Acute Renal Colic

Laryssa Patti; Stephen Leslie

Acute Renal Colic

Author: Laryssa Patti Editor: Stephen W. Leslie Updated: 12/23/2024 4:11:30 PM

Introduction

Acute renal colic is a severe and sudden flank pain that typically originates at the costovertebral angle and extends anteriorly and inferiorly toward the groin or testicle. This condition is usually caused by an acute urinary tract obstruction due to calculus and is often associated with nausea and vomiting.

Urolithiasis, commonly known as kidney stones, is a prevalent condition affecting approximately 1 in 11 individuals in the United States at some point in their lives. Urolithiasis typically occurs when a crystal or crystalline aggregate travels from the kidney through the genitourinary system, becoming lodged and obstructing urinary flow, usually in the ureter. This obstruction leads to proximal ureteral and renal pelvic dilation (hydroureteronephrosis), which is the primary cause of the intense pain known as renal colic.[1][2][3][4]

The intensity of pain is related to the degree of obstruction, rather than the size of the stone, although stone size can help predict the likelihood of spontaneous passage. Although kidney stones are not the only cause of flank pain, their prevalence and the severity of the pain they cause make ureterolithiasis the most likely presumptive diagnosis when sudden, severe flank pain occurs, particularly when associated with hematuria.

The nature, onset, location, and severity of the pain vary depending on the underlying cause. However, for most patients, the pain typically peaks 1 to 2 hours after its initial onset. Underlying causes of urolithiasis include inadequate hydration, aciduria, chronic urinary infections, hypercalciuria, hyperoxaluria, hyperuricosuria, and hypocitraturia. The initial evaluation of a patient presenting with acute renal colic involves laboratory testing, urinalysis, and appropriate imaging studies.

The immediate treatment of acute renal colic due to urolithiasis includes pain control, intravenous (IV) hydration, antiemetics, and antibiotics (if indicated). Patients with severe or refractory symptoms may require hospital observation or admission. In some cases, urgent surgical intervention is necessary, such as in obstructive pyelonephritis (pyonephrosis), where emergent drainage of the infected renal pelvis is required. Definitive treatment for obstructing ureteral stones may involve conservative or procedural approaches. Surgical options include cystoscopy with double J stenting, extracorporeal shockwave lithotripsy (ESWL), ureteroscopy with stone basketing, and laser therapy, as open surgery for ureteral stones is rarely necessary. Please see StatPearls' companion resource, "Ureterolithiasis," for more information.

Quality of life scores typically decrease as the frequency of kidney stone attacks increases. This decline is most noticeable when a patient experiences 5 or more lifetime episodes of renal colic, indicating that preventive measures, such as 24-hour urine testing, should be considered at that point, if not earlier.[5]

Etiology

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Etiology

Renal colic is caused by the dilation of the renal pelvis and ureteral segments. While colic usually results from acute obstruction, such as a ureteral calculus, it can also be caused by other issues, including ureteral spasms following double J stent removal or ureteroscopy. Chronic ureteral blockages, such as those caused by ureteropelvic junction obstructions, prostate cancer, cervical or pelvic cancer, ureteral scarring, or retroperitoneal fibrosis, typically do not result in acute pain or colic.

Several predictors and risk factors commonly associated with kidney stone formation are mentioned below.

Aciduria

Aciduria is the most common cause of uric acid stone formation, accounting for 5% to 10% of all urinary calculi. This may result from excessive intake of animal protein, renal tubular acidosis, or metabolic acidosis. Please see StatPearls' companion resources, "Metabolic Acidosis" and "Renal Tubular Acidosis," for more information. Treatment usually involves potassium citrate to achieve a sustained urinary pH of 6.5. Sodium bicarbonate may also be used, although it delivers a significant sodium load. Please see StatPearls' companion resources, "Hyperuricosuria" and "Uric Acid Nephrolithiasis," for more information.

Cystinuria

Cystinuria is an autosomal recessive genetic disorder characterized by elevated urinary cystine levels. Cystine stones are highly resistant to shockwave therapy and typically require laser therapy for effective fragmentation. Preventive measures include aggressive hydration, aiming to produce at least 3000 mL of urine daily, and urinary alkalinization to a pH of 7.5 or higher, as cystine becomes significantly more soluble in alkaline urine. Please see StatPearls' companion resource, "Cystinuria," for more information.

Hypercalciuria

Hypercalciuria, the most common chemical promoter of nephrolithiasis, is defined as urinary calcium excretion of 250 mg or more per day. This often results from increased intestinal calcium absorption, elevated renal calcium excretion (renal calcium leak), excessive vitamin D intake, hyperparathyroidism, metabolic acidosis, or idiopathic causes. Treatment strategies include moderating dietary calcium intake, normalizing vitamin D levels, correcting phosphate deficiencies (which can elevate vitamin D levels), administering oral phosphate supplements, and using thiazide diuretics to reduce renal calcium excretion. Please see StatPearls' companion resource, "Hypercalciuria," for more information.

Hyperoxaluria

Hyperoxaluria is typically defined as urinary oxalate excretion of 40 mg or more per day, with optimal levels being 25 mg/d or less. Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information. Oxalate is a potent promoter of calcium oxalate urolithiasis; therefore, reducing elevated oxalate levels is critical, particularly in patients producing calcium oxalate stones. Dietary oxalate intake should be reduced by limiting high-oxalate foods such as spinach, rhubarb, and collard greens. Taking oral calcium citrate supplementation with meals can enhance intestinal oxalate binding, reducing absorption and lowering urinary oxalate levels. Although most cases of hyperoxaluria are secondary, specific medications are available for treating primary hyperoxaluria. Please see StatPearls' companion resource, "Hyperoxaluria," for more information.

Hyperuricosuria

Hyperuricosuria, characterized by excessive urinary uric acid, contributes to the formation of both uric acid and calcium oxalate stones. Patients with calcium stones and elevated urinary uric acid levels can benefit from dietary modifications, such as reducing excessive animal protein intake, or medical management with allopurinol or febuxostat. Most uric acid stones are effectively treated with potassium citrate and urinary alkalinization. The optimal urinary uric acid level is 600 mg daily or less. Please see StatPearls' companion resources, "Hyperuricosuria" and "Uric Acid Nephrolithiasis," for more information.

Hypocitraturia

Hypocitraturia is typically defined as urinary citrate excretion of 320 mg or less per day, although this threshold does not account for factors such as urinary pH, stone composition, volume, or concentration. Clinicians are advised to prioritize achieving optimal urinary citrate concentrations of approximately 300 mg/L of urine daily. In managing aciduria or uric acid stones, urinary pH is more critical than absolute citrate levels, with an optimal target pH of 6.5 or higher. Potassium citrate is the preferred oral citrate supplement, although sodium bicarbonate may also be. Please see StatPearls' companion resources, "Uric Acid Nephrolithiasis" and "Hypocitraturia and Renal Calculi," for more information.

Relative Dehydration and Inadequate Urinary Volume

Relative dehydration and inadequate urinary volume, particularly levels below 1 L/d, significantly increase the concentration of solutes (indicated by urine osmolarity exceeding 600 mOsm/kg) and promote urinary stasis. This can result in solute supersaturation and subsequent stone formation. The optimal daily urine volume for individuals prone to kidney stones is 2500 mL, with 2000 mL as the minimum acceptable threshold.[6] Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information. The average daily urinary fluid volume in most individuals is approximately 1300 mL. Inadequate urinary fluid excretion is the most common single cause of urolithiasis.

Urinary Tract Infections

Urinary tract infections caused by urease-producing bacteria lead to ammoniagenesis and increased urinary pH, creating conditions that promote the formation of struvite (infection) or triple phosphate (magnesium, calcium, and ammonium) calculi. Staghorn stones are typically composed of this material. Treatment involves infection control and complete removal of all infected stone material. In selected cases, acetohydroxamic acid, a urease inhibitor, may be used.[6] Please see StatPearls' companion resource, "Struvite and Triple Phosphate Renal Calculi," for more information.

Epidemiology

The annual incidence of urolithiasis in North America and Europe is 0.5%. Among those diagnosed with urolithiasis, 50% will experience a recurrent stone within 10 years or less if preventive measures are not implemented.[7] According to the National Institutes of Health, approximately 6% of women and 11% of men in the United States will experience a kidney stone attack at some point in their lives. Over 1.2 million emergency department visits a year in the United States are due to acute renal colic, with about 20% of patients requiring hospital admission.[8][9]

Over the past 30 years, the global incidence of kidney stone disease has steadily increased and continues to rise.[10][11] Most kidney stones (over 70%) occur in individuals aged 20 to 50, with men being more affected than women at a ratio of approximately 2:1. However, the incidence in women is increasing.[10] Patients with obesity, hypertension, a family history of nephrolithiasis, irritable bowel syndrome, and diabetes have an increased risk of developing kidney stones.[12][13][14]

Hispanics and Blacks have a lower overall risk of kidney stones compared to Whites, who have the highest risk.[15] This difference is likely attributed to cultural dietary preferences, geographical location (warmer climates), and socioeconomic factors rather than genetic differences.[10] New stone formers have a 26% median probability of at least one additional symptomatic renal colic attack within 5 years of their initial stone event.[16] The lifetime risk of at least one other stone ranges from approximately 60% to 80%.[17]

The likelihood of a repeat episode of renal colic is increased in patients with the following risk factors:

Bariatric surgery (especially Roux-en-Y gastric bypass)
Cardiovascular disease
Chronic renal failure
Diabetes
Enteric hyperoxaluria
First stone at a younger age
History of cystine or uric acid stones
Hypertension
Malabsorption
Metabolic syndrome
Obesity
Positive family history of kidney stones
Previous renal colic episodes or kidney stone surgery
Primary hyperoxaluria
Untreated hyperparathyroidism
White ethnicity (compared to Black, Hispanic, or Asian) [18][19]

Pathophysiology

As a kidney stone moves through the renal collecting system, it can significantly disrupt urine flow in the genitourinary tract by causing either constant or intermittent obstruction and hydronephrosis of the ureter. This leads to urine backing up into the kidney, ureteral dilation, pyelolymphatic backflow, and stretching of the renal capsule, which triggers pain by releasing prostaglandins.

Intermittent obstruction often causes more prolonged discomfort and pain than constant blockage, as compensatory mechanisms can partially offset the increased ureteral intraluminal pressure. Acute ureteral obstruction leads to a decrease in the glomerular filtration rate (GFR) of the affected kidney, while increasing urine excretion by the unaffected kidney, accompanied by severe, excruciating pain.

Complete obstruction of the ureter can result in the eventual loss of renal function, with damage potentially becoming irreversible after just 1 to 2 weeks. Additionally, urinary flow obstruction for an extended interval carries the risk of renal calyx rupture, which can potentially lead to the development of a urinoma.

A kidney stone generally does not cause pain or discomfort unless it becomes infected or causes urinary obstruction. The severity of pain is determined by the degree of ureteral obstruction, not the size of the stone. Consequently, a larger stone may pass without pain, while a small 2- to 3-mm stone can cause significant discomfort. Intermittent obstruction, where the stone blocks and releases as it moves, is also possible.

Urinary calculi can become impacted at various points in the urinary tract, but they most commonly occur at the following 3 anatomical sites where the ureter is narrowest:

The ureteropelvic junction, where the renal pelvis narrows abruptly to meet the ureter.
Near the pelvic brim, where the ureter makes an acute posterior turn just distal to the iliac bifurcation.
The ureterovesical junction, the narrowest portion of the ureter, where the ureter tunnels transversely through the muscular bladder wall.

Please see StatPearls' companion resource, "Anatomy, Abdomen and Pelvis Ureter," for more information.

Pain arises from a combination of factors, including ureteral muscle spasms, increased proximal ureteral dilation, enhanced peristalsis driven by intrinsic ureteral pacemakers, localized inflammatory changes induced by the stone, renal swelling with capsular stretching, edema, and irritation. These processes activate submucosal stretch receptors in the ureter, renal pelvis, and capsule, triggering prostaglandin release, which directly causes pain. The stretching of the renal pelvis, peripelvic renal capsule, and renal calyces closely resembles the pain experienced by patients with renal colic.

The immediate effect of a newly obstructing ureteral stone is an increase in proximal intraluminal pressure, leading to distension of the renal pelvis and heightened ureteral peristalsis. Peak renal pelvic pressure from a high-grade obstruction typically occurs within 2 to 5 hours of complete ureteral obstruction.

Additional renal changes following complete ureteral obstruction include pyelolymphatic and pyelovenous backflow. Interstitial renal edema develops, significantly increasing lymphatic drainage from the affected kidney and stretching the renal capsule, which stimulates renal capsular stretch receptors and causes pain. Over time, a state of equilibrium is often achieved as proximal ureteral dilation increases, permitting some urine to bypass the obstruction. This, along with other compensatory mechanisms, typically alleviates pain and stabilizes the condition.

Pain fibers primarily travel through preganglionic sympathetic nerves and the ascending spinothalamic tracts. When the stone reaches the intramural ureter, involvement of the nervi erigentes can lead to bladder symptoms such as frequency, urgency, dysuria, hesitancy, and difficulty voiding.[20] Please see StatPearls' companion resources, "Physiology, Bladder" and "Physiology, Urination," for more information.

Renal blood flow increases for up to 90 minutes after the initial ureteral blockage before gradually diminishing. This is due to vasodilation of the afferent preglomerular arterial blood supply. Within 5 hours of the obstruction, renal blood flow and ureteral intraluminal pressures return to normal levels or even decrease further.

Renal blood flow gradually decreases over time, dropping to approximately half of the usual baseline by day 3. This decline continues over time, and by 8 weeks, renal blood flow is only 12% of its normal baseline value. Despite this, dilation and hydroureteronephrosis often persist, while ureteral peristalsis nearly disappears. By this point, renal blood flow in the contralateral kidney has increased.

Nausea and vomiting are commonly reported in more than half of patients with classic renal colic caused by acute obstructing ureteral calculi. This association arises from a shared embryological innervation pathway between the kidneys and the gastrointestinal tract, mediated by afferent fibers of the vagus nerve and the celiac axis. These symptoms can be exacerbated by the gastrointestinal adverse effects of nonsteroidal anti-inflammatory drugs (NSAIDs) and opioid medications. Notably, nausea and vomiting are not directly linked to pain intensity, as other highly painful conditions do not typically produce such adverse effects.

The severity of the pain does not reliably correlate with stone size or the likelihood of spontaneous expulsion.[21] Fortunately, acute renal colic pain is self-limited and lasts around 24 hours. Subsequently, the blocked ureter usually ceases further stretching, and it reaches equilibrium. Severe pain or other symptoms persisting for more than 3 days are likely to require surgical intervention.

Studies have identified characteristics that may help predict which patients are more likely to fail conservative management of acute renal colic. A previous history of renal colic weakly correlates with a failure of conservative treatment; however, factors such as gender, degree of hydronephrosis, initial pain level, stone size, shape, or location cannot reliably predict the need for surgical intervention.[22] Generally, the larger and more proximal the stone, the greater the likelihood that surgical intervention will eventually be required.

History and Physical

Patients with renal colic typically present with an acute onset of flank pain radiating inferiolaterally to the lower abdomen, groin, or testicle. They often describe a dull, constant discomfort, which is interspersed with colicky episodes of intense, sharp pain. The constant discomfort is usually due to the stretching of the renal capsule from obstruction, while the colicky pain results from peristalsis of the ureteral smooth muscle. Many patients report associated nausea or vomiting, and most (85%) will exhibit gross or microscopic hematuria. As the kidney stone moves distally toward the bladder, the patient may experience increasing lower urinary tract symptoms, such as dysuria, urinary frequency, urgency, or difficulty urinating.

Patients experiencing renal colic often present with severe, excruciating pain. These patients are typically unable to find a comfortable position and may be writhing or pacing constantly, in contrast to patients with an acute abdomen, who generally prefer to remain still. Please see StatPearls' companion resource, "Acute Abdomen," for more information.

The physical exam typically reveals flank pain or discomfort and may also show abdominal pain. The skin may be cool or diaphoretic. A personal or family history of kidney stones, recent ureteroscopic surgery, or removal of a double-J stent is often noted.

In cases of recent ureteroscopy or immediate post-removal of a double-J stent, the history alone can often provide the diagnosis. The pain in these instances is caused by ureteral spasm, which can mimic an obstruction and lead to proximal ureteral and renal dilation, even without a stone. While the pain can be as intense as that caused by an obstructing ureteral stone, it is typically self-limited and resolves over time. However, some patients may require a drainage procedure or the placement of a new double-J stent.

Patients taking topiramate, protease inhibitors (such as atazanavir and indinavir), acetazolamide, sulphadiazine, ephedrine, and guaifenesin are at higher risk of developing drug-related urolithiasis.[23][24][25]

Evaluation

Diagnosis relies on a comprehensive approach that includes the patient's history, physical examination, laboratory tests, and imaging studies.[7]

Urinalysis

Urinalysis reveals microscopic or gross hematuria in 85% of stone patients and should also be assessed for crystalluria, pH levels, and signs of infection (such as white blood cells [WBCs] and bacteria). A urinary pH greater than 7.5 may suggest a urease-producing bacterial infection, while a pH below 5.5 may indicate the presence of uric acid calculi. If there are signs of infection, a urine culture should be obtained. Please see StatPearls' companion resources, "Uric Acid Nephrolithiasis" and "Struvite and Triple Phosphate Renal Calculi," for more information.

