Acute Renal Colic

Laryssa Patti; Stephen Leslie

Acute Renal Colic

Author: Laryssa Patti Editor: Stephen W. Leslie Updated: 6/6/2024 9:17:06 AM

Introduction

Acute renal colic is a severe form of sudden flank pain that typically originates over the costovertebral angle and extends anteriorly and inferiorly towards the groin or testicle. Acute renal colic is generally caused by acute obstruction of the urinary tract by a calculus and is frequently associated with nausea and vomiting.

Urolithiasis, also known as kidney stones, is a common condition affecting about 1 of every 11 individuals in the United States at some point. Urolithiasis is usually caused by a crystal or crystalline aggregate traveling from the kidney through the genitourinary system and becoming stuck, obstructing urinary flow, typically in the ureter. This obstruction results in proximal ureteral and renal pelvic dilation (hydroureteronephrosis), which is the immediate cause of the intense pain known as renal colic.[1][2][3][4]

The degree of pain is related to the degree of obstruction and not the size of the stone, although stone size can be a reasonable predictor of the likelihood of spontaneous passage. While kidney stones are not the only cause of flank pain, their frequency and the severity of the pain they cause make ureterolithiasis the most likely presumptive diagnosis when sudden, severe flank pain occurs, especially when associated with hematuria.

While the nature and onset of the pain depend on the underlying cause, its exact location, and severity, for most patients, the pain peaks about 1 to 2 hours after its initial onset.

Underlying causes of urolithiasis include inadequate hydration, aciduria, chronic urinary infection, hypercalciuria, hyperoxaluria, hyperuricosuria, and hypocitraturia.

The initial evaluation of a patient who presents with acute renal colic includes laboratory testing, urinalysis, and appropriate imaging studies.

The immediate treatment of acute renal colic due to ureterolithiasis starts with pain control, IV hydration, antiemetics, and antibiotics (if indicated). Patients with difficult-to-control symptoms may need hospital admission. Some situations may require urgent surgical intervention, such as obstructive pyelonephritis (pyonephrosis), where the infected renal pelvis needs to be drained emergently.

Definitive treatment of obstructing ureteral stones may be conservative or procedural. 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 indicated.[5] See StatPearls' companion reference, "Ureterolithiasis," for more information.[5]

Quality of life scores tend to lower as kidney stone attacks increase. This was most obvious when the total number of lifetime renal colic events reached 5 or more, suggesting that preventive measures, such as 24-hour urine testing, should be done at that point, if not earlier.[6]

Etiology

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Etiology

Renal colic is caused by dilation of the renal pelvis and ureteral segments. While colic usually results from an acute obstruction such as a ureteral calculus, it may also be due to various other problems and disorders, such as ureteral spasms immediately after double J stent removal or ureteroscopy.

Similar ureteral blockages from chronic sources (such as ureteropelvic junction obstructions, prostate, cervical, or pelvic cancer, ureteral scarring, and retroperitoneal fibrosis, among others) do not generally cause acute pain or colic.

There are multiple predictors and risk factors for kidney stone formation. The following are the most common:

Aciduria is the most common cause of uric acid stone formation, which accounts for 5% to 10% of all urinary calculi.[7][8] Aciduria may be caused by excessive ingestion of animal meat protein, renal tubular acidosis, or metabolic acidosis.[9][10] Treatment usually involves potassium citrate sufficient to reach a sustained urinary pH of 6.5.[8] Sodium bicarbonate may also be used but delivers a significant sodium load. See StatPearls' companion reference, "Uric Acid Nephrolithiasis."[8]

Cystinuria is an inheritable autosomal recessive familial genetic disorder that causes high urinary cystine levels. Cystine stones are resistant to shockwave therapy and usually require laser therapy for fragmentation. Preventive therapy consists of aggressive hydration (3,000 mL of urine daily or more) and urinary alkalinization to a pH of 7.5 or more, as cystine becomes far more soluble when the urine is alkaline.[11] See StatPearls' companion reference, "Cystinuria."[11]

Hypercalciuria, the most commonly identified chemical promoter of nephrolithiasis, is defined as 250 mg or more of urinary calcium per day.[12] Hypercalciuria is often due to increased intestinal calcium absorption, high renal calcium excretion (renal calcium leak), excessive Vitamin D intake, hyperparathyroidism, metabolic acidosis, or idiopathic.[12] Treatment consists of moderating dietary calcium intake, normalizing Vitamin D levels, correcting phosphate deficiencies (that increase Vitamin D levels), oral phosphate supplements, and using thiazides to reduce renal calcium excretion.[12]

Hyperoxaluria is usually defined as 40 mg or more of urinary oxalate excretion daily, while optimal levels are 25 mg daily or less.[13][14] Oxalate is a very potent promoter of calcium oxalate urolithiasis, so every effort should be made to reduce it if levels are elevated or the patient is producing calcium oxalate stones.[13] Dietary oxalate should be reduced by limiting high oxalate foods such as spinach, rhubarb, and collard greens.[13] There is no specific medication for hyperoxaluria, but oral calcium citrate supplementation with meals can increase intestinal oxalate binding, preventing its absorption and lowering urinary oxalate levels.[13] See StatPearls' companion reference, "Hyperoxaluria."[13]

Hyperuricosuria, excessive urinary uric acid, contributes to both uric acid and calcium oxalate stone formation.[7] Patients who form calcium stones with excessive urinary uric acid can be treated by limiting excessive dietary animal protein ingestion or medically with allopurinol or febuxostat.[7] Most uric acid stones are best treated with potassium citrate and urinary alkalinization.[8] The optimal level of urinary uric acid is 600 mg daily or less.[7] See StatPearls' companion reference, "Hyperuricosuria."[7]

Hypocitraturia is usually defined as 320 mg or less of urinary citrate excretion daily, but this ignores urinary pH, stone composition, urinary volume and concentration, and other factors.[15] Therefore, it is suggested that clinicians focus more on achieving optimal urinary citrate levels and concentrations of approximately 300 mg of citrate per liter of urine daily.[15] When treating aciduria or uric acid stones, the actual urinary citrate level is less important than the urinary pH, which should be 6.5 or higher optimally.[8] Potassium citrate is the recommended oral citrate supplement, but sodium bicarbonate may also be used.[15] See StatPearls' companion reference, "Hypocitraturia and Renal Calculi."[15]

Relative dehydration and inadequate urinary volume, particularly less than 1 liter per day, greatly increase the concentration of solutes (indicated by urine with an osmolarity greater than 600 mOsm/Kg) and promote urinary stasis, which can cause supersaturation of solutes, leading to urinary stone formation. The optimal daily urine volume for stone formers is 2,500 mL, with a minimum acceptable level of 2,000 mL.[14][16] (The average daily urinary fluid volume in normal individuals without stones is 1,300 mL.) Inadequate urinary fluid excretion is the most common single cause of urolithiasis.

Urinary tract infections by urease-producing bacteria lead to ammoniagenesis and increased urinary pH. This produces conditions that promote the formation of struvite, infection, or triple (magnesium, calcium, ammonium) phosphate calculi.[17] Staghorn stones are typically composed of this material. Treatment requires infection control and complete removal of all infected stone material.[17] Acetohydroxaminc acid, a urease inhibitor, can be used in selected cases.[16][17] See StatPearls' companion reference, "Struvite and Triple Phosphate Renal Calculi," for more information."[17]

Epidemiology

The yearly incidence of urolithiasis in North America and Europe is 0.5%. Of those diagnosed with urolithiasis, 50% will have a recurrent stone within 10 years or less from the initial presentation if preventive measures are not taken.[18]

According to the National Institute of Health, about 6% of women and 11% of men in the US will experience a stone attack sometime in their lives.

