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Acute Kidney Injury

Editor: Khalid Bashir Updated:

Acute kidney injury (AKI), previously called acute renal failure (ARF), denotes a sudden and often reversible reduction in kidney function, as measured by glomerular filtration rate (GFR).[1][2][3] However, immediately after a renal insult, blood urea nitrogen (BUN) or creatinine levels may be within the normal range. The only sign of acute kidney injury may be a decline in urine output. AKI can lead to the accumulation of water, sodium, and other metabolic products. It can also result in several electrolyte disturbances. It is a very common condition, especially among hospitalized patients. It can be seen in up to 7% of hospital admissions and 30% of ICU admissions. There is no clear definition of AKI; however, several different criteria have been used in research studies, such as RIFLE, AKIN (Acute Kidney Injury Network), and KDIGO (Kidney Disease: Improving Global Outcomes) criteria. Among these, KDIGO is the most recent and most commonly used tool. According to KDIGO, AKI is the presence of any of the following:

  1. Increase in serum creatinine by 0.3 mg/dL or more (26.5 micromoles/L or more) within 48 hours
  2. Increase in serum creatinine to 1.5 times or more baseline within the prior seven days
  3. Urine volume less than 0.5 mL/kg/h for at least 6 hours


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The impetus for glomerular filtration is the difference in the pressures between the glomerulus and the Bowman space. This pressure gradient is affected by the renal blood flow and is under the direct control of the combined resistances of afferent and efferent vascular pathways. Nevertheless, whatever the cause of AKI, renal blood flow reduction is a common pathologic pathway for declining glomerular filtration rate. Pathophysiology of AKI has always been traditionally divided into three categories: prerenal, renal, and post-renal. Each of these categories has several different causes associated with it.[4][5]

The prerenal form of AKI is because of any cause of reduced blood flow to the kidney. This may be part of systemic hypoperfusion resulting from hypovolemia or hypotension or maybe due to selective hypoperfusion to the kidneys, such as those resulting from renal artery stenosis and aortic dissection. However, tubular and glomerular function tends to stay normal. A few examples with the mechanism of prerenal AKI are listed below:

  1. Hypovolemia: hemorrhage, severe burns, and gastrointestinal fluid losses such as diarrhea, vomiting, and high ostomy output.
  2. Hypotension from the decreased cardiac output: cardiogenic shock, massive pulmonary embolism, acute coronary syndrome
  3. Hypotension from systemic vasodilation: septic shock, anaphylaxis, anesthesia administration, hepatorenal syndrome
  4. Renal vasoconstriction: NSAIDs, iodinated contrast, amphotericin B, calcineurin inhibitors, 
  5. Glomerular efferent arteriolar vasodilation: ACE inhibitors, angiotensin receptor blockers

Intrinsic renal causes include conditions that affect the glomerulus or tubule, such as acute tubular necrosis and acute interstitial nephritis. This underlying glomerular or tubular injury is associated with the release of vasoconstrictors from the renal afferent pathways. Prolonged renal ischemia, sepsis, and nephrotoxins are the most common ones. It is worth mentioning that prerenal injury can convert into a renal injury if the offending factor's exposure is prolonged enough to cause cellular damage. A few examples of this mechanism are listed below:

  1. Acute tubular necrosis: ischemia from prolonged prerenal injury, drugs such as aminoglycosides, vancomycin, amphotericin B, and pentamidine; rhabdomyolysis, intravascular hemolysis
  2. Acute interstitial nephritis: Drugs such as beta-lactam antibiotics, penicillins, NSAIDs, proton pump inhibitors (PPIs), 5-ASA; infections, autoimmune conditions (SLE, IgG related disease)
  3. Glomerulonephritis: anti-glomerular basement membrane disease, immune complex-mediated diseases such as SLE, post-infectious glomerulonephritis, cryoglobulinemia, IgA nephropathy, Henoch-Schonlein purpura.
  4. Intratubular obstruction: monoclonal gammopathy seen in multiple myeloma, tumor lysis syndrome, and toxins such as ethylene glycol. 