Hematuria

Hematuria is present in 85% of acute renal colic cases caused by calculi.[26] While the presence of hematuria suggests a stone, it is not definitive, and its absence does not conclusively rule out the presence of a stone.[26]

Laboratory Studies

Laboratory studies should include a basic metabolic panel with serum calcium and creatinine levels to assess renal function, dehydration, acid-base status, and electrolyte balance.[7] Serum uric acid should also be checked. A complete blood count (CBC) may be considered to evaluate for leukocytosis if there is concern for infection; however, a mild elevation in WBC count (up to 15,000 WBCs per microliter) is common due to WBC demargination and is not necessarily indicative of an infection.[7][27][28]

A 24-hour urine collection for prophylactic testing should be considered for interested patients, particularly those at high risk or recurrent stone formers. However, all patients with a history of urolithiasis should be informed about this option.[7]

Parathyroid Hormone Levels

Parathyroid hormone levels should be obtained if hypercalcemia is present or if primary hyperparathyroidism is suspected. If possible, urine should be strained to capture stones for chemical analysis to help determine optimal preventive prophylactic measures.

Further metabolic testing, including a 24-hour urine collection for volume, pH, calcium, oxalate, uric acid, citrate, sodium, magnesium, and potassium concentrations, should be considered for high-risk first-time, pediatric, or recurrent stone formers. In addition, it is highly recommended for nephrolithiasis patients with solitary and transplanted kidneys, renal failure, and gastrointestinal bypass (eg, Roux-en-Y) or those at high anesthesia risk.

Renal Ultrasonography

Renal ultrasonography can assess hydronephrosis, measure the resistive index, and track larger renal stones, particularly uric acid stones. However, it may miss stones smaller than 3 mm and is not a reliable imaging modality for visualizing ureteral calculi.[29][30] The degree of perinephric fluid can help predict the extent of obstruction.[3] While it is not always possible to visualize ureteral calculi with ultrasound, identifying ureteral jets in the bladder can aid in assessing obstruction. Obstruction of the ureter typically leads to a decrease in the frequency of ureteral jets compared to the contralateral side.[29]

Ultrasound offers the advantage of not exposing patients to ionizing radiation, can visualize radiolucent stones, and can be performed quickly at the bedside by emergency department (ED) physicians or ultrasound technologists in radiology. Ultrasound is the recommended imaging modality for pregnant patients. However, if ultrasonography is inadequate or nondiagnostic, low-dose unenhanced computed tomography (CT) scanning may be considered during the second and third trimesters.[31]

Ultrasonography alone may be sufficient for diagnosis in select cases, particularly in patients with a history of recurrent ureterolithiasis.[32][33] In these instances, a flat abdominal x-ray of the kidney, ureter, and bladder (KUB) is typically recommended for tracking and follow-up. However, relying solely on ultrasound may result in incorrect management in about one-fifth of patients, as it provides insufficient information on stone size, shape, or location.[34]

Renal resistive index: As determined by ultrasound, this index is a valuable tool for diagnosing ureteral obstructions. This index is calculated as (peak systolic velocity−end diastolic velocity)/peak systolic velocity, with normal values typically being 0.7 or less. Higher values indicate either obstruction or intrinsic renal disease.[35][36][37][38][39] A high resistive index in a single kidney in a patient with renal colic on that side strongly suggests acute ureteral obstruction, such as from ureterolithiasis.[35][37][38] Medical renal disease typically results in elevated but similar resistive index levels bilaterally.

Ultrasound is the preferred modality for evaluating a pregnant patient with suspected renal colic. Studies have shown that using ultrasound as the primary imaging method does not increase complications compared to CT. Ultrasound is also effective for monitoring patients with uric acid renal calculi.[40] However, while ultrasound may be suggestive, a negative result does not definitively rule out a ureteral stone or renal colic.

Abdominal x-Ray (KUB)

A plain abdominal x-ray (KUB) can identify many stones, but 10% to 20% of renal calculi are radiolucent and not visible on plain films. The x-ray provides limited information on hydronephrosis, obstruction, or internal renal anatomy and is less useful in obese patients. Additionally, bowel gas, the bony pelvis, and abdominal organs may interfere with stone visualization.

A KUB is recommended in all kidney stone cases when an unenhanced CT scan is positive, and the exact location of the stone is known. This helps identify stones that can be tracked with follow-up KUB, potentially making them amenable to lithotripsy. The KUB also provides a more accurate depiction of the stone's shape and offers valuable surgical orientation.

Cost-Effective Imaging With Renal Ultrasound and Abdominal x-Ray (KUB)

Combining renal ultrasonography with a KUB offers a cost-effective and efficient alternative to CT scans by reducing costs, limiting radiation exposure, and maintaining good diagnostic efficacy.[40][41]

Renal ultrasound: This technique effectively demonstrates hydronephrosis, measures the resistive index to indicate obstruction, and identifies radiolucent renal calculi. However, it is less reliable for detecting ureteral calculi or stones smaller than 3 mm.

Abdominal x-ray (KUB): The KUB is sensitive for detecting urinary calcifications but cannot visualize radiolucent stones or provide information on renal function, hydronephrosis, or ureteral obstruction.

Symptomatic stones are likely to cause hydronephrosis or obstruction, be visible on ultrasound, or be directly identified on the KUB.[40][41] Combining KUB radiography with renal ultrasonography achieves a reported diagnostic accuracy of 90% for obstructing stones, with a specificity of 93% and a sensitivity of 88%.[42]

Non-Contrast or Helical Computed Tomography Scans

Unenhanced CT scans (non-contrast or helical CT) are the gold standard for diagnosing suspected renal colic, offering a sensitivity of 98%, specificity of 100%, and a negative predictive value of 97%.[43][44][45][46][47][48] This imaging modality provides rapid identification of stones, determines their location and size, and identifies associated findings such as hydroureter, hydronephrosis, or ureteral edema. Additionally, it can help detect alternative causes of pain, such as an abdominal aortic aneurysm or malignancy.[40]

CT scans are recommended for patients with acute renal colic and no prior history of nephrolithiasis to guide management. However, CT scans tend to underestimate stone size by approximately 12% compared to IV pyelography or KUB radiography.[49] CT scans using low-dose and ultra-low-dose radiation protocols are highly recommended for pediatric and pregnant patients to minimize radiation exposure while maintaining diagnostic efficacy for urolithiasis detection.[50][51][52][53] Low-dose CT delivers approximately half the radiation of a standard scan, and ultra-low-dose protocols further reduce exposure by an additional 55%.[50][51][54][55] The positive predictive value of low-dose CT in these cases is 95.8%.[56][57]

While most urinary stones, including the relatively radiolucent cystine, dihydroxyadenine, xanthine, and uric acid calculi, are visible on CT scans, some stone compositions may not be detected. These include stones formed from antiviral protease inhibitors and their metabolites,[58][59] such as atazanavir and indinavir.[60][61][62][63][64][65] A contrast study is required when these stones are suspected.[59][64] However, CT scans expose patients to significant radiation and can be costly.

In some patients with a history of renal colic who present with pain similar to previous episodes of obstructing urolithiasis, ultrasonography may be sufficient. Although ultrasound is less sensitive (60% to 76%) than CT for detecting calculi smaller than 5 mm, it can reliably identify hydronephrosis and other signs of ureteral obstruction, such as an increased resistive index in the affected kidney and unilateral blocked ureteral jets. If the stone passes before imaging can be performed, residual inflammation may still be present and identifiable, such as hydronephrosis, stranding, or pain, even if no stone is specifically or definitively identified.

The American College of Obstetricians and Gynecologists (ACOG) and the American Urological Association (AUA) now support the selective and judicious use of low-dose, non-contrast CT imaging during pregnancy in cases where ultrasound is diagnostically insufficient.[56][66]

Magnetic Resonance Pyrography

Magnetic resonance pyelography has a lower positive predictive value (80%) for identifying urinary stones compared to CT, but it does not use ionizing radiation. Magnetic resonance urography may be indicated for patients who have a contraindication to ionizing radiation but an inadequate ultrasound evaluation for urinary stones. [56][57][67][68] The European Association of Urology (EAU) recommends it as a second-line imaging modality after ultrasound in equivocal clinical situations. This offers an alternative to ureteroscopic surgery and provides a safer option than CT scanning during pregnancy.[56][67][68]

Ureteroscopic Surgery

Ureteroscopic surgery with laser lithotripsy and double J stent placement is a reasonable option when the clinical presentation strongly suggests urolithiasis, especially if symptoms such as pain are prolonged or difficult to control.[56] Ureteroscopic surgery can be safely performed in pregnant patients with urolithiasis, yielding good outcomes and a negative ureteroscopy rate of only 14%.[57][69][70][71]

Urosepsis

Urosepsis is a potentially life-threatening organ dysfunction caused by a dysregulated host response to an infection originating from a urological source.[72][73] Urosepsis is characterized by symptoms such as hypotension, tachycardia (>90 beats/min), tachypnea (>20 breaths/min), pyuria, and leukocytosis (>12,000/μL [12 × 10⁹/L]).[74] Mild leukocytosis, up to 15,000/μL (15 × 10⁹/L), can be common in acute renal colic without infection.[7][27][28] Acidosis (serum pH <7.35) may also be present.[75]

Patients with renal colic who also have a fever of 100°F (37.8°C) or higher, significant leukocytosis (>15,000 WBCs/mm³), pyuria, hypotension, or unexplained tachycardia should be considered at risk for urosepsis and obstructive pyelonephritis, especially if they have diabetes. Please see StatPearls' companion resource, "Urosepsis," for more information. The recommended treatment for patients with acute renal colic caused by an obstructing ureteral stone and signs of systemic infection, sepsis, or obstructive pyelonephritis is urgent drainage of the renal pelvis, either through cystoscopy with double J stenting or via percutaneous nephrostomy. Please see StatPearls' companion resource, "Complicated Urinary Tract Infections," for more information.

As it is not possible to clinically distinguish acute pyelonephritis from obstructive pyelonephritis, imaging is necessary when the diagnosis is uncertain, especially in diabetic patients or those at increased surgical or anesthesia risk. Ultrasonography is typically sufficient for this purpose, but an unenhanced CT scan may be considered definitive if the results are uncertain or equivocal. Various urosepsis serum biomarkers have significant potential to identify septic patients earlier.[76] Please see StatPearls' companion resources, "Urosepsis," "Bacterial Sepsis," and "Laboratory Evaluation of Sepsis," for more information.

Urosepsis biomarkers for early diagnosis: The selection of biomarkers for diagnosing early urosepsis depends on factors such as cost, test availability, and physician familiarity with interpreting laboratory results. Below is a review of some clinically useful serum biomarkers.

C-reactive protein: C-reactive protein (CRP) is an inexpensive and readily available laboratory indicator of infection and inflammation. CRP is slower to react to bacterial sepsis than procalcitonin, and it is not specific for bacterial infections. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[77][78]
- CRP is produced in the liver when serum interleukin-6 (IL-6) is stimulated.[78]
- The serum concentration of CRP begins to increase 6 hours after the initial inflammatory event, doubling every 8 hours, and peaks by 36 to 50 hours, approximately twice as long as procalcitonin.[78][79][80]
- A commonly used cutoff level of 50 mg/L is used to identify bacterial sepsis.[77]
- The half-life of CRP is 19 hours.[81]

Please see StatPearls' companion resource, "C Reactive Protein," for more information.

Interleukin-6: IL-6 may be a more effective biomarker for tracking disease progression than procalcitonin, lactic acid, or CRP.[82][83][84][85]
- IL-6 is a proinflammatory cytokine intimately involved in host defense mechanisms and has been proposed as a laboratory biomarker for sepsis.[86]
- IL-6 is produced by immune and stromal cells, including endothelial cells, fibroblasts, endothelial cells, macrophages, monocytes, and T-lymphocytes.[83][87][88]
- A threshold level of 52.6 pg/mL or higher has been suggested for identifying sepsis.[83]
- IL-6 levels peak at around 12 hours, with a half-life of about 1 hour.[89][90]

Lactic acid (lactate): Lactic acid (lactate) levels in the serum are normally less than 2 mmol/L (18.2 mg/dL). Elevated levels indicate infection, and levels exceeding 4 mmol/L (36.4 mg/dL) are considered severe, often suggesting sepsis, particularly if they increase rapidly. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[91]
- Serum lactic acid levels reflect relative tissue hypoxia, but recent research suggests they also represent an adaptive chemical response to abnormal metabolism and serve as a marker of elevated endogenous catecholamine levels. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[92]
- A reduction in lactic acid levels is a good indicator of tissue recovery.[92]
- If lactate is initially elevated, a repeat measurement in 6 hours is recommended,[93] with some guidelines suggesting rechecking levels every 2 hours for critically ill patients initially.[94]
- Lactate and lactic acid levels are similar but not chemically equivalent, so the normal ranges in the specific laboratory should be verified. The half-life of serum lactate is approximately 20 minutes.

Neutrophil-to-lymphocyte ratio: The neutrophil-to-lymphocyte (NLR) ratio is more elevated in patients with worsening sepsis and is also higher in older individuals.[95]
- Normal and abnormal thresholds for NLR have not been conclusively defined, but levels above 3.75 to 4 are commonly associated with sepsis and urosepsis.[95]
- This test has the advantages of being inexpensive, readily available, easily calculated, and immediately available.[95][96][97][98]

Pentraxin-3: Pentraxin-3 (PTX3) is an inflammatory serum protein produced early in the inflammatory process by various cell types.
- PTX3 activates the complement immune system pathway, dendritic cells, and macrophages.
- The protein also promotes the identification of pathogenic bacteria and serves as an antibody precursor.[84][99][100]
- Several studies suggest that PTX3 could be a useful laboratory marker for sepsis and a prognostic indicator, comparable to IL-6.[83][84][101][102][103][104]
- PTX3 has a relatively short half-life of 1 to 4 hours.[105][106]

Procalcitonin: Procalcitonin is a precursor of calcitonin and is a valuable marker for assessing the severity of bacterial infections and monitoring disease progression. Please see StatPearls' companion resource, "Laboratory Evaluation of Sepsis," for more information.[92][107]
- Procalcitonin correlates well with the degree of leukocytosis and CRP levels for infection monitoring.[77][107]
- Procalcitonin is considered superior to CRP as a sepsis marker because it is more specific to bacterial infections; it rises earlier (peaking at 6-12 hours) and normalizes faster. Please see StatPearls' companion resource, "Procalcitonin," for more information.[107][108]
- Normal procalcitonin levels are typically below 0.1 μg/L, although patients with renal failure may have higher baseline levels.[107][109]
- A low or normal procalcitonin level does not completely rule out a bacterial infection. Please see StatPearls' companion resource, "Procalcitonin," for more information.[107]
- Procalcitonin has a half-life of about 24 hours.[107] Please see StatPearls' companion resource, "Procalcitonin," for more information.[107]

Considerations for the Evaluation of Renal Colic in Pregnancy

Pregnancy can complicate the diagnosis and management of renal colic. The pressure from the gravid uterus on surrounding structures can alter the flow of urine from the renal pelvis to the urinary bladder. Additionally, pregnant patients may excrete higher levels of calcium in their urine.[110]

Ultrasound is the preferred first-line study for evaluating renal colic in pregnancy, as it poses no risk of ionizing radiation. However, the results may be nondiagnostic or equivocal.[56] Options for management include conservative measures and observation, low-dose CT imaging, magnetic resonance urography, or ureteroscopic surgery. Ureteroscopic surgery can be safely performed in pregnant patients with urolithiasis, with good outcomes and a negative ureteroscopy rate of only 14%.[57][69][70][71]

Placement of a double J stent or performing a percutaneous nephrostomy is a less invasive method to temporize the clinical situation until after delivery, allowing more definitive diagnostic and therapeutic measures to be safely performed without jeopardizing the pregnancy.

Surgical intervention is more likely and typically performed earlier in pregnant patients with acute renal colic who present with the following conditions:

Anterior-posterior diameter of the renal pelvis of greater than 18 mm
Abnormal ureteral anatomy
Continuous pain lasting 4 or more days
Difficulty controlling pain
Elevated serum creatinine levels
Extrarenal pelvis
Fever
Elevated leukocytosis
High stone density (>700 Hounsfield units)
High serum CRP levels
Higher degree of hydronephrosis
Higher NLR
Increased fetal body weight
Larger (≥8 mm) ureteral calculi
Multiple previous stone surgical procedures
Stone volume of 0.2 cc or more
Ureteral stone length of 9 mm or more
Ureteral wall thickness of more than 2 mm [111][112][113]

Patients diagnosed with kidney stones during pregnancy should have close obstetrical follow-up, as those admitted for renal colic are at up to a 2-fold increased risk of preterm labor. This may be mediated by oxytocin release in response to maternal dehydration caused by nausea and vomiting.[114]

Treatment / Management

Management of Acute Renal Colic Symptoms

Immediate management includes providing adequate analgesia, antiemetics, and IV hydration. Antibiotics should be administered if the patient presents with systemic signs of infection or has infected urine. NSAIDs and opioids are considered first-line therapies for analgesia.