Over 1.2 million emergency department visits a year in the US are due to acute renal colic, with about 20% of patients requiring hospital admission.[19][20]

Over the last 30 years, the global incidence of kidney stone disease has steadily increased, and it continues to do so.[21][22]

Most stones (over 70%) occur in people aged 20 to 50. They are more common in men than women by a factor of about 2:1, but the rate of increase in females is higher.[21]

Patients with obesity, hypertension, a positive family history of nephrolithiasis, irritable bowel syndrome, and diabetes are at increased risk for kidney stone formation.[23][24][25]

Hispanics and Blacks have the lowest overall risk of kidney stones, compared to Whites, who have the highest.[26] This is likely due to cultural dietary preferences, geographical location trends (warmer climate), and socioeconomic factors rather than genetic differences.[21]

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.[27] The lifetime risk of at least one other stone is roughly 60% to 80%.[28]

The chances of a repeat renal colic attack are increased in patients with the following risk factors: [29][30]

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 (Not Black, Hispanic, or Asian)

Pathophysiology

As a stone moves from the renal collecting system, it can significantly affect the genitourinary tract by causing either constant or intermittent obstruction and hydronephrosis of the ureter. This results in urine backing up into the kidney, ureteral dilation, pyelolymphatic backflow, and stretching of the renal capsule.

Intermittent obstruction often causes longer-lasting discomfort and pain than a constant blockage, where compensatory mechanisms can somewhat offset the increased ureteral intraluminal pressure.

An acute ureteral obstruction causes a decrease in the glomerular filtration rate of the affected kidney and increases urine excretion by the unaffected kidney, as well as very severe, excruciating pain.

Complete obstruction of the ureter can lead to the eventual loss of renal function, with damage becoming irreversible, possibly starting at just 1 to 2 weeks. Additionally, there is a risk of rupture of a renal calyx with the development of a urinoma.

In general, a stone in the kidney itself does not cause pain or discomfort unless it becomes infected or causes some degree of urinary obstruction. The severity of pain is dependent on the degree of ureteral obstruction, not on the size of the stone. Therefore, a larger stone can pass painlessly, while a small 2- to 3-mm stone can cause tremendous discomfort. Intermittent obstruction from a stone that blocks and releases as it rotates or swivels is also possible.

Urinary calculi can become impacted anywhere in the urinary tract, but most commonly at 1 of 3 locations where the ureter is anatomically narrow:

At the ureteropelvic junction, where the renal pelvis narrows abruptly to meet the ureter.
Near the pelvic brim, the ureter makes an acute posterior turn just distal to the iliac bifurcation.
At the ureterovesical junction, where the ureter tunnels transversely through the muscular bladder wall. This is the narrowest portion of the ureter.[31]

Pain results from a combination of ureteral muscle spasms, increased proximal ureteral dilation and peristalsis from activation of intrinsic ureteral pacemakers, stone-induced localized inflammatory changes, renal swelling with capsular stretching, edema, and irritation. These processes stimulate submucosal stretch receptors in the ureter, renal pelvis, and capsule, which directly cause pain.

Of all the factors that can contribute to flank pain and renal colic, stimulation by stretching the renal pelvis, the peripelvic renal capsule, and the calyces most closely mimics typical renal colic.

Unfortunately, the severity of the pain does not reliably predict stone size or likelihood of spontaneous expulsion.[32] Fortunately, acute renal colic pain typically lasts only about 24 hours, after which the blocked ureter reaches an equilibrium as new stretching generally stops by that point. Severe pain or other symptoms lasting more than 3 days are likely to require surgical intervention.

Various parameters have been looked at to help predict which patients are more likely to fail conservative management of their acute renal colic and require surgery. A previous history of renal colic weakly correlated with a failure of conservative treatment, but neither gender, degree of hydronephrosis, initial degree of pain, stone size, shape, or location could reliably predict which patients would ultimately require surgical intervention.[33] In general, the larger and more proximal the stone, the greater the likelihood of eventually requiring surgical intervention.

The immediate effect of a newly obstructing ureteral stone is to increase proximal intraluminal pressure, which initially distends the renal pelvis and increases ureteral peristalsis. Peak renal pelvic pressure from a high-grade obstruction is usually obtained within 2 to 5 hours of a complete ureteric obstruction.

Other renal changes after a complete ureteral blockage include pyelolymphatic and pyelovenous backflow. Interstitial renal edema develops, significantly increasing lymphatic drainage from the affected kidney and stretching the renal capsule. This stretching directly leads to painful stimuli from the renal capsular stretch receptors.

Often, a state of equilibrium will be achieved as the increasing proximal ureteral dilation allows some urine to pass around the obstruction, which is enough, along with the other compensatory measures, to relieve the pain and achieve stability.

Pain fibers are primarily through the preganglionic sympathetic nerves and the ascending spinothalamic tracts. When the stone approaches the intramural ureter, the nervi erigentes can become involved, which can cause various bladder symptoms, including frequency, urgency, dysuria, hesitancy, and difficulty in voiding.[34][35][36]

Renal blood flow increases for 90 minutes after initial ureteral blockage before diminishing. This is caused by vasodilation of the afferent preglomerular arterial blood supply. Within 5 hours after the ureteral obstruction, renal blood flow and ureteral intraluminal pressures have dropped back to normal or even lower.

Over time, renal blood flow tends to diminish slowly. By 3 days, the renal blood flow has dropped to about half of the usual baseline. This trend gradually continues over time. By 8 weeks, renal blood flow is only 12% of its previous normal baseline value. Even then, the dilation and hydroureteronephrosis usually remain, but ureteral peristalsis has almost disappeared. Renal blood flow in the contralateral kidney has increased at this point.

Nausea and vomiting are associated with classic renal colic in about half or more of patients with acute obstructing ureteral calculi. This is due to a common innervation pathway between the kidneys and the gastrointestinal tract embryologically through afferents of the vagus nerve and celiac axis. This effect can be exacerbated by nonsteroidal anti-inflammatory drugs (NSAIDs) and opioid medications that have gastrointestinal adverse effects. Nausea and vomiting are not from the intensity of the pain, as other extremely painful disorders do not produce such adverse effects.

History and Physical

Patients with renal colic typically present with acute or sudden onset of flank pain radiating inferiolaterally to the lower abdomen, groin, or testicle. Patients often report a dull, constant level of discomfort with colicky episodes of markedly increased pain. The constant discomfort is often due to stretching of the renal capsule due to obstruction, whereas the colicky pain is caused by peristalsis of the ureteral smooth muscle.

Many patients report associated nausea or vomiting, and most (85%) will have gross or microscopic hematuria.

As the stone migrates distally and approaches the bladder, the patient may experience increasing lower urinary tract symptoms such as dysuria, urinary frequency, urgency, or difficulty in urination.

Patients experiencing renal colic may present in very severe, excruciating pain. Classically, these patients are unable to find a comfortable position and are often writhing or constantly pacing, compared to patients with an acute abdomen who typically want to remain absolutely still.[37]

The physical exam will reveal flank pain or discomfort but may also demonstrate abdominal pain, and the skin may be cool or diaphoretic.

There is often a personal or family history history of stones, recent ureteroscopic surgery, or removal of a double J stent.

In the case of a recent ureteroscopy or immediately after removing a double J stent, the history alone can provide the diagnosis. In these cases, the pain is due to ureteral spasm, which effectively causes an obstruction with resultant proximal ureteral and renal dilation even without a stone. The pain can be just as intense as from an obstructing ureteral stone but is usually limited and will resolve with time. However, some patients may need a drainage procedure or placement of a double J stent.

Patients taking topiramate, protease inhibitors, acetazolamide, protease inhibitors (atazanavir, indinavir), sulphadiazine, ephedrine, and guaifenesin will be at higher risk of drug-related urolithiasis.[38][39][40]

Evaluation

The diagnosis is made through a combination of the history and physical exam, laboratory testing, and imaging studies.[18]

Urinalysis shows some degree of microscopic or gross hematuria in 85% of stone patients but should also be evaluated for crystalluria, pH, and signs of infection (eg, white blood cells, bacteria). Urinary pH greater than 7.5 may suggest a urease-producing bacterial infection, while urinary pH values less than 5.5 may indicate the presence of uric acid calculi.[8][17] If there are signs of infection, a urine culture should be obtained.

