Acute kidney injury (AKI), formerly known as acute renal failure (ARF) denotes a sudden and often reversible reduction in the kidney function, as measured by glomerular filtration rate (GFR).  There is no clear definition of AKI. Several different criteria have been used in research studies such as RIFLE, AKIN (Acute Kidney Injury Network) or KDIGO (Kidney Disease: Improving Global Outcomes) criteria. However, KDIGO is the most recent and most commonly used. According to KDIGO, AKI is the presence of any of the following:
Pre-renal includes any reduced blood flow to the kidney. This may be part of a systemic hypoperfusion resulting from hypovolemia or hypotension; or may be due to selective hypoperfusion to the kidneys such as those resulting from renal artery stenosis, aortic dissection.
Renal includes acute tubular necrosis which can result from several different causes. Prolonged renal ischemia, sepsis, and nephrotoxins being the most common ones. It is worthwhile mentioning that pre-renal injury can convert into renal injury if the exposure to offending factor is prolonged enough to cause cellular damage.
Post-renal mainly includes obstructive causes which lead to congestion of the filtration system and thus eventually lead to shutting down of the kidneys. The most common ones being renal/ureteral calculi, tumors or any urethral obstruction. Another noteworthy fact is that a unilateral obstruction may not always present as AKI especially if the obstruction is gradual such as a tumor because a normal working contralateral kidney may be able to compensate for the function of the affected kidney. Therefore, the most common etiology of post-renal AKI is bladder outlet obstruction.
AKI is a very commonly seen in patients admitted to the hospital. It is often an important factor that contributes to decision to hospitalize for other conditions, if not being the sole reason for hospitalization. AKI is one of the most clinically impactful diseases since it affects patient management to a great extent regarding the treatment options for their primary disease. Most drugs or procedures that use contrast media may need to delay due to co-existent AKI. Most of the drugs are renally excreted, and dosages might need to be adjusted to account for the reduced renal function. Sometimes, it may even necessitate frequent monitoring of drug levels, for example, Vancomycin. AKI is thus an important contributor to longer hospital stays and patient morbidity. 
Pathogenesis of AKI is etiology driven. The common endpoint in all acute tubular necrosis is a cellular insult either secondary to ischemia or direct toxins which result in effacement of the brush border and eventually cell death thus shutting down the function of tubular cells.
The history and physical exam should focus on determining the etiology of AKI and the timeline of progression. If the history points towards hypovolemia or hypotension, then the treatment is guided towards volume repletion. The physician needs to look for inciting events such as diarrhea, nausea, vomiting which may have caused volume loss or any over the counter drugs such as NSAIDs or other nephrotoxins. One of the important signs to look for on physical exam is orthostatic vital signs since they are an important clue for hypovolemia and in an appropriate clinical context would guide treatment. History and physical are very important in AKI because more often than not, labs are unable to provide a clear answer as to the etiology of AKI.
All patients presenting with AKI warrant a basic lab panel including a basic metabolic panel. Sometimes, urine electrolytes can be helpful in suggesting an etiology of the AKI. Renal ultrasound can be helpful if obstructive causes are suspected. However, routine renal ultrasound for every patient with AKI is not warranted. Urine sediment examination can also provide important clues as to the etiology such as muddy brown casts seen in acute tubular necrosis. 
There are markers of tubular function that can be calculated to help distinguish an etiology like the fractional excretion of sodium and urea, urine osmolality but the sensitivity of all these markers is very poor, and they are affected by many drugs very commonly used in clinical practice such as diuretics. Therefore, no single marker can be reliably used in isolation to distinguish pre-renal from renal causes of AKI, which is a common misconception in clinical practice.
With the exception of post-renal AKI, most cases are an overlap between pre-renal and acute tubular necrosis type of AKI.  The best way to determine if the AKI is pre-renal or not is a fluid challenge. If the clinical scenario doesn't contradict it, all patients with acute renal dysfunction should receive a fluid challenge. They require close monitoring of the urine output and renal function. If the renal function improves with fluid, that is the best indicator of a pre-Renal AKI. Acute tubular necrosis is very slow to recover and can take weeks to months for complete recovery of renal function. It may not normalize at all sometimes. Another important thing to consider for these patients is to avoid any further insult to the kidneys such as nephrotoxic drugs. Any and all medications need to be renally dosed once a patient develops AKI. Sometimes, AKI may need short-term renal replacement therapy till the kidney function recovers. This is seen especially in the oliguric phase of acute tubular necrosis, where the patient is prone to develop multiple electrolyte and acid-base abnormalities as well as fluid overload.
Mild AKI can often be managed, outpatient. AKI more often than not is a co-existent problem for hospitalized patients and usually is appropriate for these patients to be on the general medical floor unless they also have an electrolyte imbalance or significant volume overload, in which case, they may require a higher level of care. The most important issues to realize for clinicians dealing with AKI is to appropriately adjust the dose of any medications these patients are taking and avoiding nephrotoxic medications as much as possible. The other important thing to consider is an appropriate fluid challenge whenever possible.
AKI does have significant morbidity and mortality. The aim today is to try and prevent the condition in the first place by employing a multidisciplinary team approach. All healthcare workers must be aware of the condition and its causes. The pharmacist should ensure that at the first signs of creatinine elevation that the patient is on no nephrotoxic medications. The nurse should ensure that the patient is well hydrated prior to any contrast study and is making adequate urine. For those who do develop AKI, the nurse should educate the patient on agents to avoid to prevent worsening of the renal injury. Plus, close follow up with a nephrologist is highly recommended. Finally, the patient should have a dietary consult because the restriction of salt and fluid are vital when managing AKI. Similarly, the patient should avoid a high potassium diet when there is renal dysfunction. Because AKI induces a catabolic state, the patient should be encouraged to eat at least 1800 calories per day. (Level V)
The outcomes for patients with AKI depends on the cause of the renal dysfunction, the presence of any underlying kidney disease and duration of the renal dysfunction. In the past, it was widely believed that AKI was fully reversible in all patients. Studies now show that in patients with a low eGFR, not only is there a higher risk of progressing to end-stage renal disease but it also increases the mortality rate. In addition, AKI can also worsen the quality of life compared to the general population. Individuals who have a sudden increase in creatinine, usually tend to have the worst prognosis. Today, in-hospital mortality for patients with AKI varies between 30-50%, especially when dialysis is required. Negative prognostic factors include:
Over the long term, at least 12-15% of patients with AKI may require permanent dialysis. Mortality is increased in patients with high APACHE lll score, advanced age and persistent elevation of creatinine. (Level V)
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