Nonsteroidal anti-inflammatory drugs: NSAIDs are typically the first-line treatment for pain relief, as they are often as effective as, or even more effective than, opioids, while avoiding the complications associated with opioid usage.[115][116][117][118][119][120] These medications reduce the production of arachidonic acid metabolites, which mediate pain receptor activation, thereby alleviating pain caused by renal capsule distension. Additionally, NSAIDs inhibit prostaglandin production, further decreasing pain receptor activity and reducing ureteral contractions. However, this inhibition may result in some degree of platelet dysfunction. Please see StatPearls' companion resources, "Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)" and "Ketorolac," for more information. (A1)

Additionally, NSAIDs induce contraction of the efferent arterioles of the glomerulus, lowering the GFR and reducing hydrostatic pressure across the glomerulus. As patients with renal colic often cannot tolerate oral medications, parenteral options such as ketorolac (15-30 mg IV or intramuscular [IM]) or diclofenac (37.5 mg IV) are commonly used.[121][122][115] Please see StatPearls' companion resources, "Ketorolac" and "Diclofenac," for more information.(A1)

Ketorolac, an injectable NSAID commonly used for renal colic, is generally considered equivalent to or superior to opioids in treating acute ureterolithiasis pain while being safer with fewer significant adverse effects.[115][116][117][123] As a result, ketorolac and similar NSAIDs are typically preferred for the initial management of pain in acute renal colic. Ketorolac can also be administered as a continuous IV infusion, usually at a rate of 3 to 5 mg/h.[124][125][126][127] Please see StatPearls' companion resources, "Ketorolac" and "Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)," for more information.(A1)

Ketorolac may be used in combination with IV acetaminophen, although this is generally not recommended for more than a few days, despite no specific negative interactions being noted. No published data support the efficacy of this combination for treating renal colic. Ketorolac (an FDA pregnancy category C drug) is contraindicated in patients with renal failure (GFR <30 mL/min), a history of gastrointestinal bleeding, an allergy to aspirin or NSAIDs, or in pregnant women. Please see StatPearls' companion resource, "Ketorolac," for more information.

Additional steroidal medications, such as dexamethasone (8 mg IV), have been shown to improve pain relief in renal colic patients compared to ketorolac alone.[117][128] (A1)

Opioid pain medications: Opioids such as morphine sulfate (0.1 mg/kg IV or IM) or hydromorphone (0.02 mg/kg IV or IM) can be effective for analgesia, particularly when other treatments, such as ketorolac, have failed or their maximum dose is insufficient. Please see StatPearls' companion resources, "Morphine" and "Hydromorphone," for more information. However, opioids carry risks of respiratory depression, reduced gastrointestinal motility, nausea, sedation, and dependence with prolonged use. There is also a risk of dependence associated with prolonged opiate use.[129] Please see StatPearls' companion resources, "Opioid Withdrawal" and "Opioid Use Disorder," for more information. The administration of IV morphine following ketorolac has demonstrated effectiveness in providing additional analgesia for patients with inadequate pain relief.[117](B2)

Intravenous acetaminophen: IV acetaminophen has shown comparable effectiveness to ketorolac in a meta-analysis. However, the available data are insufficient to recommend it over standard analgesics. IV acetaminophen can be safely used in combination with NSAIDs and opioids.[130][131]

Intravenous lidocaine: IV lidocaine has been used effectively for pain relief in acute renal colic, with positive results reported.[132][133][134] The standard protocol involves injecting 100 to 120 mg of lidocaine in 100 mL of normal saline IV over 10 minutes. The drug is particularly effective for intractable renal colic unresponsive to standard therapy, typically providing relief within 3 to 5 minutes. No adverse events have been reported.[135] (A1)

The benefit of adding lidocaine to patients who have already received ketorolac remains unclear, as studies on this are conflicting. However, salvage therapy with lidocaine has also been reported in some cases.[136]

Intradermal sterile water injection therapy: This has proven effective in relieving the pain of acute renal colic, showing results roughly equivalent to NSAIDs.[137][138][139][140][141][142][143] Pain relief is not achieved when normal saline is used in place of sterile water. The injections are administered directly into the flank at the point of greatest tenderness. The mechanism underlying this surprising result remains unclear. However, most experts suggest it involves diffuse noxious inhibitory control or a pain-gating mechanism.[142][144] In addition, it may also produce localized inflammation, triggering the cutaneous A-afferents, leading to endorphin release or working through physiological distraction.[144][145] (A1)

The technique is simple, safe, inexpensive, and free of significant adverse effects, with the option for repetition as needed. This does not interfere with other pain management methods. Therefore, intradermal water injection therapy shows promise and warrants further investigation for potential clinical use in managing acute renal colic pain.

Antiemetics: Antiemetics should be used as needed for symptomatic relief in patients with acute renal colic. Data regarding the relative effectiveness of antiemetic drugs for controlling nausea and vomiting are limited in these patients. Please see StatPearls' companion resource, "Antiemetic Medications," for more information. Limited studies suggest that ondansetron (4-8 mg IV or PO) may be the preferred drug in these situations. Please see StatPearls' companion resource, "Antiemetics, Selective 5-HT3 Antagonists," for more information.[146][147] The use of additional agents to optimize symptom relief when ondansetron alone is insufficient remains unclear. Please see StatPearls' companion resource, "Ondansetron," for more information.

Intravenous fluid hydration: Intravenous fluid hydration is recommended as an adjunct to the initial treatment of acute renal colic. Although no evidence suggests that empiric fluids can help "flush out" a stone, many patients who are dehydrated due to decreased oral intake, nausea, or vomiting benefit from supplemental IV hydration.

Nerve blocks: Nerve blocks can be beneficial, particularly in cases of chronic flank pain.[148] An anesthetic injection is typically administered near the 11th or 12th intercostal nerve area. The reported efficacy of nerve blocks suggests a musculoskeletal or neuropathic etiology. Paravertebral, splanchnic, and intercostal nerve blocks have all demonstrated varying degrees of effectiveness in relieving flank pain.[149][150][151](B3)

Reported randomized clinical trials of alternative analgesic agents: Reported randomized clinical trials of alternative analgesic agents for pain relief in acute renal colic often use morphine and other opioid-based medications as rescue drugs, complicating the assessment of their reported relative effectiveness.[152] Future randomized controlled studies should define therapeutic success as achieving total or near-total pain relief rather than relying on unquantified pain relief.[152](A1)

Kidney stone prophylaxis: Kidney stone prophylaxis through 24-hour urine testing should be considered for all urolithiasis patients, particularly those at high risk or with recurrent stones. This includes patients with solitary or horseshoe kidneys, renal failure, abnormal ureteral anatomy, pediatric patients, cystine stone formers, and those with high surgery or anesthesia risks. The success of 24-hour urine testing largely depends on the patient's commitment to long-term treatment recommendations and dietary modifications.

The AUA guidelines recommend informing even first-time stone formers about 24-hour urine testing and prophylactic therapy.[7] Comprehensive guidelines for interpreting 24-hour urine tests and optimizing treatment selection are available for free download. Calcium loading tests for patients with hypercalciuria are no longer recommended. Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information.[7][153][154]

Behavior modification, dietary adjustments, and general urolithiasis prevention strategies should be discussed with all kidney stone patients. Common recommendations include:

Patients are advised to increase fluid intake to optimize urine output, aiming for at least 2000 mL, with an optimal goal of 2500 mL of urine daily.
Patients with calcium stones and elevated urine calcium should limit sodium and meat protein intake while maintaining a moderate calcium intake of 1000 to 1200 mg daily.
Thiazide diuretics and a salt-restricted diet are recommended for those with high urinary calcium to reduce the amount of urinary calcium.
Individuals with calcium stones and low urinary citrate, or those with uric acid stones and high urinary uric acid, should increase their intake of fruits and vegetables while reducing their intake of nondairy animal protein.
Uric acid stone formers are typically treated with potassium citrate (a urinary alkalinizer) to achieve an optimal urinary pH of 6.5 or higher.
Hyperuricosuric calcium stone formers may benefit from allopurinol or febuxostat.
Patients with hyperoxaluria should be encouraged to reduce their intake of oxalate-rich foods (eg, spinach, nuts, chocolates, and green leafy vegetables), maintain a moderate calcium intake, or use calcium citrate supplementation with meals high in oxalates (usually lunch and dinner), and increase their fluid intake.
Cystine stone formers require significant urine volumes of 3000 mL or more daily, along with a urine pH of 7.5 or higher, to optimize cystine solubility. Potassium citrate is the preferred urinary alkalinizer, and tiopronin or other thiol medications can help lower urinary cystine levels.[6]

Please see StatPearls' companion resources, "Hyperuricosuria," "Hypercalciuria," "Hyperoxaluria," "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," "Hypocitraturia and Renal Calculi," "Struvite and Triple Phosphate Renal Calculi," and "Uric Acid Nephrolithiasis," for more information.

Treatment of Ureterolithiasis

Medical expulsive therapy: This is generally recommended, particularly for smaller stones in the distal ureter.[7][48] Alpha-1 adrenergic receptors are found in increasing concentrations in the distal ureter, and blocking these receptors with alpha-blocking medications (such as tamsulosin, alfuzosin, nifedipine, and silodosin) may assist in the expulsion of the stone by relaxing and dilating the distal ureter.[48][155][156][157][158][159][160][161]. However, data from randomized controlled trials regarding the effectiveness of these medications in improving spontaneous stone passage rates are somewhat mixed.[47][48][155][162](A1)

The consensus opinion and the recommendation from the AUA guidelines indicate that medical expulsive therapy is helpful for smaller stones in the lower or distal ureter and is generally recommended. However, such treatment will likely have limited benefits for larger stones in the proximal ureter.[47][155][163][164][165][166][167](A1)

Tamsulosin: This is the most frequently used agent, typically prescribed at a dose of 0.4 mg orally daily. While alfuzosin and tamsulosin were found to be roughly comparable, nifedipine appeared to be less effective overall than other agents used for medical expulsive therapy.[161]

(A1)

Mirabegron: This is a beta-3 adrenoceptor agonist usually used for bladder overactivity and has shown a beneficial effect on facilitating spontaneous ureteral stone passage. A recent systematic review and meta-analysis of randomized controlled trials found that the drug improved the spontaneous expulsion rate of ureteral calculi, particularly for smaller stones (less than 6 mm) located in the distal ureter.[168][169] However, mirabegron did not reduce the time for spontaneous expulsion or help with pain management.[169] Data on using mirabegron with alpha-blocker medications for medical expulsive therapy of ureteral calculi are unavailable.

(A1)

Tadalafil: This has been suggested as an agent for medical expulsive therapy, but the results of studies are conflicting, and it cannot be recommended as a standalone treatment.[170][171][172][173]

(A1)

Silodosin: This has been shown to be superior to both tamsulosin and alfuzosin in several recent systematic reviews, comparisons, and meta-analyses of agents used for medical expulsive therapy.[156][174][175][176] If silodosin is selected for medical expulsive therapy, the higher dose (8 mg) is recommended, as the 4 mg dose has been shown to be inferior, with reduced expulsion rates and increased pain.[177]

(A1)

Various combinations of medical expulsive drugs have been studied, such as tadalafil with either tamsulosin or silodosin, which appeared to be somewhat more effective than single agents or other combinations.[178][179] However, further high-quality studies are needed to determine the relative efficacy and optimal composition of such combination treatments for medical expulsive therapy of ureteral calculi.[178](A1)

Antibiotics: Antibiotic use in patients with acute renal colic should generally be reserved for patients with acute renal colic who have clinical or laboratory evidence of a urinary tract infection. A microscopic urinalysis showing at least 10 WBCs per high-power field (HPF) (or more WBCs than RBCs), bacteriuria, or positive nitrites on the urine dipstick would indicate the need for antibiotics.

Systemic signs of infection include leukocytosis, fever, tachycardia, lactic acidosis, elevated procalcitonin, or other indicators of a possible urinary or systemic infection. Notably, patients with kidney stones may initially appear stable with typical vital signs but can rapidly develop urosepsis from obstructive pyelonephritis, becoming critically ill within hours. High-risk patients include older adults (who may not show signs of infection until sepsis is advanced), those with diabetes, those with solitary kidneys, and those with a history of urinary tract infections or who are immunocompromised.

While inappropriate, unjustified, and excessive antibiotic use is discouraged, consideration should be given to administering antimicrobials in high-risk individuals, particularly those with diabetes presenting with acute renal colic who are not yet septic. Some of these patients may later develop urosepsis and obstructive pyelonephritis.

Definitive surgical management of impacted ureteral stones: Definitive surgical management can be achieved through several procedures, including ESWL, which uses high-energy shock waves to fragment stones, ureteroscopy with stone basketing, laser or electrohydraulic stone fragmentation, or, in rare cases, open surgery.[47] Please see StatPearls' companion resources, "Ureterolithiasis," "Extracorporeal Shockwave Lithotripsy," and "Ureteroscopy," for more information.

Laparoscopic and robotic surgery are alternative procedural options, typically reserved for complex or unusual clinical situations.[180][181][182] In the presence of infection, a double J stent or percutaneous nephrostomy may be used to facilitate urinary drainage of the affected renal unit, with definitive stone therapy deferred until the infection has resolved.[47][183][184](A1)

Indications for Surgical Intervention in Ureterolithiasis

The indications for surgical intervention in ureterolithiasis causing renal colic depend on the following factors:

Evidence of worsening kidney failure or renal damage from prolonged obstruction.
Failure to pass ureteral stones after 4 to 6 weeks, with or without medical expulsive therapy.
Intractable or persistent pain, nausea, or vomiting lasting more than 3 days.
New onset of anuria that coincides with the ureteral obstruction.
Likely or suspected obstructive pyelonephritis (pyonephrosis).
Patient preference for intervention.
Pregnant patients who have not responded to conservative management.
Recurrent urinary tract infections related to the stone disease.
The stone's size, shape, and position significantly influence the likelihood of spontaneous passage, as mentioned below.
- Larger, angular-shaped, and proximal ureteral calculi are less likely to pass spontaneously without intervention.
- Stones larger than 10 mm will generally require surgery.
- Stones exceeding 7 mm are much less likely to pass spontaneously and often necessitate surgery.
- Stones 4 mm or smaller have a 90% to 95% spontaneous passage rate and rarely require a procedure.
Solitary kidney or simultaneous, bilateral ureteral obstruction.
Presence of a urinary tract infection, where drainage procedures are performed until the infection is resolved.[47][185][186][187]

(B3)

Double J stent placement: Double J stent placement can promptly relieve pain and symptoms associated with ureteral obstruction, facilitate drainage of an infected renal unit until the infection is resolved, and dilate the ureter to aid subsequent ureteroscopy. However, routine preoperative use is generally discouraged unless infection is present, as it involves additional anesthesia and operating room procedures.

Obstructive pyelonephritis or pyonephrosis: Obstructive pyelonephritis or pyonephrosis is a potentially life-threatening condition in which an obstructed kidney, caused by a ureteral or renal calculus, becomes infected, leading to progressive urosepsis. Prompt surgical drainage of the renal pelvis is essential, as antibiotics alone are insufficient to resolve the condition.[183][188][189][190][191] Please see StatPearls' companion resource, "Complicated Urinary Tract Infections," for more information. Mortality from obstructive pyelonephritis remains significant, reported to be as high as 7.4%, even with treatment.(B2)

The standard technique for draining the renal pelvis is placing a double J stent cystoscopically. However, a general anesthetic is needed. The procedure also requires manipulating a guide wire and stent past the obstructive stone, and it may not be successful in every case. Please see Statpearls' companion resource, "Double J Placement Methods Comparative Analysis," for more information.