Hematuria is present in 85% of acute renal colic cases caused by calculi.[41] While the presence of hematuria suggests a stone, it is not definitive, nor does its absence conclusively prove that a stone is not present.[41]

Laboratory studies should include a basic metabolic panel (BMP) with serum calcium and creatinine levels, which should be obtained to assess renal function, dehydration, acid-base status, and electrolyte balance.[18] Serum uric acid should also be checked. A complete blood count (CBC) can be considered to evaluate for leukocytosis if there is a concern for infection, although a mild elevation of WBCs (up to 15,000 WBCs per microliter) is common secondary to white blood cell demargination and is not necessarily indicative of an infection.[18][42][43]

A 24-hour urine collection for prophylactic testing should be considered later for interested patients, especially if high-risk or recurrent stone-formers. However, all patients with a history of urolithiasis should be informed of this option.[18]

Parathyroid hormone (PTH) levels should be obtained if hypercalcemia is present or 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, such as a 24-hour urine collection for volume, pH, calcium, oxalate, uric acid, citrate, sodium, magnesium, and potassium concentrations, should be considered in high-risk first-time, pediatric or recurrent stone formers. It is highly recommended in nephrolithiasis patients with solitary kidneys, renal failure, transplanted kidneys, gastrointestinal (GI) bypass (eg, Roux-n-Y), and any patient with high or increased anesthesia risk.

Renal ultrasonography can be used to establish hydronephrosis, measure the resistive index, and track larger renal stones (especially uric acid), but it will often miss stones smaller than 3 mm in size and is not a reliable imaging modality for visualizing ureteral calculi.[44][45] The degree of perinephric fluid can reasonably predict the degree of obstruction.[3] Visualizing ureteral calculi with ultrasound is not always easy, but identifying ureteral jets in the bladder can be helpful when trying to determine obstruction.[44]

Ultrasound has the advantage of not exposing the patient to ionizing radiation, can visualize even radiolucent stones, and can be done quickly at the bedside in the emergency department by ER physicians or through radiology. It is the recommended imaging modality of choice in pregnant patients, although low-dose unenhanced CT scanning may be done during the second and third trimester when ultrasonography is inadequate or nondiagnostic.[46]

Ultrasonography alone may be sufficient to verify a diagnosis in selected cases, especially in patients with a history of recurrent ureterolithiasis.[47][48] In such cases, a flat abdominal x-ray is usually recommended for tracking and follow-up. However, using ultrasound alone may lead to incorrect management in about one-fifth of patients as it provides insufficient information on stone size, shape, or location.[49]

The renal resistive index, as determined by ultrasound, can be very useful in diagnosing ureteral obstructions. It is defined as (peak systolic velocity-end diastolic velocity)/peak systolic velocity where normal is typically 0.7 or less, and higher levels indicate either obstruction or intrinsic renal disease.[50][51][52][53][54]

A high resistive index in just one kidney in a patient with renal colic affecting that side would be highly suggestive of acute ureteral obstruction, such as from ureterolithiasis.[50][52][53]

Medical renal disease would tend to have elevated but similar levels bilaterally.

Ultrasound is the modality of choice for evaluating a pregnant patient with concern for renal colic. Studies have shown that using ultrasonography as a primary imaging modality does not lead to an increase in complications in comparison to CT. Ultrasound is also a good way to continue to assess a patient with uric acid renal calculi.[55] While suggestive, negative ultrasonography of the kidneys does not definitively rule out a ureteral stone or renal colic.

A plain abdominal x-ray (KUB) can identify many stones, but 10% to 20% of renal calculi are not visible as they are radiolucent. It provides little information regarding hydronephrosis, obstruction, or internal renal anatomy and is of limited benefit 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 the unenhanced computerized tomography (CT) scan is positive, and the exact location of the stone is known. This helps clearly identify stones that can be tracked by follow-up KUB and, therefore, might be amenable to lithotripsy. The KUB also more accurately depicts the shape of the stone and provides good surgical orientation.

As many CT scans ordered in the emergency department patients use IV contrast, it is suggested that a KUB be routinely performed on all patients with possible ureterolithiasis before the CT so any IV contrast administered will not interfere with identifying any urinary calculi.

Combining renal ultrasonography with a KUB can be very cost-effective and efficient as an alternative to CT scans with lower cost, reduced radiation, and good efficacy.[55][56]

Renal ultrasound can easily demonstrate hydronephrosis, measure the resistive index as an indicator of obstruction, and identify even radiolucent renal calculi. However, it has difficulty detecting ureteral calculi or stones smaller than 3 mm in size.

The KUB has good sensitivity for detecting urinary calcifications but will not visualize radiolucent stones and provides no information on renal function, hydronephrosis, or possible ureteral obstruction.

Symptomatic stones will likely produce hydronephrosis or obstruction (visible on ultrasound) or be seen directly on the KUB.[55][56] Combining KUB radiography with renal ultrasonography provides a reported diagnostic accuracy for an obstructing stone of 90%, a specificity of 93%, and a sensitivity of 88%.[57]

Unenhanced CT scans are the gold standard for the initial diagnosis of suspected renal colic, with a sensitivity of 98%, specificity of 100%, and negative predictive value of 97%.[58][59][60][61][62][63] This modality allows rapid identification of stone, provides information as to the location and size of the stone along with any associated hydroureter, hydronephrosis, or ureteral edema, and can give information regarding potential other etiologies of pain (eg, abdominal aortic aneurysm, malignancy).[55]

CT should be performed in patients with acute renal colic and no previous history of nephrolithiasis to guide management. Remember that CT scans will underestimate stone size compared to an intravenous pyelogram or abdominal x-ray (KUB) by about 12%.[64]

Evaluation of Renal Colic in Pregnancy

Ultrasound is the obvious first-line study, but the results may be nondiagnostic or equivocal.[65] Options include conservative measures and observation, low-dose CT scan imaging, magnetic resonance urography, or ureteroscopic surgery.

Ureteroscopic surgery with laser lithotripsy and double J stent placement is a reasonable option in such cases if the clinical presentation is strongly suggestive of urolithiasis and symptoms like pain are prolonged or difficult to control.[65] Ureteroscopic surgery can be safely performed in pregnant patients with urolithiasis, with good outcomes reported and a negative ureteroscopy rate of only 14%.[66][67][68][69]

Surgical intervention is more likely in pregnant patients with acute renal colic who present with any of the following:

Continuous pain for four or more days
Difficult to control pain
Elevated serum creatinine levels
Fever
Greater degree of hydronephrosis
Greater degree of leukocytosis
High serum C-reactive protein
Higher neutrophil/lymphocyte ratio
Increased fetal body weight
Larger (≥8 mm) ureteral calculig [70][71]

CT scans using low-dose and ultra-low-dose radiation protocols are recommended, especially for pediatric and pregnant patients, as they dramatically reduce patient radiation exposure without seriously affecting the scans' diagnostic efficacy for detecting urolithiasis.[72][73][74][75] A low-dose CT delivers about half the radiation of a standard dose scan, and an ultra-low-dose protocol reduces the exposure by another 55%.[72][73][76][77] The positive predictive value of low-dose CT in such cases is 95.8%.[65][66]

While most urinary stones—including the relatively radiolucent cystine, dihdroxyadenine, xanthine, and uric acid calculi—will appear on CT scans, a few stone compositions will not, mostly consisting of antiviral protease inhibitor medications and their metabolites.[78][79] These include atazanavir and indinavir.[80][81][82][83][84][85] A contrast study will be needed when such stones are suspected.[79][84]