Post-renal causes mainly include obstructive causes, which lead to congestion of the filtration system, leading to a shift in the filtration driving forces. The most common ones are renal/ureteral calculi, tumors, blood clots, 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 compensate for the function of the affected kidney. Therefore, the most common etiology of post-renal AKI is bladder outlet obstruction.

AKI is very commonly seen in patients admitted to the hospital. In the United States, 1% of all hospital admissions have AKI on admission. It is often an important factor in making the decision to hospitalize for other conditions, if not being the sole reason for hospitalization. During hospitalization, the approximate incidence rate of acute kidney injury is 2% to 5%, and it develops in up to 67% of patients admitted to the intensive care unit. AKI is one of the most clinically impactful diseases since it affects patient management to a great extent in terms of the treatment options for their primary disease. Most drugs or procedures that use contrast media may need to be delayed due to co-existent AKI. Most of the drugs are renally excreted, and dosages might need to be adjusted on account of the reduced renal function. Sometimes, it may even necessitate frequent monitoring of drug levels, for example, vancomycin. Furthermore, a huge percentage, approximately 95%, of nephrologist consultations are related to AKI. AKI is thus an important contributor to more extended hospital stays and patient morbidity.[6][7][8]

The pathogenesis of AKI is etiology-driven. The common endpoint in all types of acute tubular necrosis is a cellular insult either secondary to ischemia or direct toxins, which results in effacement of the brush border and eventually cell death, thus shutting down the function of tubular cells. Intratubular obstruction by pigments such as myoglobin or crystals such as uric acid in tumor lysis syndrome or immunoglobulin light chains, as seen in monoclonal gammopathy, may also lead to the same result. On the other hand, the mechanism of injury in glomerulonephritis may be due to direct immune-mediated injury of the vessels or immune complex deposition leading to an immune response and damage to the glomeruli.

Histopathology can reliably differentiate the intrinsic renal pattern of AKI from others; however, histopathology may not be reliable at narrowing down a specific cause in every situation. Renal biopsy is an invasive procedure and is usually only pursued in cases where a significant impact on management is expected, such as suspected glomerulonephritis. In those cases, immunofluorescence patterns and electron microscopy can help differentiate between various causes.

History and Physical

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 providers need 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. Differentiating between AKI and chronic kidney disease (CKD) is essential, as CKD itself is not an uncommon risk factor for AKI. This can be achieved with the help of history in which one may find features suggestive of CKD, such as chronic fatigue, anorexia, nocturia, disturbed sleep-wake cycle, polyuria, and pruritis. Moreover, a careful review of past medical history to reveal any co-morbid conditions can also help narrow down the etiology of AKI, for instance, cirrhosis and a history of blood clots requiring anticoagulation. History and physical examination are essential in AKI because, more often than not, labs are unable to provide a clear answer as to the etiology of AKI.

The most common causes of AKI in hospitalized patients are in this order:

  1. ATN – 45%
  2. Prerenal disease – 21%
  3. Acute superimposed on CKD – 13%
  4. Urinary tract obstruction – 10% (most often due to benign prostatic hypertrophy in older men)
  5. Glomerulonephritis or vasculitis – 4%
  6. AIN – 2%
  7. Atheroemboli – 1%

A history of urine output is important, which may give clues to the cause of AKI. Following are some associations:

  1. Oliguria - favors AKI.
  2. Sudden anuria - suggests acute urinary tract obstruction, acute glomerulonephritis, or vascular catastrophe.
  3. Gradually diminishing urine output - may be secondary to urethral stricture or bladder outlet obstruction due to causes such as prostate enlargement.

Performing a detailed examination is imperative as it provides extremely valuable information in establishing the etiology of AKI. A crucial part of the physical exam should be orthostatic vital signs since they are an important clue for hypovolemia and, in an appropriate clinical context, would guide treatment. Several organ systems need to be examined to find clues regarding the cause of AKI. Some of them are given below:

  1. Skin - livedo reticularis, digital ischemia, butterfly rash, and purpuras to suggest vasculitis. Track marks to suggest endocarditis in an IV drug abuser.
  2. Eyes and ears - jaundice in liver disease, band keratopathy in multiple myeloma, signs of diabetes mellitus, atheroemboli in retinopathy, and signs of hypertension. Keratitis, iritis, and uveitis in autoimmune vasculitis. Hearing loss in Alport disease. 
  3. Cardiovascular system - pulse rate, blood pressure, and jugulovenous pulse in establishing volume status. Irregular rhythm may indicate electrolyte imbalance-related arrhythmias. Pericardial friction rub in uremic pericarditis.