If the ureteral obstruction is significant or the patient is critically ill and too unstable for general anesthesia, percutaneous nephrostomy is the preferred method for renal drainage. This approach requires only minimal sedation and local anesthesia, minimizes manipulation of the infected renal unit, and eliminates the risk of unsuccessful bypass with a double J stent.[192][193][194][195][196][197][198] Details on the technique for percutaneous nephrostomy are available in other resources.[196][197] Please see StatPearls' companion resource, "Percutaneous Nephrostomy," for more information.(A1)

Delays in the surgical decompression of obstructive pyelonephritis can increase the risk of death by approximately 30%.[199][200] These delays were often associated with minority patient populations, lower socioeconomic status, and weekend presentations, highlighting critical areas for improvement.[199] Delaying treatment, especially postponing drainage procedures beyond 2 days, significantly increases morbidity and mortality.[200]

Evidence suggests that third-generation cephalosporins may be the preferred antibiotics in these cases, although surgical intervention remains the primary treatment.[201] Most patients with obstructive pyelonephritis who undergo timely drainage can safely proceed with definitive ureterolithiasis surgery within 1 to 2 weeks.[202]

Risk Factors for Obstructive Pyelonephritis in Ureterolithiasis

Risk factors for developing obstructive pyelonephritis in patients with ureterolithiasis include:

Greater degree of hydronephrosis
Diabetes
Elevated CRP, lactic acid, procalcitonin, or NLR levels
Increasing patient age
Lower serum albumin
Perinephric fat stranding on imaging
Positive nitrites on urinalysis
Pyuria
Renal failure
Size of obstructing stone larger than 5 mm
Thrombocytopenia [203][204][205][206][207][208][209]

(B2)

Differential Diagnosis

Numerous conditions can cause flank pain that may simulate renal colic, including:

Abdominal aortic aneurysm dissection
Acute mesenteric ischemia
Angiomyolipomas
Appendicitis
Biliary colic
Bowel obstruction
Cholecystitis
Costochondritis
Dietl crisis
Diverticulitis
Double J stenting or removal
Ectopic pregnancy
Endometriosis
Focal nephronia
Hepatitis
Herpes zoster
Iliac aneurysms
Irritable bowel syndrome
Lobar pneumonia
Local mass or growth
Neurological disorders and neuropathic pain
Nutcracker syndrome
Musculoskeletal conditions
Ovarian cyst torsion
Pancreatitis
Papillary necrosis
Pelvic pain syndrome
Perinephric abscess
Peritonitis
Pleural pain
Polycystic kidney disease
Post-ureteroscopy
Prostatitis
Pyelonephritis
Referred pain from the back
Renal abscess
Renal hematoma
Renal infarct
Renal neoplasm
Renal vein thrombosis
Renovascular compromise
Retroperitoneal disorders
Retroperitoneal fibrosis
Spinal disc disorders
Spinal tumor or fracture
Splenic infarction
Ureteral compression (iatrogenic, neoplasms, and scarring)
Ureteral spasms
Ureteral stricture
Ureteroceles
Ureteropelvic junction obstruction
Urinary tract infection
Wunderlich syndrome (a rare condition with spontaneous renal subcapsular and/or retroperitoneal bleeding and hematoma formation)

Prognosis

The prognosis depends on the clinical situation, stone size and location, the patient’s anatomy, clinical history, and comorbidities. Smaller stones (<5 mm) located in the distal ureter are highly likely to pass spontaneously. However, the larger the stone size and the more proximal its location in the ureter, the less likely it is to pass without intervention. If the kidney becomes infected, urgent surgical intervention to drain the renal pelvis may be necessary to prevent urosepsis, embolic ischemia, limb amputations, and death.

All patients with urinary calculi should be provided information about 24-hour urine testing for prophylactic treatment. This testing is especially recommended for children, patients with renal failure, solitary kidneys, recurrent stone formers, or those at high surgical or anesthetic risk.

Complications

Possible complications include:

Embolic ischemia
Failure of spontaneous stone passage
Forniceal (calyceal) rupture with extravasation
Hematuria
Intractable pain, nausea, or vomiting
Obstructive pyelonephritis (pyonephrosis)
Pyelolymphatic backflow
Renal failure or damage
Sepsis
Ureteral scarring or stricture
Urinary tract infection

Deterrence and Patient Education

Patients should be informed about the possibility of identifying chemical risk factors for future stone formation through a 24-hour urine test. The analysis of these results can guide specific recommendations regarding dietary changes, lifestyle modifications, or medications to help reduce the risk of additional stones, although prevention is not always guaranteed.

Testing is recommended for high-risk individuals, including those with significant comorbidities, solitary or horseshoe kidneys, recurrent stone formation, children, and patients with elevated surgical or anesthetic risks. The effectiveness of the preventive therapy program largely depends on patient motivation and discipline. Patients who are committed to minimizing their risk of future stones will benefit the most, as long-term compliance with the treatment is essential.

Even without specific testing, general recommendations include increasing fluid intake to produce at least 2000 mL of urine daily, with an optimal goal of 2500 mL. Calcium intake should be moderate, as both insufficient and excessive amounts are discouraged. Dietary adjustments should include reducing excessive sodium, animal protein, and high-oxalate foods.

Patients with cystine stones face a significantly high risk of recurrence and require specialized treatment to remain stone-free. Prophylactic measures include maintaining aggressive hydration to produce 3000 to 3500 mL of urine daily and alkalinizing the urine to achieve a pH of 7.5. Please see StatPearls' companion resource, "Cystinuria," for more information.

Pearls and Other Issues

The size and location of the calculus, along with the patient's level of discomfort, help predict the likelihood of spontaneous stone passage. About 90% of stones smaller than 5 mm pass within 4 weeks, while up to 95% of stones larger than 8 mm are likely to become impacted and require intervention.

Hospital admission is indicated for significant renal stones in a solitary kidney, severe kidney injury, infected renal stones, intractable pain or nausea, urinary extravasation, or sepsis.

Patients with infected stones (eg, nephrolithiasis accompanied by evidence of a urinary tract infection) require urgent and specialized treatment. The infected stone is a nidus for infection, leading to urinary stasis and impairing the body's ability to manage the infection. In many cases, these stones must be completely removed through surgery to prevent recurrent infections and the formation of new stones.

As it is not possible to clinically differentiate acute pyelonephritis (a medical condition treated with antibiotics) from pyonephrosis (obstructive pyelonephritis), a potentially life-threatening condition requiring urgent surgical intervention and drainage, imaging is essential in nearly all cases of acute flank pain. This is particularly important if patients admitted for pyelonephritis do not improve with medical therapy.

Ultrasound may be sufficient but is not always definitive. If the results are equivocal, insufficient, or negative, a non-contrast CT may be necessary, as obstructive pyelonephritis can still be present even with a routine renal ultrasound.

Intervention is recommended for a stone that has not moved or passed after 4 to 6 weeks, even if the patient remains asymptomatic. This is due to the risk of ureteral scarring and other complications. Convincing an asymptomatic patient to undergo surgery can be challenging, but explaining the need for the procedure early in the course of treatment can be effective. This allows patients to understand that the procedure is necessary to protect the kidneys and ureters from permanent damage if a stone or obstruction is stuck and not resolving on its own.

An infected kidney or urinary tract infection with obstructing ureterolithiasis is considered an urgent surgical emergency. Please see StatPearls' companion resource, "Complicated Urinary Tract Infections," for more information.[188][189][190] In the most serious cases or when there is a significant ureteral stone burden, percutaneous renal drainage is preferred over double J stents.[192][193][194][195]

All stone material should be collected and sent for chemical analysis. Urine tests collected over a 24-hour period are essential for long-term preventive therapy but require high levels of patient dedication and compliance for success. Despite this, they should be offered to all patients with nephrolithiasis.

24-Hour urine testing is particularly recommended in the following situations:

Abnormal urinary tract anatomy
Chronic diarrhea
Family history of nephrolithiasis
First stone before or at age 21
High anesthesia or surgical risk
Irritable bowel syndrome
Morbid obesity
Nephrocalcinosis
Preexisting renal failure
Prior ureteral or urinary stone surgery
Stone composition primarily other than calcium oxalate or struvite (cystine, calcium phosphate, and uric acid)
Recurrent urinary tract infections
Recurrent urolithiasis
Reimplanted ureter(s)
Renal failure (GFR<60 mL/min due to obstructive calculi)
Solitary kidney
Underlying predisposing condition (eg, bypass surgery, short-bowel syndrome, and enteric hyperoxaluria)
Ureteropelvic junction obstruction

Please see StatPearls' companion resource, "24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines," for more information.[210]

Enhancing Healthcare Team Outcomes

The management of renal stones is most effective when conducted by an interprofessional healthcare team, which includes a nephrologist, ED physician, radiologist, urologist, dietitian or nutritionist, and primary care provider. Although most renal stones will pass spontaneously within 4 weeks, stones larger than 7 mm may require surgical intervention. Stones measuring 10 mm or larger typically necessitate surgery.

Healthcare providers, including nurse practitioners who treat patients with kidney stones, should consult with a urologist when ureteral stones fail to pass after 4 to 6 weeks, with or without medical expulsive therapy. Urologic nurses play a key role in treatment by monitoring patients, offering ongoing support and education, and updating the team on any changes in patient status. Pharmacists ensure prescribed medications are dosed appropriately, check for potential drug interactions, and provide patient education.

Ethical considerations are crucial when determining treatment options and respecting patient autonomy in decision-making. Responsibilities within the interprofessional team of healthcare providers should be clearly defined, with each member contributing their specialized knowledge and skills to optimize patient care. Effective interprofessional communication fosters a collaborative environment where information is shared, questions are encouraged, and concerns are addressed promptly.

Lastly, care coordination is essential to ensure seamless and efficient patient care. Physicians, advanced practitioners, nurses, pharmacists, and other healthcare professionals must collaborate to streamline the patient's journey from diagnosis through treatment and follow-up. This coordination minimizes errors, reduces delays, and enhances patient safety, ultimately leading to improved outcomes and patient-centered care that prioritizes the well-being and satisfaction of individuals affected by nephrolithiasis.

References

[1]

Ganti S, Sohil P. Renal Colic: A Red Herring for Mucocele of the Appendiceal Stump. Case reports in emergency medicine. 2018:2018():2502183. doi: 10.1155/2018/2502183. Epub 2018 Dec 6 [PubMed PMID: 30631605]

Level 3 (low-level) evidence

[2]

Kutilek S, Plasilova I, Chrobok V. Two Different Causes of Paediatric Hypercalcaemia. Sultan Qaboos University medical journal. 2018 Aug:18(3):e389-e392. doi: 10.18295/squmj.2018.18.03.022. Epub 2018 Dec 19 [PubMed PMID: 30607285]

[3]

Nadav G, Eyal K, Noam T, Yeruham K. Evaluation of the clinical significance of sonographic perinephric fluid in patients with renal colic. The American journal of emergency medicine. 2019 Oct:37(10):1823-1828. doi: 10.1016/j.ajem.2018.12.040. Epub 2018 Dec 20 [PubMed PMID: 30595428]

[4]

Gandhi A, Hashemzehi T, Batura D. The management of acute renal colic. British journal of hospital medicine (London, England : 2005). 2019 Jan 2:80(1):C2-C6. doi: 10.12968/hmed.2019.80.1.C2. Epub [PubMed PMID: 30592663]

[5]

Tapiero S, Limfuco L, Bechis SK, Sur RL, Penniston KL, Nakada SY, Antonelli JA, Streeper NM, Sivalingam S, Viprakasit DP, Averch TD, Okhunov Z, Patel RM, Chi T, Pais VM Jr, Chew BH, Bird VG, Andonian S, Bhojani N, Canvasser NE, Landman J. The impact of the number of lifetime stone events on quality of life: results from the North American Stone Quality of Life Consortium. Urolithiasis. 2021 Aug:49(4):321-326. doi: 10.1007/s00240-020-01238-y. Epub 2021 Jan 6 [PubMed PMID: 33409555]

Level 2 (mid-level) evidence

[6]

Terry RS, Preminger GM. Metabolic evaluation and medical management of staghorn calculi. Asian journal of urology. 2020 Apr:7(2):122-129. doi: 10.1016/j.ajur.2019.12.007. Epub 2019 Dec 17 [PubMed PMID: 32257805]

[7]

Pearle MS, Goldfarb DS, Assimos DG, Curhan G, Denu-Ciocca CJ, Matlaga BR, Monga M, Penniston KL, Preminger GM, Turk TM, White JR, American Urological Assocation. Medical management of kidney stones: AUA guideline. The Journal of urology. 2014 Aug:192(2):316-24. doi: 10.1016/j.juro.2014.05.006. Epub 2014 May 20 [PubMed PMID: 24857648]

[8]

Hill AJ, Basourakos SP, Lewicki P, Wu X, Arenas-Gallo C, Chuang D, Bodner D, Jaeger I, Nevo A, Zell M, Markt SC, Eisner BH, Shoag JE. Incidence of Kidney Stones in the United States: The Continuous National Health and Nutrition Examination Survey. The Journal of urology. 2022 Apr:207(4):851-856. doi: 10.1097/JU.0000000000002331. Epub 2021 Dec 2 [PubMed PMID: 34854755]

Level 3 (low-level) evidence

[9]

Eaton SH, Cashy J, Pearl JA, Stein DM, Perry K, Nadler RB. Admission rates and costs associated with emergency presentation of urolithiasis: analysis of the Nationwide Emergency Department Sample 2006-2009. Journal of endourology. 2013 Dec:27(12):1535-8. doi: 10.1089/end.2013.0205. Epub 2013 Nov 19 [PubMed PMID: 24251430]

[10]

Stamatelou K, Goldfarb DS. Epidemiology of Kidney Stones. Healthcare (Basel, Switzerland). 2023 Feb 2:11(3):. doi: 10.3390/healthcare11030424. Epub 2023 Feb 2 [PubMed PMID: 36766999]

[11]

Romero V, Akpinar H, Assimos DG. Kidney stones: a global picture of prevalence, incidence, and associated risk factors. Reviews in urology. 2010 Spring:12(2-3):e86-96 [PubMed PMID: 20811557]

[12]

Аgenosov MP, Каgan OF, Khеyfets VK. [Features of urolithiasis in patients of advanced and senile age.]. Advances in gerontology = Uspekhi gerontologii. 2018:31(3):368-373 [PubMed PMID: 30584876]

Level 3 (low-level) evidence

[13]

D'Costa MR, Pais VM, Rule AD. Leave no stone unturned: defining recurrence in kidney stone formers. Current opinion in nephrology and hypertension. 2019 Mar:28(2):148-153. doi: 10.1097/MNH.0000000000000478. Epub [PubMed PMID: 30531469]

Level 3 (low-level) evidence

[14]

Raja AS, Pourjabbar S, Ip IK, Baugh CW, Sodickson AD, O'Leary M, Khorasani R. Impact of a Health Information Technology-Enabled Appropriate Use Criterion on Utilization of Emergency Department CT for Renal Colic. AJR. American journal of roentgenology. 2019 Jan:212(1):142-145. doi: 10.2214/AJR.18.19966. Epub 2018 Nov 7 [PubMed PMID: 30403534]

[15]

Abufaraj M, Xu T, Cao C, Waldhoer T, Seitz C, D'andrea D, Siyam A, Tarawneh R, Fajkovic H, Schernhammer E, Yang L, Shariat SF. Prevalence and Trends in Kidney Stone Among Adults in the USA: Analyses of National Health and Nutrition Examination Survey 2007-2018 Data. European urology focus. 2021 Nov:7(6):1468-1475. doi: 10.1016/j.euf.2020.08.011. Epub 2020 Sep 6 [PubMed PMID: 32900675]

Level 3 (low-level) evidence

[16]

Ferraro PM, Curhan GC, D'Addessi A, Gambaro G. Risk of recurrence of idiopathic calcium kidney stones: analysis of data from the literature. Journal of nephrology. 2017 Apr:30(2):227-233. doi: 10.1007/s40620-016-0283-8. Epub 2016 Mar 11 [PubMed PMID: 26969574]

[17]

Morton AR, Iliescu EA, Wilson JW. Nephrology: 1. Investigation and treatment of recurrent kidney stones. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2002 Jan 22:166(2):213-8 [PubMed PMID: 11829004]

[18]

Wang K, Ge J, Han W, Wang D, Zhao Y, Shen Y, Chen J, Chen D, Wu J, Shen N, Zhu S, Xue B, Xu X. Risk factors for kidney stone disease recurrence: a comprehensive meta-analysis. BMC urology. 2022 Apr 19:22(1):62. doi: 10.1186/s12894-022-01017-4. Epub 2022 Apr 19 [PubMed PMID: 35439979]

Level 1 (high-level) evidence

[19]

Taylor EN, Stampfer MJ, Curhan GC. Diabetes mellitus and the risk of nephrolithiasis. Kidney international. 2005 Sep:68(3):1230-5 [PubMed PMID: 16105055]

Level 2 (mid-level) evidence

[20]

Yoshimura N, Chancellor MB. Neurophysiology of lower urinary tract function and dysfunction. Reviews in urology. 2003:5 Suppl 8(Suppl 8):S3-S10 [PubMed PMID: 16985987]

[21]

Gourlay K, Splinter G, Hayward J, Innes G. Does pain severity predict stone characteristics or outcomes in emergency department patients with acute renal colic? The American journal of emergency medicine. 2021 Jul:45():37-41. doi: 10.1016/j.ajem.2021.02.049. Epub 2021 Feb 23 [PubMed PMID: 33647760]

[22]

González-Padilla DA, González-Díaz A, García-Rojo E, Abad-López P, Santos-Pérez de la Blanca R, Hernández-Arroyo M, Teigell-Tobar J, Peña-Vallejo H, Rodríguez-Antolín A, Cabrera-Meirás F. Analgesic refractory colic pain: Is prolonged conservative management appropriate? The American journal of emergency medicine. 2021 Jun:44():137-142. doi: 10.1016/j.ajem.2021.02.018. Epub 2021 Feb 15 [PubMed PMID: 33618037]

[23]

Daudon M, Frochot V, Bazin D, Jungers P. Drug-Induced Kidney Stones and Crystalline Nephropathy: Pathophysiology, Prevention and Treatment. Drugs. 2018 Feb:78(2):163-201. doi: 10.1007/s40265-017-0853-7. Epub [PubMed PMID: 29264783]

[24]

Assimos DG, Langenstroer P, Leinbach RF, Mandel NS, Stern JM, Holmes RP. Guaifenesin- and ephedrine-induced stones. Journal of endourology. 1999 Nov:13(9):665-7 [PubMed PMID: 10608519]