However, CT scans expose patients to a significant radiation burden, and they can be costly. In some patients with a history of renal colic that present with pain similar to previous obstructing urolithiasis, it may be sufficient to perform ultrasonography. While ultrasound is significantly less sensitive (60% to 76%) than CT for identifying calculi less than 5 mm, it can reliably detect hydronephrosis and other evidence of ureteral obstruction (increased resistive index in the affected kidney, unilateral blocked ureteral jets). If the stone should pass before imaging can be performed, some evidence of residual inflammation may remain and be identified, 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 allow the selective and judicious use of low-dose, non-contrast CT imaging in pregnancy for cases where ultrasound is diagnostically insufficient.[65][86]

Magnetic resonance urography does not enjoy the high positive predictive value and sensitivity of CT scans for ureteral calculi, but it does not use any ionizing radiation and offers improved detection rates for urinary stones, particularly when ultrasound alone is inadequate. Magnetic resonance urography enjoys a positive predictive value of 80%, which is not as good as CT scanning but avoids using X-rays.[65][66][87][88] It is therefore recommended by the European Association of Urology (EAU) as the second-line imaging modality after ultrasound in equivocal clinical situations as an alternative to ureteroscopic surgery as it is safer than CT scanning during pregnancy.[65][87][88]

Ureteroscopic surgery with laser lithotripsy and/or double J stent placement is a reasonable option in such cases if the clinical presentation is strongly suggestive of urolithiasis and symptoms like pain are prolonged or difficult to control.[65][69] Ureteroscopic surgery can be safely done in pregnant patients with urolithiasis, with good outcomes reported and a negative ureteroscopy rate of only 14%.[66][67][68][69] Placement of a double J stent or performing a percutaneous nephrostomy is less invasive means of temporizing the clinical situation until after delivery when more definitive diagnostic and therapeutic measures can be safely performed without jeopardizing the fetus or the pregnancy.

The degree of hydronephrosis on imaging does not always correlate well with the pain intensity or the likelihood of spontaneous passage. In general, the presence of minimal-to-moderate hydronephrosis from a stone does not appear to affect the spontaneous stone passage rate significantly, but severe hydronephrosis suggests a reduced passage rate and earlier surgical intervention may be warranted.[89]

Surgical intervention is more likely and typically earlier in pregnant patients with acute renal colic who present with the following: [70][71][90]

Anterior-posterior diameter of the renal pelvis of greater than 18 mm
Abnormal ureteral anatomy
Continuous pain for four or more days
Difficult to control pain
Elevated serum creatinine levels
Extrarenal pelvis
Fever
Greater degree of leukocytosis
Greater stone density (>700 Hounsfield units)
High serum C-reactive protein
Higher degree of hydronephrosis
Higher neutrophil/lymphocyte ratio
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

Urosepsis

Urosepsis is defined as a potentially life-threatening organ dysfunction caused by a dysregulated host response to infection originating from a urological source.[91][92] It is characterized by symptoms and signs including hypotension, tachycardia (>90 beats/min), tachypnea (>20 breaths/min), pyuria, and leukocytosis (>12,000 per μL [12 × 10⁹ per L]).[93] Remember that mild leukocytosis up to 15,000 per μL (15 × 10⁹ per L) is common in acute renal colic without infection.[18][42][43] Acidosis (serum pH <7.35) may also be present.[94]

Any patients with renal colic who also have a fever of 100 °F (37.8 °C) or more, significant leukocytosis (>15,000 WBCs/mm³), pyuria, hypotension, or unexplained tachycardia should be considered at risk for urosepsis and obstructive pyelonephritis, especially if diabetic.[95]

The recommended treatment for patients with acute renal colic from an obstructing ureteral stone and signs of systemic infection, sepsis, or obstructive pyelonephritis is urgent drainage of the renal pelvis, either with cystoscopy and double J stenting or via a percutaneous nephrostomy.[96]

Since there is no way to distinguish acute from obstructive pyelonephritis clinically, imaging is required when the diagnosis is uncertain, particularly in diabetic patients and those at increased surgical or anesthesia risk. Ultrasonography is usually sufficient for this purpose, but an unenhanced CT scan would be considered definitive if the results are uncertain or equivocal.

There is great potential for using various urosepsis serum biomarkers early to identify septic patients sooner.[97] See StatPearls' companion references, "Urosepsis," "Bacterial Sepsis," and "The Laboratory Evaluation of Sepsis," for more detailed information."[95][98][99]

The selection of specific biomarkers to help diagnose early urosepsis will depend on cost, test availability, and physician familiarity with the interpretation of the laboratory study. Some of the more clinically useful of such serum biomarkers are briefly reviewed below:

C-reactive protein (CRP) is an inexpensive, readily available laboratory indicator of infection and inflammation, but it is slower to react to bacterial sepsis than procalcitonin, and it is not specific for bacterial infections.[99][100][101]
- The protein is produced in the liver when stimulated by serum IL-6.[101]
- The serum concentration of CRP increases 6 hours after the initial inflammatory event, doubles every 8 hours, and peaks by 36 to 50 hours, roughly twice as long as procalcitonin.[101][102][103]
- A cutoff level of 50 mg/L for identifying bacterial sepsis is generally used.[100]
- The half-life of CRP is 19 hours.[104]
- See StatPearls' companion reference, "C Reactive Protein."[105]

Interleukin 6 (IL-6) may be an even better biomarker for tracking disease progression than procalcitonin, lactic acid, or CRP.[106][107][108][109]
- IL-6 is a proinflammatory cytokine intimately involved in host defense mechanisms and has been proposed as a laboratory biomarker for sepsis.[110]
- It is manufactured by immune and stromal cells, including endothelial cells, fibroblasts, endothelial cells, macrophages, monocytes, and T-lymphocytes.[107][111][112]
- A value of 52.6 pg/mL or more has been suggested as the threshold level for identifying sepsis.[107]
- IL-6 levels peak at 12 hours, and it has a half-life of about 1 hour.[113][114]

Lactic acid (lactate) in the serum is normally less than 2 mmol/L (18.2 mg/dL). Higher titers are consistent with infection, and levels greater than 4 mmol/L (36.4 mg/dL) are considered severe and suggestive of sepsis, especially if rising rapidly.[99][115]
- Serum lactic acid level is a reflection of relative tissue hypoxia, but recent data indicate it is a chemical, adaptive response to abnormal metabolism as well as a marker of higher endogenous catecholamine levels.[99][116]
- A reduction in lactic acid levels is a good indicator of tissue recovery.[116]
- A repeat level in 6 hours is recommended if it is found to be elevated initially.[117]
- It has been suggested that levels be rechecked in critical patients every 2 hours.[118]
- Note that lactate and lactic acid levels are similar but not exactly chemically equivalent, so check the normal ranges in the specific laboratory.
- The half-life of serum lactate is about 20 minutes.

The neutrophil-to-lymphocyte (NLR) ratio is higher in patients with worsening sepsis but is also elevated in older individuals.[119]
- Normal and abnormal levels have not been conclusively defined, but levels above 3.75 to 4 appear consistent with sepsis and urosepsis.[119]
- This test has the advantages of being inexpensive, readily available, easily calculated, and immediately available.[119][120][121][122]

Pentraxin 3 (PTX3) is an inflammatory serum protein produced early in the inflammatory process by various cell types.
- It activates the complement immune system pathway, as well as dendritic cells and macrophages, promotes the identification of pathogenic bacteria, and serves as an antibody precursor.[108][123][124]
- A number of studies have suggested PTX3 could be a useful laboratory marker of sepsis and a prognostic indicator, roughly comparable to IL-6.[107][108][125][126][127][128]
- Pentraxin 3 has a relatively short half-life of 1 to 4 hours.[129][130]

Procalcitonin, a calcitonin precursor, is a useful specific indicator for the severity of bacterial infections and is useful for tracking disease progression.[99][116][131]
- It correlates well with the degree of leukocytosis and C-reactive protein levels for infection monitoring.[100][131]
- Procalcitonin is considered superior to C-reactive protein as a sepsis marker because it is more specific for bacterial infections; it rises earlier (peaks at 6 to 12 hours) and normalizes faster.[131][132][133]
- Normal levels of procalcitonin are typically lower than 0.1 μg/L, but patients with renal failure may have higher baseline levels.[131][134]
- A low or normal procalcitonin level does not completely or definitively rule out a bacterial infection.[131][133]
- Procalcitonin has a half-life of about 24 hours.[131]
- See StatPearls' companion reference, "Procalcitonin."[131][133]

Treatment / Management

Management of Acute Renal Colic

Immediate intervention is with adequate analgesia, antiemetics, and IV hydration. Antibiotics should be given if the patient shows any systemic signs of infection or has infected urine. Nonsteroidal anti-inflammatory drugs (NSAIDs) and opiates are first-line therapies for analgesia. NSAIDs work in 2 ways in renal colic.