Evaluation of AKI should include a thorough search for all possible etiologies of AKI, including prerenal, renal, and post-renal disease. The timing of the onset of AKI can be beneficial when dealing with hospitalized patients. For example, if a patient's labs are being checked every day and creatinine suddenly starts to rise on the fourth day of admission, then an inciting factor can usually be found in 24 to 48 hours preceding the onset. It is imperative to look for any radiologic studies that might have been done involving the use of iodinated contrast agents, which are not an uncommon cause of AKI. It is also imperative to review the list of medications that the patient is receiving, as they may be contributing to renal failure. Therefore, in view of decreased renal function, the doses of such drugs need to be modified. ACE inhibitors and ARBs are often the co-contributors to AKI. A good physical exam can also be helpful sometimes, e.g., the presence of a drug rash may point to acute interstitial nephritis being the etiology. Cyanotic toes could suggest cholesterol emboli in a patient post-cardiac catheterization.

All patients presenting with AKI warrant a basic lab panel, including a basic metabolic panel. Sometimes, urine electrolytes can help suggest an etiology of the AKI. Urine protein, urine osmolality, and urine albumin to creatinine ratios can also be helpful clues in determining the etiology of AKI. Older patients without any obvious etiology should also be subjected to serum and urine protein electrophoresis (SPEP and UPEP) to rule out monoclonal gammopathy and multiple myeloma. Renal ultrasound can be helpful if obstructive causes are suspected. However, routine renal ultrasound for every patient with AKI is not warranted. CT non-contrast is another important radiographic modality and can be used to look for nephrolithiasis or urolithiasis. Urine sediment examination can also provide important clues as to the etiology, such as muddy brown casts seen in acute tubular necrosis. Sterile pyuria is the most sensitive sign of acute interstitial nephritis.[9][10]

A kidney biopsy is an excellent but infrequently utilized tool. It is usually indicated in patients with rapidly declining renal function without apparent cause or to find out the exact etiology of AKI in a setting where multiple etiologies could be responsible. It is a test with a number of risks, such as bleeding, particularly in patients with platelet dysfunction from uremia.

There are markers of tubular function that can be calculated to help distinguish prerenal causes from renal/postrenal, like the fractional excretion of sodium and urea and urine osmolality; however, 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 prerenal from renal causes of AKI, which is a common misconception in clinical practice.

Lastly, attention also needs to be paid to the overall clinical picture. It is important to assess the volume status of the patient to exclude possible cardiorenal or hepatorenal syndrome. Cardiorenal syndrome is usually due to poor glomerular filtration due to venous congestion and a lack of forward flow due to poor cardiac output. Hepatorenal syndrome is due to the differential distribution of circulation volume with systemic vasodilation and splanchnic vasoconstriction, leading to the diversion of blood into the periphery and paucity of blood supply to the kidneys.

Treatment / Management

Except for post-renal AKI, most cases overlap between pre-renal and acute tubular necrosis types of AKI.[11][12] 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 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. Diuretics may be required during the oliguric phase of ATN if significant volume overload develops. Another important thing to consider for these patients is to avoid any further insult to the kidneys, such as nephrotoxic drugs. Any and the doses of all medications need to be renally adjusted once a patient develops AKI. Another vital step is to limit the dietary ingestion of potassium and phosphorus.