[25]

Roedel MM, Nakada SY, Penniston KL. Sulfamethoxazole-induced sulfamethoxazole urolithiasis: a case report. BMC urology. 2021 Sep 17:21(1):133. doi: 10.1186/s12894-021-00894-5. Epub 2021 Sep 17 [PubMed PMID: 34535099]

Level 3 (low-level) evidence

[26]

Minotti B, Treglia G, Pascale M, Ceruti S, Cantini L, Anselmi L, Saporito A. Prevalence of microhematuria in renal colic and urolithiasis: a systematic review and meta-analysis. BMC urology. 2020 Aug 8:20(1):119. doi: 10.1186/s12894-020-00690-7. Epub 2020 Aug 8 [PubMed PMID: 32770985]

Level 1 (high-level) evidence

[27]

Alleemudder A, Tai XY, Goyal A, Pati J. Raised white cell count in renal colic: Is there a role for antibiotics? Urology annals. 2014 Apr:6(2):127-9. doi: 10.4103/0974-7796.130554. Epub [PubMed PMID: 24833823]

[28]

Toyoda Y, Naitoh Y, Miyamoto K, Hiromoto Y, Maruyama K, Haraguchi C. Leucocytosis and severe pain due to ureteral calculi. Hinyokika kiyo. Acta urologica Japonica. 1988 Aug:34(8):1357-61 [PubMed PMID: 3195403]

[29]

Sim KC. Ultrasonography of acute flank pain: a focus on renal stones and acute pyelonephritis. Ultrasonography (Seoul, Korea). 2018 Oct:37(4):345-354. doi: 10.14366/usg.17051. Epub 2017 Nov 26 [PubMed PMID: 29382187]

[30]

Tamm EP, Silverman PM, Shuman WP. Evaluation of the patient with flank pain and possible ureteral calculus. Radiology. 2003 Aug:228(2):319-29 [PubMed PMID: 12819343]

[31]

. Committee Opinion No. 723: Guidelines for Diagnostic Imaging During Pregnancy and Lactation. Obstetrics and gynecology. 2017 Oct:130(4):e210-e216. doi: 10.1097/AOG.0000000000002355. Epub [PubMed PMID: 28937575]

Level 3 (low-level) evidence

[32]

Al-Balushi A, Al-Shibli A, Al-Reesi A, Ullah QZ, Al-Shukaili W, Baawain S, Al-Dhuhli H, Al-Shamsi M, Al-Hubaishi A, Al-Atbi AYH. The Accuracy of Point-of-Care Ultrasound Performed by Emergency Physicians in Detecting Hydronephrosis in Patients with Renal Colic. Sultan Qaboos University medical journal. 2022 Aug:22(3):351-356. doi: 10.18295/squmj.9.2021.130. Epub 2022 Aug 25 [PubMed PMID: 36072079]

[33]

Wang RC, Fahimi J, Dillon D, Shyy W, Mongan J, McCulloch C, Smith-Bindman R. Effect of an ultrasound-first clinical decision tool in emergency department patients with suspected nephrolithiasis: A randomized trial. The American journal of emergency medicine. 2022 Oct:60():164-170. doi: 10.1016/j.ajem.2022.08.015. Epub 2022 Aug 10 [PubMed PMID: 35986979]

Level 1 (high-level) evidence

[34]

Ganesan V, De S, Greene D, Torricelli FC, Monga M. Accuracy of ultrasonography for renal stone detection and size determination: is it good enough for management decisions? BJU international. 2017 Mar:119(3):464-469. doi: 10.1111/bju.13605. Epub 2016 Aug 17 [PubMed PMID: 27459091]

[35]

Piazzese EM, Mazzeo GI, Galipò S, Fiumara F, Canfora C, Angiò LG. The renal resistive index as a predictor of acute hydronephrosis in patients with renal colic. Journal of ultrasound. 2012 Dec:15(4):239-46. doi: 10.1016/j.jus.2012.10.003. Epub 2012 Oct 14 [PubMed PMID: 23730388]

[36]

Nicolau C, Claudon M, Derchi LE, Adam EJ, Nielsen MB, Mostbeck G, Owens CM, Nyhsen C, Yarmenitis S. Imaging patients with renal colic-consider ultrasound first. Insights into imaging. 2015 Aug:6(4):441-7. doi: 10.1007/s13244-015-0396-y. Epub 2015 May 21 [PubMed PMID: 25994497]

[37]

Viyannan M, Kappumughath Mohamed S, Nagappan E, Balalakshmoji D. Doppler sonographic evaluation of resistive index of intra-renal arteries in acute ureteric obstruction. Journal of ultrasound. 2021 Dec:24(4):481-488. doi: 10.1007/s40477-020-00539-7. Epub 2020 Nov 18 [PubMed PMID: 33210264]

[38]

Onur MR, Cubuk M, Andic C, Kartal M, Arslan G. Role of resistive index in renal colic. Urological research. 2007 Dec:35(6):307-12 [PubMed PMID: 17957364]

[39]

Tublin ME, Bude RO, Platt JF. Review. The resistive index in renal Doppler sonography: where do we stand? AJR. American journal of roentgenology. 2003 Apr:180(4):885-92 [PubMed PMID: 12646425]

[40]

Brisbane W, Bailey MR, Sorensen MD. An overview of kidney stone imaging techniques. Nature reviews. Urology. 2016 Nov:13(11):654-662. doi: 10.1038/nrurol.2016.154. Epub 2016 Aug 31 [PubMed PMID: 27578040]

Level 3 (low-level) evidence

[41]

Fulgham PF, Assimos DG, Pearle MS, Preminger GM. Clinical effectiveness protocols for imaging in the management of ureteral calculous disease: AUA technology assessment. The Journal of urology. 2013 Apr:189(4):1203-13. doi: 10.1016/j.juro.2012.10.031. Epub 2012 Oct 22 [PubMed PMID: 23085059]

[42]

Thungkatikajonkit P, Wongwaisayawan S, Wibulpolprasert A, Viseshsindh W, Kaewlai R. Is Combined Ultrasound with Radiography Sufficient for the Diagnosis of Obstructive Ureteric Stone in Patients with Acute Flank Pain? Journal of medical ultrasound. 2020 Apr-Jun:28(2):86-91. doi: 10.4103/JMU.JMU_49_19. Epub 2019 Dec 10 [PubMed PMID: 32874866]

[43]

Niemann T, Kollmann T, Bongartz G. Diagnostic performance of low-dose CT for the detection of urolithiasis: a meta-analysis. AJR. American journal of roentgenology. 2008 Aug:191(2):396-401. doi: 10.2214/AJR.07.3414. Epub [PubMed PMID: 18647908]

Level 1 (high-level) evidence

[44]

Katz DS, Hines J, Rausch DR, Perlmutter S, Sommer FG, Lumerman JH, Friedman RM, Lane MJ. Unenhanced helical CT for suspected renal colic. AJR. American journal of roentgenology. 1999 Aug:173(2):425-30 [PubMed PMID: 10430148]

[45]

Teichman JM. Clinical practice. Acute renal colic from ureteral calculus. The New England journal of medicine. 2004 Feb 12:350(7):684-93 [PubMed PMID: 14960744]

[46]

Bhojani N, Paonessa JE, El Tayeb MM, Williams JC Jr, Hameed TA, Lingeman JE. Sensitivity of Noncontrast Computed Tomography for Small Renal Calculi With Endoscopy as the Gold Standard. Urology. 2018 Jul:117():36-40. doi: 10.1016/j.urology.2018.03.041. Epub 2018 Apr 3 [PubMed PMID: 29625137]

[47]

Assimos D, Krambeck A, Miller NL, Monga M, Murad MH, Nelson CP, Pace KT, Pais VM Jr, Pearle MS, Preminger GM, Razvi H, Shah O, Matlaga BR. Surgical Management of Stones: American Urological Association/Endourological Society Guideline, PART II. The Journal of urology. 2016 Oct:196(4):1161-9. doi: 10.1016/j.juro.2016.05.091. Epub 2016 May 27 [PubMed PMID: 27238615]

[48]

Assimos D, Krambeck A, Miller NL, Monga M, Murad MH, Nelson CP, Pace KT, Pais VM Jr, Pearle MS, Preminger GM, Razvi H, Shah O, Matlaga BR. Surgical Management of Stones: American Urological Association/Endourological Society Guideline, PART I. The Journal of urology. 2016 Oct:196(4):1153-60. doi: 10.1016/j.juro.2016.05.090. Epub 2016 May 27 [PubMed PMID: 27238616]

[49]

Dundee P, Bouchier-Hayes D, Haxhimolla H, Dowling R, Costello A. Renal tract calculi: comparison of stone size on plain radiography and noncontrast spiral CT scan. Journal of endourology. 2006 Dec:20(12):1005-9 [PubMed PMID: 17206892]

[50]

Aggarwal G, Adhikary SD. Assessment of the efficacy of reduced-radiation noncontrast computed tomography scan compared with the standard noncontrast computed tomography scan for detecting urolithiasis: A prospective single-center study. Current urology. 2023 Mar:17(1):18-24. doi: 10.1097/CU9.0000000000000162. Epub 2022 Nov 7 [PubMed PMID: 37692141]

[51]

Rodger F, Roditi G, Aboumarzouk OM. Diagnostic Accuracy of Low and Ultra-Low Dose CT for Identification of Urinary Tract Stones: A Systematic Review. Urologia internationalis. 2018:100(4):375-385. doi: 10.1159/000488062. Epub 2018 Apr 12 [PubMed PMID: 29649823]

Level 1 (high-level) evidence

[52]

Roberts MJ, Williams J, Khadra S, Nalavenkata S, Kam J, McCombie SP, Arianayagam M, Canagasingham B, Ferguson R, Khadra M, Varol C, Winter M, Sanaei F, Loh H, Thakkar Y, Dugdale P, Ko R. A prospective, matched comparison of ultra-low and standard-dose computed tomography for assessment of renal colic. BJU international. 2020 Sep:126 Suppl 1():27-32. doi: 10.1111/bju.15116. Epub 2020 Jun 23 [PubMed PMID: 32573114]

[53]

Chi BH, Chang IH, Lee DH, Park SB, Kim KD, Moon YT, Hur T. Low-Dose Unenhanced Computed Tomography with Iterative Reconstruction for Diagnosis of Ureter Stones. Yonsei medical journal. 2018 May:59(3):389-396. doi: 10.3349/ymj.2018.59.3.389. Epub [PubMed PMID: 29611401]

[54]

Planz VB, Posielski NM, Lubner MG, Li K, Chen GH, Nakada SY, Pickhardt PJ. Ultra-low-dose limited renal CT for volumetric stone surveillance: advantages over standard unenhanced CT. Abdominal radiology (New York). 2019 Jan:44(1):227-233. doi: 10.1007/s00261-018-1719-5. Epub [PubMed PMID: 30073402]

[55]

Rob S, Bryant T, Wilson I, Somani BK. Ultra-low-dose, low-dose, and standard-dose CT of the kidney, ureters, and bladder: is there a difference? Results from a systematic review of the literature. Clinical radiology. 2017 Jan:72(1):11-15. doi: 10.1016/j.crad.2016.10.005. Epub 2016 Oct 31 [PubMed PMID: 27810168]

Level 1 (high-level) evidence

[56]

Chan K, Shakir T, El-Taji O, Patel A, Bycroft J, Lim CP, Vasdev N. Management of urolithiasis in pregnancy. Current urology. 2023 Mar:17(1):1-6. doi: 10.1097/CU9.0000000000000181. Epub 2023 Feb 16 [PubMed PMID: 37692143]

[57]

White WM, Johnson EB, Zite NB, Beddies J, Krambeck AE, Hyams E, Marien T, Shah O, Matlaga B, Pais VM Jr. Predictive value of current imaging modalities for the detection of urolithiasis during pregnancy: a multicenter, longitudinal study. The Journal of urology. 2013 Mar:189(3):931-4. doi: 10.1016/j.juro.2012.09.076. Epub 2012 Sep 24 [PubMed PMID: 23017526]

[58]

Akhavan Sepahi M, Mosavimovahed M. Best Imaging Method for Detection of Renal Stones. Medical journal of the Islamic Republic of Iran. 2021:35():160. doi: 10.47176/mjiri.35.160. Epub 2021 Dec 3 [PubMed PMID: 35341086]

[59]

Wu DS, Stoller ML. Indinavir urolithiasis. Current opinion in urology. 2000 Nov:10(6):557-61 [PubMed PMID: 11148725]

Level 3 (low-level) evidence

[60]

Schwartz BF, Schenkman N, Armenakas NA, Stoller ML. Imaging characteristics of indinavir calculi. The Journal of urology. 1999 Apr:161(4):1085-7 [PubMed PMID: 10081843]

[61]

Arumainayagam N, Gresty H, Shamsuddin A, Garvey L, DasGupta R. Human immunodeficiency virus (HIV)-related stone disease - a potential new paradigm? BJU international. 2015 Nov:116(5):684-6. doi: 10.1111/bju.12971. Epub 2015 Jun 3 [PubMed PMID: 25346053]

[62]

Chu G, Rosenfield AT, Anderson K, Scout L, Smith RC. Sensitivity and value of digital CT scout radiography for detecting ureteral stones in patients with ureterolithiasis diagnosed on unenhanced CT. AJR. American journal of roentgenology. 1999 Aug:173(2):417-23 [PubMed PMID: 10430147]

[63]

Chong SL, Ng YH. Obstructive uropathy and severe acute kidney injury from renal calculi due to adenine phosphoribosyltransferase deficiency. World journal of pediatrics : WJP. 2016 May:12(2):243-5. doi: 10.1007/s12519-015-0073-8. Epub 2015 Dec 18 [PubMed PMID: 26684317]

[64]

Jiménez Herrero MC, Petkov Stoyanov V, Gutiérrez Sánchez MJ, Martín Navarro JA. Litiasis due to 2,8-dihydroxyadenine, usefulness of the genetic study. Nefrologia. 2019 Mar-Apr:39(2):206-207. doi: 10.1016/j.nefro.2018.08.002. Epub 2018 Oct 30 [PubMed PMID: 30389108]

[65]

Ceballos-Picot I, Daudon M, Harambat J, Bensman A, Knebelmann B, Bollée G. 2,8-Dihydroxyadenine urolithiasis: a not so rare inborn error of purine metabolism. Nucleosides, nucleotides & nucleic acids. 2014:33(4-6):241-52. doi: 10.1080/15257770.2013.853780. Epub [PubMed PMID: 24940675]

[66]

Dean NS, Krambeck AE. Contemporary Use of Computed Tomography (CT) Imaging in Suspected Urolithiasis in Pregnancy. Current urology reports. 2023 Sep:24(9):443-449. doi: 10.1007/s11934-023-01171-8. Epub 2023 Jun 14 [PubMed PMID: 37314612]

[67]

Masselli G, Weston M, Spencer J. The role of imaging in the diagnosis and management of renal stone disease in pregnancy. Clinical radiology. 2015 Dec:70(12):1462-71. doi: 10.1016/j.crad.2015.09.002. Epub 2015 Oct 9 [PubMed PMID: 26454345]

[68]

Morgan K, Rees CD, Shahait M, Craighead C, Connelly ZM, Ahmed ME, Khater N. Urolithiasis in pregnancy: Advances in imaging modalities and evaluation of current trends in endourological approaches. Actas urologicas espanolas. 2022 Jun:46(5):259-267. doi: 10.1016/j.acuroe.2022.03.005. Epub 2022 May 9 [PubMed PMID: 35551890]

Level 3 (low-level) evidence

[69]

Juliebø-Jones P, Beisland C, Gjengstø P, Baug S, Ulvik Ø. Ureteroscopy during pregnancy: Outcomes and lessons learned over 4 decades at a tertiary center in Norway. Current urology. 2023 Mar:17(1):7-12. doi: 10.1097/CU9.0000000000000157. Epub 2022 Oct 8 [PubMed PMID: 37692136]

[70]

Jin X, Liu B, Xiong Y, Wang Y, Tu W, Shao Y, Zhang L, Wang D. Outcomes of ureteroscopy and internal ureteral stent for pregnancy with urolithiasis: a systematic review and meta-analysis. BMC urology. 2022 Sep 14:22(1):150. doi: 10.1186/s12894-022-01100-w. Epub 2022 Sep 14 [PubMed PMID: 36104697]

Level 1 (high-level) evidence

[71]

Gull S, Para SA, Singh S, Ansari FM, Kumar M, Ashraf W. Safety and Efficacy of Ureteroscopic Laser Lithotripsy in the Management of Ureteric Calculi in Pregnancy-Experience of a Tertiary Care Center. Journal of obstetrics and gynaecology of India. 2024 Apr:74(2):131-135. doi: 10.1007/s13224-023-01889-y. Epub 2023 Nov 30 [PubMed PMID: 38707872]

[72]

Napolitano LM. Sepsis 2018: Definitions and Guideline Changes. Surgical infections. 2018 Feb/Mar:19(2):117-125. doi: 10.1089/sur.2017.278. Epub [PubMed PMID: 29447109]

[73]

Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23:315(8):801-10. doi: 10.1001/jama.2016.0287. Epub [PubMed PMID: 26903338]