NSAIDs are generally preferred initially as they avoid the side effects of opioid use and are quite effective, being roughly equivalent or even superior to opioids for pain relief.[135][136][137][138][139][140] They decrease the production of arachidonic acid metabolites, which mediate pain receptors, alleviating pain caused by distension of the renal capsule.[141] They also block the production of prostaglandins, which decreases pain receptor activity and reduces ureteral contractions, although it may also cause some platelet dysfunction.[141][142](A1)

Additionally, they cause contraction of the efferent arterioles to the glomerulus, causing a reduction in glomerular filtration and reducing hydrostatic pressure across the glomerulus. Because patients with renal colic are frequently unable to tolerate oral medications, parenteral NSAIDs such as ketorolac (15-30 mg IV or IM) or diclofenac (37.5 mg IV) are most commonly used.[143][144][135][142][145](A1)

Ketorolac, an injectable NSAID often used for renal colic, is equivalent or superior overall to opioids in treating the pain of acute ureterolithiasis while being safer and risking fewer significant side effects.[135][136][137][142][146] Therefore, ketorolac and similar NSAID medications are generally preferred for the initial management of pain in patients with acute renal colic.[141][142] Ketorolac can also be used as a continuous IV drip, typically at 3 to 5 mg/h.[142][147][148][149][150](A1)

Adding 8 mg of dexamethasone improved pain relief in renal colic patients compared to ketorolac alone.[137][151] The use of IV morphine after ketorolac was also found to be beneficial in patients requiring additional analgesia.[137](A1)

Ketorolac may be used together with IV acetaminophen, but this is not generally recommended for more than a few days, even though no specific negative interactions have been noted. There is no published data on the efficacy of this combination for renal colic.

Ketorolac cannot be used in patients with renal failure (GFR <30 mL/min), a history of gastrointestinal bleeding, aspirin or NSAID allergy, or pregnant women (category C).[142]

Opioid pain medications, such as morphine sulfate (0.1 mg/kg IV or IM) or hydromorphone (0.02 mg/kg IV or IM), can also be used effectively for analgesia, especially when other measures, such as ketorolac, have failed or their maximum dose provides insufficient analgesia.[152][153] However, opiates are associated with respiratory depression, decreased gastrointestinal motility, increased nausea, and sedation. There is also a risk of dependence associated with prolonged opiate use.[154][155][156](B3)

Intravenous acetaminophen has demonstrated rough equivalence to ketorolac in a meta-analysis, but the overall data is insufficient to recommend it over standard analgesics, although it can safely be used together with NSAIDs and opioids.[157][158]

Intravenous lidocaine has been used for pain relief from acute renal colic, with good results reported.[159][160][161] The protocol is to inject lidocaine 100 to 120 mg in 100 mL of normal saline intravenously over 10 minutes for pain management. It has been quite effective for intractable renal colic unresponsive to standard therapy and typically starts to work in 3 to 5 minutes. No adverse events have been reported.[162] (A1)

It is unclear if adding lidocaine to patients who have received ketorolac provides much additional benefit as studies are conflicting, but salvage therapy with lidocaine has also been reported.[163]

Intradermal sterile water injection therapy has been demonstrated to be effective in relieving the pain of acute renal colic, roughly equivalent to NSAIDs.[164][165][166][167][168][169][170] Pain relief does not occur when normal saline is used instead of sterile water. The injections are done directly into the flank at the site of greatest tenderness. The mechanism for this surprising result is still unclear.[169](A1)

Most experts believe it is through diffuse noxious inhibitory control or a pain inhibition gate control mechanism.[169][171] It may also produce localized inflammation, triggering the A cutaneous afferents, leading to endorphin release or working through physiological distraction.[171][172]

The technique is simple, safe, inexpensive, has no significant side effects, and can be repeated as needed. It also does not interfere with the use of any other method of pain management. Therefore, intradermal water injection therapy appears worthy of additional study and possible clinical use for analgesic relief in acute renal colic situations.

Antiemetics should be used as needed for symptomatic relief. There is a general lack of strong data regarding the relative effectiveness of antiemetic drugs used for symptom control of nausea and vomiting in patients with acute renal colic.[173] The limited studies available suggest that ondansetron may be the drug of choice in these situations.[174][175][176][177] It is unclear what additional agents can be used to optimize symptom relief when ondansetron alone is insufficient.

Intravenous fluid hydration is a recommended adjunct to the initial treatment of acute renal colic. Although there is no evidence to support that empiric fluid will help “flush out” a stone, many patients are dehydrated secondary to decreased oral intake, nausea, or vomiting and benefit from additional intravenous hydration.

Nerve blocks can often be helpful, especially in cases of chronic flank pain.[178] An anesthetic injection is typically administered proximal to the 11th or 12th intercostal nerve area. The good reported efficacy of a nerve block suggests a musculoskeletal or neuropathic etiology. Paraveterbral, splanchnic, and intercostal nerve blocks have all shown varying degrees of efficacy in relief from flank pain.[179][180][181](B3)

Reported randomized clinical trials of alternative analgesic agents for pain relief in patients with acute renal colic frequently use morphine and other opioid-based medications as rescue drugs, which makes it difficult to rely on their reported relative effectiveness.[182] It is recommended that future randomized controlled studies define the success of therapy as being the total or near-total pain relief and not merely unquantified pain relief.[182](A1)

Kidney stone prophylaxis with 24-hour urine testing should be discussed and considered in all urolithiasis patients, especially in high-risk and recurrent stone formers. This would include patients with solitary or horseshoe kidneys, renal failure, abnormal ureteral anatomy, pediatrics, cystine stone formers, and those with high surgery/anesthesia risk factors. The success of 24-hour urine testing largely depends on the patient's willingness to follow treatment suggestions and dietary modifications long-term.

Since patients do not feel any differently on prophylactic therapy, it is often very tempting to cheat from time to time. When nothing "bad" happens, it becomes very easy to skip therapy for longer and longer periods or to completely stop the treatment altogether.[14]

The American Urological Association Guidelines recommend informing even first-time stone formers about 24-hour urine testing and prophylactic therapy.[18] Excellent guidelines for interpreting 24-hour urine tests and optimizing treatment selection have been published and are now available for free download.[14] See StatPearls' reference article on "24-Hour Urine Testing for Nephrolithiasis: Interpretation Guideline."[14] Calcium loading tests for patients with hypercalciuria are no longer recommended.[18][183][184]

Behavior modification, dietary adjustments, and general urolithiasis preventative measures should be discussed with all patients with kidney stones. Typical suggestions include the following:

Increase fluid intake to optimize urine output with a goal of at least 2,000 mL and, optimally, 2,500 mL of urine daily.
Patients with calcium stones and high urine calcium concentrations should limit sodium and meat protein intake while maintaining a moderate calcium diet of 1,000 mg to 1,200 mg of dietary calcium daily.
Thiazide diuretics and a salt-restricted diet are indicated in those with high urinary calcium to reduce the amount of urinary calcium.
Those 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 decreasing nondairy dietary animal protein.
Uric acid stone formers are usually best treated with potassium citrate (urinary alkalinizer) to achieve an optimal urinary pH of 6.5 or more.
Hyperuricosuric calcium stone formers can benefit from allopurinol or febuxostat.
Patients with hyperoxaluria should be encouraged to lower their oxalate intake (spinach, nuts, chocolate, green leafy vegetables), maintain a moderate calcium intake or calcium citrate supplementation with their higher oxalate meals (usually lunch and dinner), and increase their fluid intake.
Cystine stone formers need exceptional urinary volumes of 3,000 mL or more daily urine volume and a pH of 7.5 or more to optimize cystine solubility. Potassium citrate is the urinary alkalinizer of choice. Tiopronin and other thiol medications are also used to lower urinary cystine levels.[7][8][12][13][14][15][16][17]

Treatment of Ureterolithiasis

Medical expulsive therapy is generally recommended, particularly for smaller stones in the distal ureter.[18][63] Alpha-1 adrenergic receptors exist in increasing concentrations in the distal ureter.