If hyperkalemia develops, it needs to be managed in a robust manner because, in AKI patients, it can be catastrophic. Approaches to lower potassium in the body include:

  1. Dietary restriction
  2. Insulin, IV dextrose, and beta-agonists
  3. potassium-binding resins
  4. Calcium gluconate to stabilize the cardiac membrane
  5. Dialysis for nonresponsive hyperkalemia

Some AKI patients tend to develop volume overload, which should be corrected as early as possible to avoid pulmonary and cardiac complications. Euvolemic state can be achieved with the help of furosemide, which is a cornerstone in managing such patients. Usually, high doses of IV furosemide are needed to correct volume overload in AKI patients; however, it plays no role in converting oliguric AKI to non-oliguric AKI.

Sometimes, AKI may need short-term renal replacement therapy until the kidney function recovers. Dialysis is usually required to manage the complications of AKI, such as severe and nonresponsive hyperkalemia, uremic pericarditis, and pulmonary edema. 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.[13] When required, dialysis in this setting is usually performed through a double-lumen central venous catheter. Continuous renal replacement therapy can also be utilized in patients who cannot tolerate hemodialysis due to hypotension. It is a much slower, continuous type of dialysis. Correction of some of the metabolic abnormalities, along with dialysis, may be required. Metabolic acidosis is one such instance where systemic administration of citrate or bicarbonate is often required to maintain a suitable blood pH. The requirement for renal replacement therapy should be reevaluated in these patients daily while they are hospitalized and at least weekly thereafter until the kidney function is stable. Renal replacement therapy is usually required for the short term, ranging from a few days to a few weeks in most cases; however, acute tubular necrosis can take up to months to recover and may require intermittent hemodialysis support during that time.

Certain specific treatments are required for acute kidney injury in specific circumstances, such as administering vasoactive medications and colloids for the treatment of hepatorenal syndrome and cautious diuresis in cardiorenal syndrome. Acute kidney injury from various glomerulonephritides may require immunosuppressive medications for treatment. Acute interstitial nephritis, which does not recover with supportive care, may benefit from a trial of steroids. Post renal obstruction may need to be relieved operatively in certain situations. For example, benign prostatic hypertrophy may require surgical relief of bladder outlet obstruction. Urethral calculi may require stenting and lithotripsy. 

It is also important to note that in a certain situation, the risk of acute kidney injury may be decreased by taking some measures. For example, in high-risk patients such as those with compromised renal function at baseline, it may be beneficial to administer peri-procedure intravenous fluids to prevent contrast-induced nephropathy when performing cardiac catheterization.

Differential Diagnosis

Acute kidney injury can occur in patients with preexisting chronic renal failure. Therefore, it is crucial to make every effort to preclude all the reversible factors. The best indicator of reversibility is the rate at which the renal function declines. For instance, accelerated worsening of renal function should prompt the search for the cause. Differentials to be considered in AKI include:

  1. Renal calculi
  2. Sickle cell anemia
  3. Chronic renal failure
  4. Dehydration
  5. Gastrointestinal bleeding
  6. Heart failure
  7. Urinary tract infection
  8. Protein overloading
  9. Diabetic ketoacidosis
  10. Urinary obstruction


Most acute kidney injury cases recover entirely with supportive management; however, the prognosis mostly depends on the etiology of AKI and the presence or absence of antecedent kidney disease or declined eGFR. Most pre-renal AKI cases recover completely with correction of the underlying insult if caught early; however, the persistence of the underlying insult may lead to acute tubular necrosis, in which case the damage may not be completely reversible. The other consideration to keep in mind is that although recovery from individual episodes may be complete or partial, repeated AKI can lead to a cumulative worsening of renal function. Therefore, it is essential to follow these patients either to the normalization of renal function or until it can be decided that this will be their new baseline renal function. The in-hospital mortality rate for AKI is 40% to 50%, and the mortality for ICU patients is more than 50%. Other prognostic factors include:

  1. Older age
  2. Duration of illness
  3. Fluid balance
  4. Diuretic use
  5. The decline in urine output
  6. Hypotension
  7. Inotropic support
  8. Multiorgan involvement
  9. Sepsis
  10. Number of transfusions


Several complications may associate AKI with mortality. Some of these complications are directly associated with AKI and can easily be gauged (hyperkalemia, volume overload, metabolic acidosis, hyponatremia); however, the effect of other complications on AKI-related mortality, such as inflammation and infection, is difficult to assess. The most common complications include metabolic derangements such as:

  1. Hyperkalemia- If severe, it can lead to arrhythmias, because of which renal replacement therapy is required in cases of severe hyperkalemia.
  2. Metabolic acidosis- The kidney's inability to excrete acids leads to metabolic acidosis and may necessitate systemic administration of bicarbonate or citrate buffers.
  3. Hyperphosphatemia- can usually be prevented by decreasing dietary ingestion or using phosphate binders.
  4. Other effects include pulmonary edema from volume overload and peripheral edema from an inability to excrete body water. This is especially common in the oliguric phase of acute tubular necrosis. It may necessitate the use of diuretics or renal replacement therapy.

The other organ-related complications include 

  1. Cardiovascular - Heart failure secondary to fluid overload is attributable to oliguric AKI, arrhythmias secondary to acidotic state and electrolyte abnormalities, cardiac arrest due to metabolic derangements, and myocardial infarction, and rarely pericarditis.
  2. Gastrointestinal (GI) - Nausea, vomiting, GI bleeding, and anorexia. A mildly raised level of amylase is commonly found in patients suffering from AKI. Elevation of amylase concentration can make the diagnosis of pancreatitis difficult. Therefore, measuring lipase, which is not raised in AKI, is necessary to establish AKI diagnosis.
  3. Neurologic - CNS-related signs of uremic burden are common in AKI, and they include lethargy, somnolence, disturbed sleep-wake cycle, and cognitive impairment.

Deterrence and Patient Education

For patients that have developed AKI, there are several things they should be advised to preserve renal function, including avoiding nephrotoxic agents. NSAIDs are known to cause interstitial nephritis, which can lead to the development of AKI or the worsening of existing AKI. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are known to affect renal autoregulation, although the avoidance of these mediations in the perioperative period is currently a topic of debate.

Pearls and Other Issues

Mild AKI can often be managed on an outpatient basis. AKI, more often than not, is a coexistent problem for hospitalized patients. It is usually 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 are adjusting the dose of any medications these patients are taking and avoiding nephrotoxic medications as much as possible. The other important factor to consider is an appropriate fluid challenge whenever possible.

Enhancing Healthcare Team Outcomes

Acute kidney injury (AKI) does have significant morbidity and mortality if it is left untreated. The aim today is to try and prevent the condition in the first place by employing an interprofessional team approach. All healthcare workers must be aware of the condition, its causes, and potential complications.

At the first signs of creatinine elevation, the pharmacist should ensure that the patient is on no nephrotoxic medications. The patient should be educated that the regular consumption of NSAIDs is harmful to the kidneys. The patient should be instructed to remain compliant with his blood pressure medications since uncontrolled hypertension can worsen kidney injury.

The nurse practitioner should ensure that the patient is well hydrated and is producing adequate urine before any contrast study. For those who develop acute kidney injury, the nurse should educate the patient to avoid agents such as NSAIDs to prevent the worsening of the renal injury. Plus, close follow-up with a nephrologist is highly recommended. Finally, the patient should have a dietary consult because salt and fluid restriction are vital when managing acute kidney injury. Similarly, the patient should avoid a high-potassium diet when there is renal dysfunction. Because acute kidney injury induces a catabolic state, the patient should be encouraged to eat at least 1800 calories per day. [14][15][16] [Level 5]

Finally, the primary care provider should closely monitor renal function, and if it is found to be worsening, a prompt nephrologist consult is recommended. Only through an interprofessional approach can the morbidity of acute kidney injury be lowered. If the kidney injury is allowed to progress, end-stage renal disease is the outcome. 


The outcomes for patients with AKI depend on the cause of renal dysfunction, the presence of any underlying kidney disease, and the 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:

  • Advanced age
  • Oliguria
  • Use of vasopressors
  • Multiorgan dysfunction
  • Need for blood transfusions
  • Hypotension

Over the long term, at least 12-15% of patients with AKI may require permanent dialysis. Mortality is increased in patients with high APACHE III scores, advanced age, and persistent creatinine elevation.[17][18] [Level 5]



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