Level 3 (low-level) evidence

[74]

Gauer R, Forbes D, Boyer N. Sepsis: Diagnosis and Management. American family physician. 2020 Apr 1:101(7):409-418 [PubMed PMID: 32227831]

[75]

Suetrong B, Walley KR. Lactic Acidosis in Sepsis: It's Not All Anaerobic: Implications for Diagnosis and Management. Chest. 2016 Jan:149(1):252-61. doi: 10.1378/chest.15-1703. Epub 2016 Jan 6 [PubMed PMID: 26378980]

[76]

Wu Y, Wang G, Huang Z, Yang B, Yang T, Liu J, Li P, Li J. Diagnostic and therapeutic value of biomarkers in urosepsis. Therapeutic advances in urology. 2023 Jan-Dec:15():17562872231151852. doi: 10.1177/17562872231151852. Epub 2023 Jan 31 [PubMed PMID: 36744043]

Level 3 (low-level) evidence

[77]

Ryoo SM, Han KS, Ahn S, Shin TG, Hwang SY, Chung SP, Hwang YJ, Park YS, Jo YH, Chang HL, Suh GJ, You KM, Kang GH, Choi SH, Lim TH, Kim WY, Korean Shock Society (KoSS) Investigators. The usefulness of C-reactive protein and procalcitonin to predict prognosis in septic shock patients: A multicenter prospective registry-based observational study. Scientific reports. 2019 Apr 29:9(1):6579. doi: 10.1038/s41598-019-42972-7. Epub 2019 Apr 29 [PubMed PMID: 31036824]

Level 2 (mid-level) evidence

[78]

Pepys MB, Hirschfield GM. C-reactive protein: a critical update. The Journal of clinical investigation. 2003 Jun:111(12):1805-12 [PubMed PMID: 12813013]

[79]

Póvoa P. C-reactive protein: a valuable marker of sepsis. Intensive care medicine. 2002 Mar:28(3):235-43 [PubMed PMID: 11904651]

Level 3 (low-level) evidence

[80]

Hogarth MB, Gallimore R, Savage P, Palmer AJ, Starr JM, Bulpitt CJ, Pepys MB. Acute phase proteins, C-reactive protein and serum amyloid A protein, as prognostic markers in the elderly inpatient. Age and ageing. 1997 Mar:26(2):153-8 [PubMed PMID: 9177673]

[81]

Vigushin DM, Pepys MB, Hawkins PN. Metabolic and scintigraphic studies of radioiodinated human C-reactive protein in health and disease. The Journal of clinical investigation. 1993 Apr:91(4):1351-7 [PubMed PMID: 8473487]

[82]

Weidhase L, Wellhöfer D, Schulze G, Kaiser T, Drogies T, Wurst U, Petros S. Is Interleukin-6 a better predictor of successful antibiotic therapy than procalcitonin and C-reactive protein? A single center study in critically ill adults. BMC infectious diseases. 2019 Feb 13:19(1):150. doi: 10.1186/s12879-019-3800-2. Epub 2019 Feb 13 [PubMed PMID: 30760225]

[83]

Song J, Park DW, Moon S, Cho HJ, Park JH, Seok H, Choi WS. Diagnostic and prognostic value of interleukin-6, pentraxin 3, and procalcitonin levels among sepsis and septic shock patients: a prospective controlled study according to the Sepsis-3 definitions. BMC infectious diseases. 2019 Nov 12:19(1):968. doi: 10.1186/s12879-019-4618-7. Epub 2019 Nov 12 [PubMed PMID: 31718563]

[84]

Takahashi W, Nakada TA, Yazaki M, Oda S. Interleukin-6 Levels Act as a Diagnostic Marker for Infection and a Prognostic Marker in Patients with Organ Dysfunction in Intensive Care Units. Shock (Augusta, Ga.). 2016 Sep:46(3):254-60. doi: 10.1097/SHK.0000000000000616. Epub [PubMed PMID: 27172160]

[85]

Behnes M, Bertsch T, Lepiorz D, Lang S, Trinkmann F, Brueckmann M, Borggrefe M, Hoffmann U. Diagnostic and prognostic utility of soluble CD 14 subtype (presepsin) for severe sepsis and septic shock during the first week of intensive care treatment. Critical care (London, England). 2014 Sep 5:18(5):507. doi: 10.1186/s13054-014-0507-z. Epub 2014 Sep 5 [PubMed PMID: 25190134]

[86]

Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harbor perspectives in biology. 2014 Sep 4:6(10):a016295. doi: 10.1101/cshperspect.a016295. Epub 2014 Sep 4 [PubMed PMID: 25190079]

Level 3 (low-level) evidence

[87]

Ma L, Zhang H, Yin YL, Guo WZ, Ma YQ, Wang YB, Shu C, Dong LQ. Role of interleukin-6 to differentiate sepsis from non-infectious systemic inflammatory response syndrome. Cytokine. 2016 Dec:88():126-135. doi: 10.1016/j.cyto.2016.08.033. Epub 2016 Sep 4 [PubMed PMID: 27599258]

[88]

Spittler A, Razenberger M, Kupper H, Kaul M, Hackl W, Boltz-Nitulescu G, Függer R, Roth E. Relationship between interleukin-6 plasma concentration in patients with sepsis, monocyte phenotype, monocyte phagocytic properties, and cytokine production. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2000 Dec:31(6):1338-42 [PubMed PMID: 11095999]

[89]

Castell JV, Geiger T, Gross V, Andus T, Walter E, Hirano T, Kishimoto T, Heinrich PC. Plasma clearance, organ distribution and target cells of interleukin-6/hepatocyte-stimulating factor in the rat. European journal of biochemistry. 1988 Nov 1:177(2):357-61 [PubMed PMID: 3263918]

[90]

Maniar RN, Navaneedhan G, Ranvir S, Maniar AR, Dhiman A, Agrawal A. What Is the Normal Trajectory of Interleukin-6 and C-reactive Protein in the Hours and Days Immediately After TKA? Clinical orthopaedics and related research. 2019 Jan:477(1):41-46. doi: 10.1097/CORR.0000000000000332. Epub [PubMed PMID: 30794227]

[91]

Lee SM, An WS. New clinical criteria for septic shock: serum lactate level as new emerging vital sign. Journal of thoracic disease. 2016 Jul:8(7):1388-90. doi: 10.21037/jtd.2016.05.55. Epub [PubMed PMID: 27501243]

[92]

Kanashvili B, Saganelidze K, Ratiani L. THE ROLE OF PROCALCITONIN AND BLOOD LACTIC ACID VALUES IN PROGNOSIS OF SEPSIS AND SEPTIC SHOCK IN POLYTRAUMA PATIENTS. Georgian medical news. 2018 Jun:(279):102-107 [PubMed PMID: 30035730]

[93]

Dellinger RP, Rhodes A, Evans L, Alhazzani W, Beale R, Jaeschke R, Machado FR, Masur H, Osborn T, Parker MM, Schorr C, Townsend SR, Levy MM. Surviving Sepsis Campaign. Critical care medicine. 2023 Apr 1:51(4):431-444. doi: 10.1097/CCM.0000000000005804. Epub 2023 Mar 18 [PubMed PMID: 36928012]

[94]

Bakker J. Lactate is THE target for early resuscitation in sepsis. Revista Brasileira de terapia intensiva. 2017 Apr-Jun:29(2):124-127. doi: 10.5935/0103-507X.20170021. Epub [PubMed PMID: 28977252]

[95]

Buonacera A, Stancanelli B, Colaci M, Malatino L. Neutrophil to Lymphocyte Ratio: An Emerging Marker of the Relationships between the Immune System and Diseases. International journal of molecular sciences. 2022 Mar 26:23(7):. doi: 10.3390/ijms23073636. Epub 2022 Mar 26 [PubMed PMID: 35408994]

[96]

Martins EC, Silveira LDF, Viegas K, Beck AD, Fioravantti Júnior G, Cremonese RV, Lora PS. Neutrophil-lymphocyte ratio in the early diagnosis of sepsis in an intensive care unit: a case-control study. Revista Brasileira de terapia intensiva. 2019:31(1):64-70. doi: 10.5935/0103-507X.20190010. Epub 2019 Mar 21 [PubMed PMID: 30916236]

Level 2 (mid-level) evidence

[97]

Kaushik R, Gupta M, Sharma M, Jash D, Jain N, Sinha N, Chaudhry A, Chaudhry D. Diagnostic and Prognostic Role of Neutrophil-to-Lymphocyte Ratio in Early and Late Phase of Sepsis. Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine. 2018 Sep:22(9):660-663. doi: 10.4103/ijccm.IJCCM_59_18. Epub [PubMed PMID: 30294133]

[98]

Rehman FU, Khan A, Aziz A, Iqbal M, Mahmood SBZ, Ali N. Neutrophils to Lymphocyte Ratio: Earliest and Efficacious Markers of Sepsis. Cureus. 2020 Oct 8:12(10):e10851. doi: 10.7759/cureus.10851. Epub 2020 Oct 8 [PubMed PMID: 33178505]

[99]

Mantovani A, Garlanda C, Doni A, Bottazzi B. Pentraxins in innate immunity: from C-reactive protein to the long pentraxin PTX3. Journal of clinical immunology. 2008 Jan:28(1):1-13 [PubMed PMID: 17828584]

[100]

Garlanda C, Bottazzi B, Bastone A, Mantovani A. Pentraxins at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility. Annual review of immunology. 2005:23():337-66 [PubMed PMID: 15771574]

[101]

Hamed S, Behnes M, Pauly D, Lepiorz D, Barre M, Becher T, Lang S, Akin I, Borggrefe M, Bertsch T, Hoffmann U. Diagnostic value of Pentraxin-3 in patients with sepsis and septic shock in accordance with latest sepsis-3 definitions. BMC infectious diseases. 2017 Aug 9:17(1):554. doi: 10.1186/s12879-017-2606-3. Epub 2017 Aug 9 [PubMed PMID: 28793880]

[102]

Khana TQ, Anwar KA. Detection of Inflammatory Biomarkers Among Patients with Sepsis of Gram-Negative Bacteria: A Cross-Sectional Study. International journal of general medicine. 2023:16():3963-3976. doi: 10.2147/IJGM.S415200. Epub 2023 Aug 31 [PubMed PMID: 37670930]

Level 2 (mid-level) evidence

[103]

Davoudian S, Piovani D, Desai A, Mapelli SN, Leone R, Sironi M, Valentino S, Silva-Gomes R, Stravalaci M, Asgari F, Madera A, Piccinini D, Fedeli C, Comina D, Bonovas S, Voza A, Mantovani A, Bottazzi B. A cytokine/PTX3 prognostic index as a predictor of mortality in sepsis. Frontiers in immunology. 2022:13():979232. doi: 10.3389/fimmu.2022.979232. Epub 2022 Sep 15 [PubMed PMID: 36189302]

[104]

Wang G, Jiang C, Fang J, Li Z, Cai H. Pentraxin-3 as a predictive marker of mortality in sepsis: an updated systematic review and meta-analysis. Critical care (London, England). 2022 Jun 8:26(1):167. doi: 10.1186/s13054-022-04032-x. Epub 2022 Jun 8 [PubMed PMID: 35676730]

Level 1 (high-level) evidence

[105]

Anand S, Pakkasjärvi N, Bajpai M, Krishnan N, Goswami C, Suominen JS, Yadav DK, Goel P. Utility of Pentraxin-3 as a biomarker for diagnosis of acute appendicitis: a systematic review and meta-analysis. Pediatric surgery international. 2022 Aug:38(8):1105-1112. doi: 10.1007/s00383-022-05149-4. Epub 2022 Jun 15 [PubMed PMID: 35704081]

Level 1 (high-level) evidence

[106]

Albert Vega C, Mommert M, Boccard M, Rimmelé T, Venet F, Pachot A, Leray V, Monneret G, Delwarde B, Brengel-Pesce K, Mallet F, Trouillet-Assant S. Source of Circulating Pentraxin 3 in Septic Shock Patients. Frontiers in immunology. 2018:9():3048. doi: 10.3389/fimmu.2018.03048. Epub 2019 Jan 4 [PubMed PMID: 30687307]

[107]

Samsudin I, Vasikaran SD. Clinical Utility and Measurement of Procalcitonin. The Clinical biochemist. Reviews. 2017 Apr:38(2):59-68 [PubMed PMID: 29332972]

[108]

Becker KL, Snider R, Nylen ES. Procalcitonin in sepsis and systemic inflammation: a harmful biomarker and a therapeutic target. British journal of pharmacology. 2010 Jan 1:159(2):253-64. doi: 10.1111/j.1476-5381.2009.00433.x. Epub 2009 Nov 27 [PubMed PMID: 20002097]

[109]

Snider RH Jr, Nylen ES, Becker KL. Procalcitonin and its component peptides in systemic inflammation: immunochemical characterization. Journal of investigative medicine : the official publication of the American Federation for Clinical Research. 1997 Dec:45(9):552-60 [PubMed PMID: 9444882]

[110]

Blanco LT, Socarras MR, Montero RF, Diez EL, Calvo AO, Gregorio SAY, Cansino JR, Galan JA, Rivas JG. Renal colic during pregnancy: Diagnostic and therapeutic aspects. Literature review. Central European journal of urology. 2017:70(1):93-100. doi: 10.5173/ceju.2017.754. Epub 2016 Oct 28 [PubMed PMID: 28461996]

[111]

Haberal HB, Tonyali S. Factors predicting the need for surgical intervention for hydronephrosis during pregnancy: a systematic review of the literature. Archives of gynecology and obstetrics. 2024 May:309(5):1801-1806. doi: 10.1007/s00404-024-07391-8. Epub 2024 Feb 27 [PubMed PMID: 38413423]

Level 1 (high-level) evidence

[112]

He M, Lin X, Lei M, Xu X, He Z. The identification of pregnant women with renal colic who may need surgical intervention. BMC urology. 2022 Mar 7:22(1):30. doi: 10.1186/s12894-022-00985-x. Epub 2022 Mar 7 [PubMed PMID: 35255882]

[113]

Abushamma F, Ktaifan M, Abdallah A, Alkarajeh M, Maree M, Awadghanem A, Jaradat A, Aghbar A, Zyoud SH, Keeley FX Jr. Clinical and Radiological Predictors of Early Intervention in Acute Ureteral Colic. International journal of general medicine. 2021:14():4051-4059. doi: 10.2147/IJGM.S322170. Epub 2021 Jul 30 [PubMed PMID: 34354367]

[114]

Srirangam SJ, Hickerton B, Van Cleynenbreugel B. Management of urinary calculi in pregnancy: a review. Journal of endourology. 2008 May:22(5):867-75. doi: 10.1089/end.2008.0086. Epub [PubMed PMID: 18377238]

[115]

Zhen N, De-Sheng C, Yan-Jun Y, Hua L. The analgesic effect of ketorolac addition for renal colic pain: A meta-analysis of randomized controlled studies. The American journal of emergency medicine. 2021 May:43():12-16. doi: 10.1016/j.ajem.2020.12.073. Epub 2020 Dec 30 [PubMed PMID: 33476916]

[116]

Alghamdi YA, Morya RE, Bahathiq DM, Bokhari AF, Alaboud AK, Abdulhamid AS, Ghaddaf AA, Jamjoom M. Comparison of acetaminophen, ketamine, or ketorolac versus morphine in the treatment of acute renal colic: A network meta-analysis. The American journal of emergency medicine. 2023 Nov:73():187-196. doi: 10.1016/j.ajem.2023.08.029. Epub 2023 Aug 19 [PubMed PMID: 37679264]

Level 1 (high-level) evidence

[117]

Pourafzali SM, Sanei A, Abdolrazaghnejad A, Poursadra E. A Comparative Study of the Effect of Intravenous Morphine and Ketorolac on Pain Control in Patients with Renal Colic. Advanced biomedical research. 2023:12():45. doi: 10.4103/abr.abr_278_21. Epub 2023 Feb 25 [PubMed PMID: 37057227]

Level 2 (mid-level) evidence

[118]

Leng XY, Liu CN, Wang SC, Peng HD, Wang DG, Pan HF. Comparison of the Efficacy of Nonsteroidal Anti-Inflammatory Drugs and Opioids in the Treatment of Acute Renal Colic: A Systematic Review and Meta-Analysis. Frontiers in pharmacology. 2021:12():728908. doi: 10.3389/fphar.2021.728908. Epub 2022 Jan 27 [PubMed PMID: 35153734]

Level 1 (high-level) evidence

[119]

Pathan SA, Mitra B, Cameron PA. A Systematic Review and Meta-analysis Comparing the Efficacy of Nonsteroidal Anti-inflammatory Drugs, Opioids, and Paracetamol in the Treatment of Acute Renal Colic. European urology. 2018 Apr:73(4):583-595. doi: 10.1016/j.eururo.2017.11.001. Epub 2017 Nov 22 [PubMed PMID: 29174580]

Level 1 (high-level) evidence

[120]

Afshar K, Jafari S, Marks AJ, Eftekhari A, MacNeily AE. Nonsteroidal anti-inflammatory drugs (NSAIDs) and non-opioids for acute renal colic. The Cochrane database of systematic reviews. 2015 Jun 29:2015(6):CD006027. doi: 10.1002/14651858.CD006027.pub2. Epub 2015 Jun 29 [PubMed PMID: 26120804]