Alpha-blocker medications (alfuzosin, nifedipine, silodosin, or tamsulosin) facilitate stone passage by relaxing and dilating the ureteral lumen, particularly in the distal ureter.[63][185][186][187][188][189][190][191]. However, data from randomized control trials are somewhat mixed regarding how well these medications improved spontaneous stone passage rates.[62][63][185][192](A1)

The consensus opinion and the recommendation from the American Urologic Association Guidelines are that medical expulsive therapy appears helpful for smaller stones in the lower or distal ureter and is generally recommended, but such treatment is probably of little use for larger stones in the proximal ureter.[62][185][193][194][195][196][197](A1)

If tamsulosin is used, the only available data uses 0.4 mg, and it remains unclear how well a larger dose (0.8 mg) would perform. Alfuzosin and tamsulosin were roughly comparable, but nifedipine appeared less effective overall than other agents used for medical expulsive therapy.[191](A1)

Mirabegron, a beta-3 adrenoceptor agonist usually used for bladder overactivity, appears to have a beneficial effect on facilitating spontaneous ureteral stone passage. A recent systemic review and meta-analysis of randomized controlled trials found that the drug improved the spontaneous expulsion rate of ureteral calculi, particularly for smaller stones smaller than 6 mm in size located in the distal ureter.[198][199]
- Mirabegron did not reduce the time for spontaneous expulsion or help with pain management.[199]
- There is no data on using mirabegron with alpha-blocker medications for medical expulsive therapy of ureteral calculi.

(A1)

Tadalafil has been suggested as an agent for medical expulsion therapy, but the results of studies are somewhat conflicting, and therefore, it cannot be recommended as a single agent used alone.[200][201][202][203]

(A1)

Silodosin appeared to be superior to both tamsulosin and alfuzosin in several recent systemic reviews, comparisons, and meta-analyses of agents used for medical expulsive therapy.[186][204][205][206] If silodosin is selected for medical expulsive therapy, the higher dose (8 mg) is recommended because the lower dose of 4 mg was clearly inferior, with reduced expulsion rates and increased pain reported.[207](A1)

Various combinations of medical expulsive drugs have been studied, such as tadalafil plus either tamsulosin or silodosin, which appeared to be somewhat more effective than either single agents or other combinations.[208][209] However, further high-quality studies are required to determine the relative efficacy and optimal composition of such combination treatments when used as medical expulsive therapy for ureteral calculi.[208](A1)

Antibiotic use in patients with acute renal colic should generally be limited to patients with clinical or laboratory evidence of a urinary tract infection. A microscopic urinalysis would include at least 10 WBCs/HPF (or more WBCs than RBCs), bacteriuria, or positive nitrites on the urine dipstick.

Systemic signs of infection include leukocytosis, fever, tachycardia, lactic acidosis, elevated procalcitonin, or other signs of a possible urinary or systemic infection. Be aware that patients with stones can appear fine with typical vital signs and become deathly ill with urosepsis from obstructive pyelonephritis within just a few hours.

Patients at high risk would be older adults (who may not show signs of infection until floridly septic), patients with diabetes, patients 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 using antimicrobials in high-risk individuals, particularly patients with diabetes who present with acute renal colic and who are not yet septic. Some of these patients will return with urosepsis and obstructive pyelonephritis.

Definitive surgical management of impacted ureteral stones can be achieved using several procedures. These include extracorporeal shock wave lithotripsy, in which high energy shock waves are used to fragment stones, ureteroscopy with stone basketing, laser or electrohydraulic stone fragmentation, or rarely, open surgery.[5][62][210][211] These options are described in detail in StatPearls' companion references, "Ureterolithiasis," "Extracorporeal Shockwave Lithotripsy," and "Ureteroscopy."[5][210][211]

Laparoscopic and robotic surgery are other possible procedural options, usually reserved for unusually complex or unusual clinical situations.[212][213][214]

In the presence of infection, a double J stent or percutaneous nephrostomy may be used to help with urinary drainage of the affected renal unit, with definitive stone therapy postponed until the infection has cleared.[62][215][216](A1)

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

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 over 3 days).
New onset of anuria, coincident with the ureteral obstruction.
Obstructive pyelonephritis (pyonephrosis) is likely or suspected.
Patient personal preference.
Pregnant patients who have failed conservative management.
Recurrent urinary tract infections related to the stone disease.
The stone's size, shape, and position as larger, angular-shaped, and proximal ureteral calculi are less likely to pass spontaneously.
- Stones larger than 10 mm will generally require surgery.
- Stones larger than 7 mm are much less likely to pass and may need surgery.
- Stones 4 mm or less have a spontaneous stone passage rate of 90% to 95% and are unlikely to require a procedure.
Solitary kidney or simultaneous, bilateral ureteral obstruction.
Urinary tract infection (drainage procedures only until the infection is controlled).[62][217][218][219]

(B3)

Double J stent placement can immediately relieve pain and other symptoms of ureteral obstruction, allow an infected renal unit to drain until the infection is controlled, and dilate the ureter, facilitating ureteroscopy. However, its routine preoperative use is generally discouraged except in cases of infection, as it requires additional anesthesia and operating room procedures.

Obstructive pyelonephritis or pyonephrosis describes the potentially dangerous condition where a kidney, obstructed from a ureteral or renal calculus, becomes infected, resulting in progressive urosepsis. This condition can be life-threatening and requires immediate surgical drainage of the renal pelvis, as antibiotics alone will be ineffective.[96][215][220][221][222][223] Overall mortality from obstructive pyelonephritis is reported to be as high as 7.4%, even with treatment.(B2)

A double J stent, placed cystoscopically, is the standard technique for drainage of the renal pelvis, but a general anesthetic is needed. It also requires manipulating a guide wire and stent past the obstructive stone, and it may not be successful in every case.[224] For further details on double J stent placement, see Statpearls' companion reference article, "Double J Placement Methods Comparative Analysis."[224](B2)

If the ureteral obstruction is significant or where the patient is critically ill and too unstable for a general anesthetic, a percutaneous nephrostomy is preferable for renal drainage since it requires only minimal sedation and local anesthesia, minimizes manipulation of the infected renal unit and avoids the possibility of failing to bypass the obstruction with a double J stent successfully.[225][226][227][228][229][230][231][232](A1)

The technique for percutaneous nephrostomy is described elsewhere.[229][230][231] For details, see StatPearls' companion reference, "Percutaneous Nephrostomy."[230]

Delays in surgical decompression of obstructive pyelonephritis increase the risk of death by about 30%.[233][234] These delays were often associated with minority patient populations, lower socioeconomic status, and weekend presentations, suggesting obvious opportunities for improvement.[233] Any delay in treatment will increase morbidity and mortality, particularly if drainage procedures are postponed more than 2 days.[234]

Some evidence suggests that third-generation cephalosporins may be the preferred antibiotics in these situations, but the primary treatment remains surgical.[235]

Most patients with obstructive pyelonephritis who have a timely drainage procedure can safely undergo definitive ureterolithiasis surgery within one to 2 weeks.[236]

Risk factors for the development of obstructive pyelonephritis in patients with ureterolithiasis include the following: [237][238][239][240][241][242][243](B2)

A greater degree of hydronephrosis
Diabetes
Elevated CRP, lactic acid, procalcitonin, or neutrophil-to-lymphocyte ratio NLR
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

Differential Diagnosis

There are multiple possible causes of flank pain simulating renal colic. These include the following:

Abdominal aortic aneurysm dissection
Acute mesenteric ischemia
Angiomyolipomas
Appendicitis
Biliary colic
Bowel obstruction
Cholecystitis
Costochondritis
Dietl's crisis
Diverticulitis
Double J stenting or removal
Ectopic pregnancy
Endometriosis
Focal nephronia
Hepatitis
Herpes zoster
Iatrogenic
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, scarring)
Ureteral spasms
Ureteral stricture
Ureteroceles
Ureteropelvic junction obstruction (UPJ)
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, the size and location of the stone, the specific anatomy of the patient, their clinical history, and comorbidities.

Smaller stones (<5 mm) located in the distal ureter are highly likely to pass spontaneously. The larger the stones and more proximal in the ureter, the less likely they will pass without intervention.

If the kidney becomes infected, urgent surgical intervention to drain the renal pelvis may be necessary to avoid urosepsis, embolic ischemia, limb amputations, and death.

All patients with urinary calculi should receive information concerning 24-hour urine testing for prophylactic treatment. This testing is strongly encouraged in children, patients with renal failure, solitary kidneys, recurrent stone formers, or those at high surgical (anesthetic) risk.

Complications

Possible complications include the following:

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/damage
Sepsis
Ureteral scarring, stricture
Urinary tract infection

Deterrence and Patient Education

Patients should be informed that it is now possible to identify chemical risk factors for producing future stones. This requires a 24-hour urine test. Analysis of the test results can suggest specific changes in patients' diet, lifestyle, or medications that can reduce their risk of forming additional stones, although this is never guaranteed.

Testing is recommended in higher-risk individuals and those with significant comorbidities, solitary kidneys, horseshoe kidneys, recurrent stone formers, children, and those with a high anesthesia/surgical risk.

Patient motivation and discipline will largely determine the effectiveness of the preventive therapy program. Patients determined to minimize their risk of future stones will benefit the most as long-term compliance with treatment is required.

Even without specific testing, general advice would include increasing fluid intake sufficient to generate at least 2,000 mL of urine daily, with an optimal goal of 2,500 mL. Calcium intake should be moderate (too little and too much are not recommended), along with dietary reductions in excessive sodium, animal meat protein, and high oxalate foods.

Patients with cystine stones require special treatment as their stone risk is particularly high, and aggressive medical therapy is required to keep them stone-free.[11] Prophylactic therapy begins with aggressive hydration sufficient to generate 3,000 to 3,500 mL of urine daily and urinary alkalinization to a pH of 7.5.[11]

Pearls and Other Issues

Calculus size, location, and patient discomfort predict the likelihood of spontaneous stone passage. Approximately 90% of stones less than 5 mm pass within 4 weeks. Up to 95% of stones larger than 8 mm will likely become impacted, requiring intervention.

Indications for hospital admission include a significant renal stone in a solitary kidney, severe kidney injury, an infected renal stone, intractable pain or nausea, urinary extravasation, or sepsis.

Patients with infected stones (eg, nephrolithiasis plus evidence of urinary tract infection) require special and more urgent treatment. The infected stone acts as a nidus for infection and leads to stasis, decreasing the ability to manage infections. Frequently, these stones must be removed in their entirety operatively to prevent a repeat infection and the formation of new stones.

Since there is no way to clinically differentiate acute pyelonephritis, a medical condition treated with antibiotics, from pyonephrosis (obstructive pyelonephritis), a potentially life-threatening condition that requires urgent surgical intervention and drainage, some type of imaging is necessary in virtually all cases of acute flank pain, especially if patients admitted for pyelonephritis fail to improve on medical therapy.

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

Intervention for a stone is recommended after 4 to 6 weeks if the stone has not moved or passed, even if the patient is asymptomatic. This is due to the likelihood of ureteral scarring and other complications. It can be challenging to convince an asymptomatic patient to agree to surgery. The most effective technique may be to explain the policy early in the course of treatment so patients understand the need for a procedure to protect the kidneys and ureters from permanent damage if a stone or obstruction appears stuck and is not resolving on its own.

An infected kidney or evidence of a urinary tract infection with obstructing ureterolithiasis constitutes an urgent surgical emergency.[96][220][221][222] Percutaneous renal drainage is preferred over double J stents in the most serious cases or with a substantial ureteral stone burden.[225][226][227][228]

All stone material should be collected and sent for chemical analysis.

24-hour urine tests are the cornerstone of long-term preventive therapy, but they require very high levels of patient dedication and compliance to be successful. Nevertheless, they should be offered to all nephrolithiasis patients.

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 years
High anesthesia or surgical risk
Irritable bowel syndrome (IBS)
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, ebypass surgery, short-bowel syndrome, enteric hyperoxaluria)
Ureteropelvic junction obstruction (UPJ) [14][244]

Enhancing Healthcare Team Outcomes

The management of renal stones is best conducted by an interprofessional team that consists of a nephrologist, emergency department physician, radiologist, urologist, dietician/nutritionist, and primary care provider. Most renal stones will pass spontaneously within 4 weeks, but stones larger than 7 mm may require surgical intervention. Stones that are 10 mm in size or larger will typically require surgery.

Healthcare workers, including nurse practitioners who see patients with kidney stones, should contact the urologist when ureteral stones fail to pass after 4 to 6 weeks with or without medical expulsive therapy. Urologic nurses are involved in treatment, monitoring patients, providing continuing support and patient education, and updating the team on changes in patient status. Pharmacists review prescribed medications for appropriate dosages, check for possible drug interactions, and provide patient education.

In cases of infected ureteral stones, drainage surgical intervention will likely be required, followed by definitive treatment of the obstructing stone several weeks later. The prognosis for most patients with kidney stones is good.

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]

Glazer K, Brea IJ, Leslie SW, Vaitla P. Ureterolithiasis. StatPearls. 2024 Jan:(): [PubMed PMID: 32809509]

[6]

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

[7]

Kaur P, Bhatt H. Hyperuricosuria. StatPearls. 2024 Jan:(): [PubMed PMID: 32965872]

[8]

KC M, Leslie SW. Uric Acid Nephrolithiasis. StatPearls. 2024 Jan:(): [PubMed PMID: 32809561]

[9]

Burger M, Schaller DJ. Metabolic Acidosis. StatPearls. 2024 Jan:(): [PubMed PMID: 29489167]

[10]

Mustaqeem R, Arif A. Renal Tubular Acidosis. StatPearls. 2024 Jan:(): [PubMed PMID: 30085586]

[11]

Leslie SW, Sajjad H, Nazzal L. Cystinuria. StatPearls. 2024 Jan:(): [PubMed PMID: 29262245]

[12]

Leslie SW, Sajjad H. Hypercalciuria. StatPearls. 2024 Jan:(): [PubMed PMID: 28846247]

[13]

Shah A, Leslie SW, Ramakrishnan S. Hyperoxaluria. StatPearls. 2024 Jan:(): [PubMed PMID: 32644413]

[14]

Leslie SW, Sajjad H, Bashir K. 24-Hour Urine Testing for Nephrolithiasis: Interpretation and Treatment Guidelines. StatPearls. 2024 Jan:(): [PubMed PMID: 29494055]

[15]

Leslie SW, Bashir K. Hypocitraturia and Renal Calculi. StatPearls. 2024 Jan:(): [PubMed PMID: 33232062]