Level 1 (high-level) evidence

[121]

Kominsky HD, Rose J, Lehman A, Palettas M, Posid T, Caterino JM, Knudsen BE, Sourial MW. Trends in Acute Pain Management for Renal Colic in the Emergency Department at a Tertiary Care Academic Medical Center. Journal of endourology. 2020 Nov:34(11):1195-1202. doi: 10.1089/end.2020.0402. Epub 2020 Oct 22 [PubMed PMID: 32668985]

[122]

Motov S, Drapkin J, Butt M, Thorson A, Likourezos A, Flom P, Marshall J. Analgesic Administration for Patients with Renal Colic in the Emergency Department Before and After Implementation of an Opioid Reduction Initiative. The western journal of emergency medicine. 2018 Nov:19(6):1028-1035. doi: 10.5811/westjem.2018.9.38875. Epub 2018 Oct 18 [PubMed PMID: 30429938]

[123]

Eidinejad L, Bahreini M, Ahmadi A, Yazdchi M, Thiruganasambandamoorthy V, Mirfazaelian H. Comparison of intravenous ketorolac at three doses for treating renal colic in the emergency department: A noninferiority randomized controlled trial. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2021 Jul:28(7):768-775. doi: 10.1111/acem.14202. Epub 2021 Feb 17 [PubMed PMID: 33370510]

Level 1 (high-level) evidence

[124]

Middleton RK, Lyle JA, Berger DL. Ketorolac continuous infusion: a case report and review of the literature. Journal of pain and symptom management. 1996 Sep:12(3):190-4 [PubMed PMID: 8803382]

Level 3 (low-level) evidence

[125]

Park I, Hong S, Kim SY, Hwang JW, Do SH, Na HS. Reduced side effects and improved pain management by continuous ketorolac infusion with patient-controlled fentanyl injection compared with single fentanyl administration in pelviscopic gynecologic surgery: a randomized, double-blind, controlled study. Korean journal of anesthesiology. 2024 Feb:77(1):77-84. doi: 10.4097/kja.23217. Epub 2023 Jun 14 [PubMed PMID: 37312413]

Level 1 (high-level) evidence

[126]

Pergolizzi JV Jr, Batra A, Schmidt WK. A Randomized Controlled Trial of a Novel Formulation of Ketorolac Tromethamine for Continuous Infusion (NTM-001) in Healthy Volunteers. Advances in therapy. 2024 Feb:41(2):659-671. doi: 10.1007/s12325-023-02709-5. Epub 2023 Dec 9 [PubMed PMID: 38070041]

Level 1 (high-level) evidence

[127]

Tsu E, Mathew P, Ernst E, Vesel T. Intravenous Ketorolac Infusion for Intractable Pleuritic Pain Secondary to Metastatic Epithelioid Hemangioendothelioma. Journal of palliative medicine. 2021 Nov:24(11):1744-1748. doi: 10.1089/jpm.2021.0277. Epub 2021 Jul 22 [PubMed PMID: 34297626]

[128]

Razi A, Farrokhi E, Lotfabadi P, Hosseini SS, Saadati H, Haghighi R, Rameshrad M. Dexamethasone and ketorolac compare with ketorolac alone in acute renal colic: A randomized clinical trial. The American journal of emergency medicine. 2022 Aug:58():245-250. doi: 10.1016/j.ajem.2022.05.054. Epub 2022 Jun 2 [PubMed PMID: 35738193]

Level 1 (high-level) evidence

[129]

Glare P, Walsh D, Sheehan D. The adverse effects of morphine: a prospective survey of common symptoms during repeated dosing for chronic cancer pain. The American journal of hospice & palliative care. 2006 Jun-Jul:23(3):229-35 [PubMed PMID: 17060284]

Level 3 (low-level) evidence

[130]

Sin B, Koop K, Liu M, Yeh JY, Thandi P. Intravenous Acetaminophen for Renal Colic in the Emergency Department: Where Do We Stand? American journal of therapeutics. 2017 Jan/Feb:24(1):e12-e19. doi: 10.1097/MJT.0000000000000526. Epub [PubMed PMID: 27779484]

[131]

Kaynar M, Koyuncu F, Buldu İ, Tekinarslan E, Tepeler A, Karatağ T, İstanbulluoğlu MO, Ceylan K. Comparison of the efficacy of diclofenac, acupuncture, and acetaminophen in the treatment of renal colic. The American journal of emergency medicine. 2015 Jun:33(6):749-53. doi: 10.1016/j.ajem.2015.02.033. Epub 2015 Feb 25 [PubMed PMID: 25827597]

[132]

Motov S, Drapkin J, Butt M, Monfort R, Likourezos A, Marshall J. Pain management of renal colic in the emergency department with intravenous lidocaine. The American journal of emergency medicine. 2018 Oct:36(10):1862-1864. doi: 10.1016/j.ajem.2018.07.021. Epub 2018 Jul 9 [PubMed PMID: 30025951]

[133]

Makhoul T, Kelly G, Schult RF, Acquisto NM. Intravenous lidocaine for renal colic in the emergency department (ED). The American journal of emergency medicine. 2019 Apr:37(4):775. doi: 10.1016/j.ajem.2018.08.056. Epub 2018 Aug 23 [PubMed PMID: 30177263]

[134]

Zhong J, Hu J, Mao L, Ye G, Qiu K, Zhao Y, Hu S. Efficacy of Intravenous Lidocaine for Pain Relief in the Emergency Department: A Systematic Review and Meta-Analysis. Frontiers in medicine. 2021:8():706844. doi: 10.3389/fmed.2021.706844. Epub 2022 Jan 17 [PubMed PMID: 35111766]

Level 1 (high-level) evidence

[135]

Masic D, Liang E, Long C, Sterk EJ, Barbas B, Rech MA. Intravenous Lidocaine for Acute Pain: A Systematic Review. Pharmacotherapy. 2018 Dec:38(12):1250-1259. doi: 10.1002/phar.2189. Epub 2018 Nov 9 [PubMed PMID: 30303542]

Level 1 (high-level) evidence

[136]

Sin B, Cao J, Yang D, Ambert K, Punnapuzha S. Intravenous Lidocaine for Intractable Renal Colic Unresponsive to Standard Therapy. American journal of therapeutics. 2019 Jul/Aug:26(4):e487-e488. doi: 10.1097/MJT.0000000000000729. Epub [PubMed PMID: 29443696]

[137]

Aykanat MC, Kılıç M, Cimilli Öztürk T, Ustaalioğlu İ, Ak R. The efficacy of intradermal sterile water application in severe renal colic: a randomised clinical trial. Urolithiasis. 2023 Oct 12:51(1):121. doi: 10.1007/s00240-023-01496-6. Epub 2023 Oct 12 [PubMed PMID: 37823931]

Level 1 (high-level) evidence

[138]

Moussa M, Papatsoris AG, Chakra MA. Intradermal sterile water injection versus diclofenac sodium in acute renal colic pain: A randomized controlled trial. The American journal of emergency medicine. 2021 Jun:44():395-400. doi: 10.1016/j.ajem.2020.04.079. Epub 2020 Apr 29 [PubMed PMID: 32444296]

Level 1 (high-level) evidence

[139]

Aras B, Uruç F. Intradermal sterile water injection for acute renal colic pain. The American journal of emergency medicine. 2020 Sep:38(9):1938. doi: 10.1016/j.ajem.2020.06.047. Epub 2020 Jun 25 [PubMed PMID: 32654919]

[140]

Golcuk Y, Demir A, Yıldırım B, Acar E. Intradermal sterile water injection in acute renal colic. The American journal of emergency medicine. 2021 Feb:40():204. doi: 10.1016/j.ajem.2020.05.060. Epub 2020 May 25 [PubMed PMID: 32571630]

[141]

Mozafari J, Verki MM, Tirandaz F, Mahjouri R. Comparing Intradermal Sterile Water with Intravenous Morphine in Reducing Pain in Patients with Renal Colic: A Double-Blind Randomized Clinical Trial. Reviews on recent clinical trials. 2020:15(1):76-82. doi: 10.2174/1574887114666191118153600. Epub [PubMed PMID: 31738150]

Level 1 (high-level) evidence

[142]

Hosseininejad SM, Emami Zeydi A. Can intracutaneous sterile water injection be used as a possible treatment for acute renal colic pain in the emergency department? A short literature review. Urology annals. 2015 Jan-Mar:7(1):130-2. doi: 10.4103/0974-7796.148669. Epub [PubMed PMID: 25657569]

[143]

Lee N, Mårtensson LB. Sterile water injections for management of renal colic pain: a systematic review. Scandinavian journal of urology. 2022 Jun:56(3):255-263. doi: 10.1080/21681805.2022.2066719. Epub 2022 Apr 28 [PubMed PMID: 35481429]

Level 1 (high-level) evidence

[144]

Ahmadnia H, Younesi Rostami M. Treatment of renal colic using intracutaneous injection of sterile water. Urology journal. 2004 Summer:1(3):200-3 [PubMed PMID: 17914689]

[145]

Mårtensson L, Wallin G. Sterile water injections as treatment for low-back pain during labour: a review. The Australian & New Zealand journal of obstetrics & gynaecology. 2008 Aug:48(4):369-74. doi: 10.1111/j.1479-828X.2008.00856.x. Epub [PubMed PMID: 18837842]

[146]

Jokar A, Khademhosseini P, Ahmadi K, Sistani A, Amiri M, Sinaki AG. A Comparison of Metoclopramide and Ondansetron Efficacy for the Prevention of Nausea and Vomiting In Patients Suffered From Renal Colic. Open access Macedonian journal of medical sciences. 2018 Oct 25:6(10):1833-1838. doi: 10.3889/oamjms.2018.302. Epub 2018 Oct 18 [PubMed PMID: 30455758]

[147]

de la Encarnación Castellano C, Canós Nebot À, Caballero Romeu JP, Galán Llopis JA. Medical treatment for acute renal colic. Archivos espanoles de urologia. 2021 Jan:74(1):71-79 [PubMed PMID: 33459623]

[148]

Seyhan AU, Yılmaz E. Treatment of Renal Colic by Nerve Blockade with Lidocaine Versus Intravenous Dexketoprofen. Journal of the College of Physicians and Surgeons--Pakistan : JCPSP. 2021 Aug:31(8):921-925. doi: 10.29271/jcpsp.2021.08.921. Epub [PubMed PMID: 34320708]

[149]

Maldonado-Avila M, Del Rosario-Santiago M, Rosas-Nava JE, Manzanilla-Garcia HA, Rios-Davila VM, Rodriguez-Nava P, Vela-Mollinedo RA, Garduño-Arteaga ML. Treatment of reno-ureteral colic by twelfth intercostal nerve block with lidocaine versus intramuscular diclofenac. International urology and nephrology. 2017 Mar:49(3):413-417. doi: 10.1007/s11255-016-1479-5. Epub 2016 Dec 19 [PubMed PMID: 27995373]

[150]

Nikiforov S, Cronin AJ, Murray WB, Hall VE. Subcutaneous paravertebral block for renal colic. Anesthesiology. 2001 Mar:94(3):531-2 [PubMed PMID: 11374617]

Level 3 (low-level) evidence

[151]

Kapural L, Lee N, Badhey H, McRoberts WP, Jolly S. Splanchnic block at T11 provides a longer relief than celiac plexus block from nonmalignant, chronic abdominal pain. Pain management. 2019 Mar 1:9(2):115-121. doi: 10.2217/pmt-2018-0056. Epub 2019 Jan 25 [PubMed PMID: 30681022]

[152]

Boblewska J, Dybowski B. Methodology and findings of randomized clinical trials on pharmacologic and non-pharmacologic interventions to treat renal colic pain - a review. Central European journal of urology. 2023:76(3):212-226. doi: 10.5173/ceju.2023.92. Epub 2023 Sep 9 [PubMed PMID: 38045783]

Level 1 (high-level) evidence

[153]

Pak CY, Pearle MS, Sakhaee K. Evidence for metabolic origin of absorptive hypercalciuria Type II. Urological research. 2011 Apr:39(2):147-52. doi: 10.1007/s00240-010-0315-0. Epub 2010 Nov 10 [PubMed PMID: 21063699]

[154]

Pak CY, Sakhaee K, Pearle MS. Detection of absorptive hypercalciuria type I without the oral calcium load test. The Journal of urology. 2011 Mar:185(3):915-9. doi: 10.1016/j.juro.2010.10.067. Epub 2011 Jan 19 [PubMed PMID: 21251672]

[155]

De Coninck V, Antonelli J, Chew B, Patterson JM, Skolarikos A, Bultitude M. Medical Expulsive Therapy for Urinary Stones: Future Trends and Knowledge Gaps. European urology. 2019 Nov:76(5):658-666. doi: 10.1016/j.eururo.2019.07.053. Epub 2019 Aug 15 [PubMed PMID: 31421941]

[156]

Sharma G, Pareek T, Kaundal P, Tyagi S, Singh S, Yashaswi T, Devan SK, Sharma AP. Comparison of efficacy of three commonly used alpha-blockers as medical expulsive therapy for distal ureter stones: A systematic review and network meta-analysis. International braz j urol : official journal of the Brazilian Society of Urology. 2022 Sep-Oct:48(5):742-759. doi: 10.1590/S1677-5538.IBJU.2020.0548. Epub [PubMed PMID: 34003612]

Level 1 (high-level) evidence

[157]

Cui Y, Chen J, Zeng F, Liu P, Hu J, Li H, Li C, Cheng X, Chen M, Li Y, Li Y, Yang Z, Chen Z, Chand H, Chen H, Zu X. Tamsulosin as a Medical Expulsive Therapy for Ureteral Stones: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. The Journal of urology. 2019 May:201(5):950-955. doi: 10.1097/JU.0000000000000029. Epub [PubMed PMID: 30694932]

Level 1 (high-level) evidence

[158]

Liu C, Zeng G, Kang R, Wu W, Li J, Chen K, Wan SP. Efficacy and Safety of Alfuzosin as Medical Expulsive Therapy for Ureteral Stones: A Systematic Review and Meta-Analysis. PloS one. 2015:10(8):e0134589. doi: 10.1371/journal.pone.0134589. Epub 2015 Aug 5 [PubMed PMID: 26244843]

Level 1 (high-level) evidence

[159]

Bos D, Kapoor A. Update on medical expulsive therapy for distal ureteral stones: Beyond alpha-blockers. Canadian Urological Association journal = Journal de l'Association des urologues du Canada. 2014 Nov:8(11-12):442-5. doi: 10.5489/cuaj.2472. Epub [PubMed PMID: 25553160]

[160]

Lim I, Sellers DJ, Chess-Williams R. Current and emerging pharmacological targets for medical expulsive therapy. Basic & clinical pharmacology & toxicology. 2022 Jan:130 Suppl 1():16-22. doi: 10.1111/bcpt.13613. Epub 2021 May 26 [PubMed PMID: 33991399]

[161]

Gandhi HR, Agrawal C. The efficacy of tamsulosin vs. nifedipine for the medical expulsive therapy of distal ureteric stones: A randomised clinical trial. Arab journal of urology. 2013 Dec:11(4):405-10. doi: 10.1016/j.aju.2013.08.008. Epub 2013 Sep 14 [PubMed PMID: 26558112]

Level 1 (high-level) evidence

[162]

Pickard R, Starr K, MacLennan G, Lam T, Thomas R, Burr J, McPherson G, McDonald A, Anson K, N'Dow J, Burgess N, Clark T, Kilonzo M, Gillies K, Shearer K, Boachie C, Cameron S, Norrie J, McClinton S. Medical expulsive therapy in adults with ureteric colic: a multicentre, randomised, placebo-controlled trial. Lancet (London, England). 2015 Jul 25:386(9991):341-9. doi: 10.1016/S0140-6736(15)60933-3. Epub 2015 May 18 [PubMed PMID: 25998582]

Level 1 (high-level) evidence

[163]

Campschroer T, Zhu Y, Duijvesz D, Grobbee DE, Lock MT. Alpha-blockers as medical expulsive therapy for ureteral stones. The Cochrane database of systematic reviews. 2014 Apr 2:(4):CD008509. doi: 10.1002/14651858.CD008509.pub2. Epub 2014 Apr 2 [PubMed PMID: 24691989]

Level 1 (high-level) evidence

[164]

Talamini S, Wong D, Phillips T, Palka J, Vetter J, Chow A, Paradis A, Desai A, Sands K, Nottingham C, Venkatesh R. Improved stone quality of life in patients with an obstructing ureteral stone on alpha-blocker medical expulsive therapy. International urology and nephrology. 2024 Apr:56(4):1289-1295. doi: 10.1007/s11255-023-03865-x. Epub 2023 Nov 16 [PubMed PMID: 37971642]

Level 2 (mid-level) evidence

[165]

Campschroer T, Zhu X, Vernooij RWM, Lock TMTW. α-blockers as medical expulsive therapy for ureteric stones: a Cochrane systematic review. BJU international. 2018 Dec:122(6):932-945. doi: 10.1111/bju.14454. Epub 2018 Aug 11 [PubMed PMID: 29908037]