[16]

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]

[17]

Karki N, Leslie SW. Struvite and Triple Phosphate Renal Calculi. StatPearls. 2024 Jan:(): [PubMed PMID: 33760542]

[18]

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]

[19]

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

[20]

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]

[21]

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]

[22]

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]

[23]

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

[24]

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

[25]

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]

[26]

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

[27]

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]

[28]

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]

[29]

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

[30]

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

[31]

Lescay HA, Jiang J, Leslie SW, Tuma F. Anatomy, Abdomen and Pelvis Ureter. StatPearls. 2024 Jan:(): [PubMed PMID: 30422575]

[32]

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]

[33]

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]

[34]

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]

[35]

Lanzotti NJ, Tariq MA, Bolla SR. Physiology, Bladder. StatPearls. 2024 Jan:(): [PubMed PMID: 30860768]

[36]

Flores JL, Cortes GA, Leslie SW. Physiology, Urination. StatPearls. 2024 Jan:(): [PubMed PMID: 32965852]

[37]

Patterson JW, Kashyap S, Dominique E. Acute Abdomen. StatPearls. 2024 Jan:(): [PubMed PMID: 29083722]

[38]

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]

[39]

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]

[40]

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

[41]

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

[42]

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]

[43]

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]

[44]

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]

[45]

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]

[46]

. 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

[47]

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]

[48]

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

[49]

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]

[50]

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]

[51]

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]

[52]

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]

[53]

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]

[54]

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]

[55]

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

[56]

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]

[57]

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]

[58]

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

[59]

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]

[60]

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]

[61]

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]

[62]

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]

[63]

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]

[64]

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]

[65]

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]

[66]

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]

[67]

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]

[68]

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

[69]

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]

[70]

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

[71]

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]

[72]

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]

[73]

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

[74]

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]

[75]

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]

[76]

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]

[77]

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

[78]

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]

[79]

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

Level 3 (low-level) evidence

[80]

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]

[81]

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]

[82]

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]

[83]

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]

[84]

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]

[85]

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]

[86]

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]

[87]

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]

[88]

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

[89]

Innes GD, Scheuermeyer FX, McRae AD, Teichman JMH, Lane DJ. Hydronephrosis severity clarifies prognosis and guides management for emergency department patients with acute ureteral colic. CJEM. 2021 Sep:23(5):687-695. doi: 10.1007/s43678-021-00168-x. Epub 2021 Jul 25 [PubMed PMID: 34304393]

[90]

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]

[91]

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]

[92]

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

[93]

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

[94]

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]

[95]

Porat A, Bhutta BS, Kesler S. Urosepsis. StatPearls. 2024 Jan:(): [PubMed PMID: 29493969]

[96]

Sabih A, Leslie SW. Complicated Urinary Tract Infections. StatPearls. 2024 Jan:(): [PubMed PMID: 28613784]

[97]

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

[98]

Bullock B, Benham MD. Bacterial Sepsis. StatPearls. 2024 Jan:(): [PubMed PMID: 30725739]

[99]

Fulton II MR, Zubair M, Taghavi S. Laboratory Evaluation of Sepsis. StatPearls. 2024 Jan:(): [PubMed PMID: 37603649]

[100]

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

[101]

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

[102]

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

[103]

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]

[104]

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]

[105]

Nehring SM, Goyal A, Patel BC. C Reactive Protein. StatPearls. 2024 Jan:(): [PubMed PMID: 28722873]

[106]

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]

[107]

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]

[108]

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]

[109]

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]

[110]

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

[111]

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]

[112]

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]

[113]

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]

[114]

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]

[115]

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]

[116]

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]

[117]

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]

[118]

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]

[119]

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]

[120]

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

[121]

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]

[122]

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]

[123]

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]

[124]

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]

[125]

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]

[126]

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

[127]

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]

[128]

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

[129]

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

[130]

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]

[131]

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

[132]

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]

[133]

Cleland DA, Eranki AP. Procalcitonin. StatPearls. 2024 Jan:(): [PubMed PMID: 30969616]

[134]

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]

[135]

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]

[136]

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

[137]

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

[138]

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

[139]

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

[140]

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

[141]

Ghlichloo I, Gerriets V. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs). StatPearls. 2024 Jan:(): [PubMed PMID: 31613522]

[142]

Mahmoodi AN, Patel P, Kim PY. Ketorolac. StatPearls. 2024 Jan:(): [PubMed PMID: 31424756]

[143]

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]

[144]

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]

[145]

Alfaro RA, Davis DD. Diclofenac. StatPearls. 2024 Jan:(): [PubMed PMID: 32491802]

[146]

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

[147]

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

[148]

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

[149]

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

[150]

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]

[151]

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

[152]

Murphy PB, Bechmann S, Barrett MJ. Morphine. StatPearls. 2024 Jan:(): [PubMed PMID: 30252371]

[153]

Abi-Aad KR, Derian A. Hydromorphone. StatPearls. 2024 Jan:(): [PubMed PMID: 29261877]

[154]

Shah M, Huecker MR. Opioid Withdrawal. StatPearls. 2024 Jan:(): [PubMed PMID: 30252268]

[155]

Dydyk AM, Jain NK, Gupta M. Opioid Use Disorder. StatPearls. 2024 Jan:(): [PubMed PMID: 31985959]

[156]

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

[157]

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]

[158]

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]

[159]

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]

[160]

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]

[161]

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

[162]

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

[163]

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]

[164]

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

[165]

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

[166]

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]

[167]

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]

[168]

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

[169]

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]

[170]

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

[171]

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]

[172]

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]

[173]

Hauser JM, Azzam JS, Kasi A. Antiemetic Medications. StatPearls. 2024 Jan:(): [PubMed PMID: 30335336]

[174]

Theriot J, Wermuth HR, Ashurst JV. Antiemetics, Selective 5-HT3 Antagonists. StatPearls. 2024 Jan:(): [PubMed PMID: 30020690]

[175]

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]

[176]

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]

[177]

Griddine A, Bush JS. Ondansetron. StatPearls. 2024 Jan:(): [PubMed PMID: 29763014]

[178]

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]

[179]

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]

[180]

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

[181]

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]

[182]

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

[183]

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]

[184]

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]

[185]

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]

[186]

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

[187]

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

[188]

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

[189]

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]

[190]

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]

[191]

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

[192]

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

[193]

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

[194]

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

[195]

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

[196]

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

[197]

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

[198]

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

[199]

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

[200]

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

[201]

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

[202]

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

[203]

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]

[204]

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

[205]

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

[206]

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

[207]

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]

[208]

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

[209]

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

[210]

Manzoor H, Leslie SW, Saikali SW. Extracorporeal Shockwave Lithotripsy. StatPearls. 2024 Jan:(): [PubMed PMID: 32809722]

[211]

Wason SE, Monfared S, Ionson A, Klett DE, Leslie SW. Ureteroscopy. StatPearls. 2024 Jan:(): [PubMed PMID: 32809391]

[212]

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]

[213]

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]

[214]

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]

[215]

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]

[216]

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

[217]

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

[218]

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]

[219]

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]

[220]

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

[221]

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]

[222]

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]

[223]

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]

[224]

Leslie SW, Sajjad H. Double J Placement Methods Comparative Analysis. StatPearls. 2024 Jan:(): [PubMed PMID: 29494060]

Level 2 (mid-level) evidence

[225]

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]

[226]

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

[227]

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

[228]

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]

[229]

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]

[230]

Young M, Leslie SW. Percutaneous Nephrostomy. StatPearls. 2024 Jan:(): [PubMed PMID: 29630257]

[231]

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]

[232]

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]

[233]

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]

[234]

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]

[235]

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]

[236]

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]

[237]

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]

[238]

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]

[239]

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

[240]

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]

[241]

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]

[242]

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]

[243]

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]

[244]

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]