Level 1 (high-level) evidence

[166]

Ziaeefar P, Basiri A, Zangiabadian M, de la Rosette J, Zargar H, Taheri M, Kashi AH. Medical Expulsive Therapy for Pediatric Ureteral Stones: A Meta-Analysis of Randomized Clinical Trials. Journal of clinical medicine. 2023 Feb 10:12(4):. doi: 10.3390/jcm12041410. Epub 2023 Feb 10 [PubMed PMID: 36835945]

Level 1 (high-level) evidence

[167]

Campschroer T, Zhu X, Vernooij RW, Lock MT. Alpha-blockers as medical expulsive therapy for ureteral stones. The Cochrane database of systematic reviews. 2018 Apr 5:4(4):CD008509. doi: 10.1002/14651858.CD008509.pub3. Epub 2018 Apr 5 [PubMed PMID: 29620795]

Level 1 (high-level) evidence

[168]

Tang QL, Wang DJ, Zhou S, Tao RZ. Mirabegron in medical expulsive therapy for distal ureteral stones: a prospective, randomized, controlled study. World journal of urology. 2021 Dec:39(12):4465-4470. doi: 10.1007/s00345-021-03772-9. Epub 2021 Jul 9 [PubMed PMID: 34241685]

Level 1 (high-level) evidence

[169]

Wang Z, Chi J, Liu Y, Wu J, Cui Y, Yang C. Efficacy of mirabegron for ureteral stones: a systematic review with meta-analysis of randomized controlled trials. Frontiers in pharmacology. 2023:14():1326600. doi: 10.3389/fphar.2023.1326600. Epub 2023 Dec 20 [PubMed PMID: 38178860]

Level 1 (high-level) evidence

[170]

Belkovsky M, Zogaib GV, Passerotti CC, Artifon ELA, Otoch JP, da Cruz JAS. Tamsulosin vs. Tadalafil as medical expulsive therapy for distal ureteral stones: a systematic review and meta-analysis. International braz j urol : official journal of the Brazilian Society of Urology. 2023 Nov-Dec:49(6):668-676. doi: 10.1590/S1677-5538.IBJU.2023.0345. Epub [PubMed PMID: 37903004]

Level 1 (high-level) evidence

[171]

Abdelaal MA, El-Dydamony EM. Comparative study between Tamsulosin, Silodosin and Tadalaﬁl as a medical expulsive therapy for lower ureteral stones. Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica. 2023 Feb 22:95(1):10849. doi: 10.4081/aiua.2023.10849. Epub 2023 Feb 22 [PubMed PMID: 36924384]

Level 2 (mid-level) evidence

[172]

Falahatkar S, Akhavan A, Esmaeili S, Amin A, Kazemnezhad E, Jafari A. Efficacy of tamsulosin versus tadalafil as medical expulsive therapy on stone expulsion in patients with distal ureteral stones: A randomized double-blind clinical trial. International braz j urol : official journal of the Brazilian Society of Urology. 2021 Sep-Oct:47(5):982-988. doi: 10.1590/S1677-5538.IBJU.2020.1007. Epub [PubMed PMID: 34260175]

Level 1 (high-level) evidence

[173]

Çelik S, Akdeniz F, Afsar Yildirim M, Bozkurt O, Gursoy Bulut M, Hacihasanoglu ML, Demir O. Tadalafil versus alpha blockers (alfuzosin, doxazosin, tamsulosin and silodosin) as medical expulsive therapy for { 10 mm distal and proximal ureteral stones. Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica. 2018 Jun 30:90(2):117-122. doi: 10.4081/aiua.2018.2.117. Epub 2018 Jun 30 [PubMed PMID: 29974727]

[174]

Jung HD, Cho KS, Jun DY, Jeong JY, Moon YJ, Chung DY, Kang DH, Cho S, Lee JY. Silodosin versus Tamsulosin for Medical Expulsive Therapy of Ureteral Stones: An Updated Systematic Review and Meta-Analysis of Randomized Controlled Trials. Medicina (Kaunas, Lithuania). 2022 Dec 6:58(12):. doi: 10.3390/medicina58121794. Epub 2022 Dec 6 [PubMed PMID: 36556996]

Level 1 (high-level) evidence

[175]

Hsu YP, Hsu CW, Bai CH, Cheng SW, Chen KC, Chen C. Silodosin versus tamsulosin for medical expulsive treatment of ureteral stones: A systematic review and meta-analysis. PloS one. 2018:13(8):e0203035. doi: 10.1371/journal.pone.0203035. Epub 2018 Aug 28 [PubMed PMID: 30153301]

Level 1 (high-level) evidence

[176]

Liu XJ, Wen JG, Wan YD, Hu BW, Wang QW, Wang Y. Role of silodosin as medical expulsive therapy in ureteral calculi: a meta-analysis of randomized controlled trials. Urolithiasis. 2018 Apr:46(2):211-218. doi: 10.1007/s00240-017-0974-1. Epub 2017 Apr 1 [PubMed PMID: 28365782]

Level 1 (high-level) evidence

[177]

Pricop C, Șerban DN, Șerban IL, Cumpanas AA, Puia D. Does silodosin offer better results than tamsulosin as medical expulsive treatment after shock wave lithotripsy for single distal ureteric stones? Wideochirurgia i inne techniki maloinwazyjne = Videosurgery and other miniinvasive techniques. 2020 Dec:15(4):602-607. doi: 10.5114/wiitm.2020.92307. Epub 2020 Jan 16 [PubMed PMID: 33294076]

[178]

Liu H, Wang S, Zhu W, Lu J, Wang X, Yang W. Comparative efficacy of 22 drug interventions as medical expulsive therapy for ureteral stones: a systematic review and network meta-analysis. Urolithiasis. 2020 Oct:48(5):447-457. doi: 10.1007/s00240-019-01159-5. Epub 2019 Sep 11 [PubMed PMID: 31511921]

Level 1 (high-level) evidence

[179]

Sharma G, Kaundal P, Pareek T, Tyagi S, Sharma AP, Devana SK, Singh SK. Comparison of efficacy of various drugs used for medical expulsive therapy for distal ureter stones: A systematic review and network meta-analysis. International journal of clinical practice. 2021 Sep:75(9):e14214. doi: 10.1111/ijcp.14214. Epub 2021 Apr 20 [PubMed PMID: 33825273]

Level 1 (high-level) evidence

[180]

Suntharasivam T, Mukherjee A, Luk A, Aboumarzouk O, Somani B, Rai BP. The role of robotic surgery in the management of renal tract calculi. Translational andrology and urology. 2019 Sep:8(Suppl 4):S457-S460. doi: 10.21037/tau.2019.04.06. Epub [PubMed PMID: 31656752]

[181]

Ganpule AP, Prashant J, Desai MR. Laparoscopic and robot-assisted surgery in the management of urinary lithiasis. Arab journal of urology. 2012 Mar:10(1):32-9. doi: 10.1016/j.aju.2011.12.003. Epub 2012 Jan 29 [PubMed PMID: 26558002]

[182]

Pedro RN, Buchholz N. Laparoscopic and robotic surgery for stone disease. Urolithiasis. 2018 Feb:46(1):125-127. doi: 10.1007/s00240-017-1014-x. Epub 2017 Nov 23 [PubMed PMID: 29170855]

[183]

Borofsky MS, Walter D, Shah O, Goldfarb DS, Mues AC, Makarov DV. Surgical decompression is associated with decreased mortality in patients with sepsis and ureteral calculi. The Journal of urology. 2013 Mar:189(3):946-51. doi: 10.1016/j.juro.2012.09.088. Epub 2012 Sep 24 [PubMed PMID: 23017519]

[184]

Pearle MS, Pierce HL, Miller GL, Summa JA, Mutz JM, Petty BA, Roehrborn CG, Kryger JV, Nakada SY. Optimal method of urgent decompression of the collecting system for obstruction and infection due to ureteral calculi. The Journal of urology. 1998 Oct:160(4):1260-4 [PubMed PMID: 9751331]

Level 1 (high-level) evidence

[185]

Bartoletti R, Cai T. Surgical approach to urolithiasis: the state of art. Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases. 2008 May:5(2):142-4 [PubMed PMID: 22460997]

Level 3 (low-level) evidence

[186]

Miller OF, Kane CJ. Time to stone passage for observed ureteral calculi: a guide for patient education. The Journal of urology. 1999 Sep:162(3 Pt 1):688-90; discussion 690-1 [PubMed PMID: 10458343]

[187]

Preminger GM, Tiselius HG, Assimos DG, Alken P, Buck AC, Gallucci M, Knoll T, Lingeman JE, Nakada SY, Pearle MS, Sarica K, Türk C, Wolf JS Jr, American Urological Association Education and Research, Inc, European Association of Urology. 2007 Guideline for the management of ureteral calculi. European urology. 2007 Dec:52(6):1610-31 [PubMed PMID: 18074433]

[188]

Kumar LP, Khan I, Kishore A, Gopal M, Behera V. Pyonephrosis among Patients with Pyelonephritis Admitted in Department of Nephrology and Urology of a Tertiary Care Centre: A Descriptive Cross-sectional Study. JNMA; journal of the Nepal Medical Association. 2023 Feb 1:61(258):111-114. doi: 10.31729/jnma.8015. Epub 2023 Feb 1 [PubMed PMID: 37203981]

Level 2 (mid-level) evidence

[189]

Koch GE, Johnsen NV. The Diagnosis and Management of Life-threatening Urologic Infections. Urology. 2021 Oct:156():6-15. doi: 10.1016/j.urology.2021.05.011. Epub 2021 May 17 [PubMed PMID: 34015395]

[190]

Pasiechnikov S, Buchok O, Sheremeta R, Banyra O. Empirical treatment in patients with acute obstructive pyelonephritis. Infectious disorders drug targets. 2015:15(3):163-70 [PubMed PMID: 26321323]

[191]

Hamasuna R, Takahashi S, Nagae H, Kubo T, Yamamoto S, Arakawa S, Matsumoto T. Obstructive pyelonephritis as a result of urolithiasis in Japan: diagnosis, treatment and prognosis. International journal of urology : official journal of the Japanese Urological Association. 2015 Mar:22(3):294-300. doi: 10.1111/iju.12666. Epub 2014 Nov 16 [PubMed PMID: 25400222]

[192]

Mondal U, Viswanathan S, Sreenivasan Kodakkattil S. Percutaneous Nephrostomy in Complicated Urinary Tract Infections. Cureus. 2022 Jul:14(7):e26682. doi: 10.7759/cureus.26682. Epub 2022 Jul 9 [PubMed PMID: 35949777]

[193]

Zhang M, Jin H, Liu X. Septic Shock Induced by Acute Pyelonephritis Resulting from Kidney Stones Treated by Double-J Ureteral Stents in a Pregnant Woman: A Case Report and Literature Review. The American journal of case reports. 2022 Aug 9:23():e936967. doi: 10.12659/AJCR.936967. Epub 2022 Aug 9 [PubMed PMID: 35943910]

Level 3 (low-level) evidence

[194]

Zul Khairul Azwadi I, Norhayati MN, Abdullah MS. Percutaneous nephrostomy versus retrograde ureteral stenting for acute upper obstructive uropathy: a systematic review and meta-analysis. Scientific reports. 2021 Mar 23:11(1):6613. doi: 10.1038/s41598-021-86136-y. Epub 2021 Mar 23 [PubMed PMID: 33758312]

Level 1 (high-level) evidence

[195]

Xu ZH, Yang YH, Zhou S, Lv JL. Percutaneous nephrostomy versus retrograde ureteral stent for acute upper urinary tract obstruction with urosepsis. Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy. 2021 Feb:27(2):323-328. doi: 10.1016/j.jiac.2020.11.022. Epub 2020 Dec 10 [PubMed PMID: 33309627]

[196]

Florido C, Herren JL, Pandhi MB, Niemeyer MM. Emergent Percutaneous Nephrostomy for Pyonephrosis: A Primer for the On-Call Interventional Radiologist. Seminars in interventional radiology. 2020 Mar:37(1):74-84. doi: 10.1055/s-0039-3401842. Epub 2020 Mar 4 [PubMed PMID: 32139973]

[197]

Li AC, Regalado SP. Emergent percutaneous nephrostomy for the diagnosis and management of pyonephrosis. Seminars in interventional radiology. 2012 Sep:29(3):218-25. doi: 10.1055/s-0032-1326932. Epub [PubMed PMID: 23997415]

[198]

Zhang Z, Wang X, Chen D, Peng N, Chen J, Wang Q, Yang M, Zhang Y. Minimally invasive management of acute ureteral obstruction and severe infection caused by upper urinary tract calculi. Journal of X-ray science and technology. 2020:28(1):125-135. doi: 10.3233/XST-190576. Epub [PubMed PMID: 31796723]

[199]

Haas CR, Li G, Hyams ES, Shah O. Delayed Decompression of Obstructing Stones with Urinary Tract Infection is Associated with Increased Odds of Death. The Journal of urology. 2020 Dec:204(6):1256-1262. doi: 10.1097/JU.0000000000001182. Epub 2020 Jun 5 [PubMed PMID: 32501124]

[200]

Kamei J, Sugihara T, Yasunaga H, Matsui H, Sasabuchi Y, Fujimura T, Homma Y, Kume H. Impact of early ureteral drainage on mortality in obstructive pyelonephritis with urolithiasis: an analysis of the Japanese National Database. World journal of urology. 2023 May:41(5):1365-1371. doi: 10.1007/s00345-023-04375-2. Epub 2023 Mar 22 [PubMed PMID: 36947175]

[201]

Srougi V, Moscardi PR, Marchini GS, Berjeaut RH, Torricelli FC, Mesquita JLB, Srougi M, Mazzucchi E. Septic Shock Following Surgical Decompression of Obstructing Ureteral Stones: A Prospective Analysis. Journal of endourology. 2018 May:32(5):446-450. doi: 10.1089/end.2017.0896. Epub 2018 Mar 20 [PubMed PMID: 29439607]

[202]

Hsu CK, Young WL, Wu SY. Predictive factors for stone management timing after emergency percutaneous nephrostomy drainage in patients with infection and hydronephrosis secondary to ureteral calculi. Urolithiasis. 2022 Dec 1:51(1):1. doi: 10.1007/s00240-022-01380-9. Epub 2022 Dec 1 [PubMed PMID: 36454363]

[203]

Abi Tayeh G, Safa A, Sarkis J, Alkassis M, Khalil N, Nemr E, El Helou E. Determinants of pyelonephritis onset in patients with obstructive urolithiasis. Urologia. 2022 Feb:89(1):100-103. doi: 10.1177/03915603211035244. Epub 2021 Aug 2 [PubMed PMID: 34338097]

[204]

Kakinoki H, Tobu S, Kakinoki Y, Udo K, Uozumi J, Noguchi M. Risk Factors for Uroseptic Shock in Patients with Urolithiasis-Related Acute Pyelonephritis. Urologia internationalis. 2018:100(1):37-42. doi: 10.1159/000481801. Epub 2017 Oct 24 [PubMed PMID: 29065405]

[205]

Yamamichi F, Shigemura K, Kitagawa K, Fujisawa M. Comparison between non-septic and septic cases in stone-related obstructive acute pyelonephritis and risk factors for septic shock: A multi-center retrospective study. Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy. 2018 Nov:24(11):902-906. doi: 10.1016/j.jiac.2018.08.002. Epub 2018 Aug 30 [PubMed PMID: 30174285]

Level 2 (mid-level) evidence

[206]

Tambo M, Okegawa T, Shishido T, Higashihara E, Nutahara K. Predictors of septic shock in obstructive acute pyelonephritis. World journal of urology. 2014 Jun:32(3):803-11. doi: 10.1007/s00345-013-1166-4. Epub 2013 Sep 15 [PubMed PMID: 24037335]

[207]

Kamei J, Nishimatsu H, Nakagawa T, Suzuki M, Fujimura T, Fukuhara H, Igawa Y, Kume H, Homma Y. Risk factors for septic shock in acute obstructive pyelonephritis requiring emergency drainage of the upper urinary tract. International urology and nephrology. 2014 Mar:46(3):493-7. doi: 10.1007/s11255-013-0545-5. Epub 2013 Sep 5 [PubMed PMID: 24006032]

[208]

Cao JD, Wang ZC, Wang YL, Li HC, Gu CM, Bai ZG, Chen ZQ, Wang SS, Xiang ST. Risk factors for progression of Urolith Associated with Obstructive Urosepsis to severe sepsis or septic shock. BMC urology. 2022 Mar 28:22(1):46. doi: 10.1186/s12894-022-00988-8. Epub 2022 Mar 28 [PubMed PMID: 35346141]

[209]

Gou JJ, Zhang C, Han HS, Wu HW. Risk factors of concurrent urinary sepsis in patients with diabetes mellitus comorbid with upper urinary tract calculi. World journal of diabetes. 2023 Sep 15:14(9):1403-1411. doi: 10.4239/wjd.v14.i9.1403. Epub [PubMed PMID: 37771326]

[210]

Dawson CH, Tomson CR. Kidney stone disease: pathophysiology, investigation and medical treatment. Clinical medicine (London, England). 2012 Oct:12(5):467-71 [PubMed PMID: 23101150]