​Acute kidney injury (AKI), previously known as acute renal failure, denotes a sudden and often reversible reduction in kidney function, as measured by increased creatinine or decreased urine volume. AKI can be differentiated into prerenal, intrarenal, and postrenal etiologies, and these etiologies can be overlapping and interrelated. Distinguishing the causes of AKI is fundamental to effectively and efficiently treating AKI, which improves patient outcomes. This activity reviews the evaluation and management of acute kidney injury and highlights the role of the interprofessional team in managing patients affected by this condition.



Acute kidney injury (AKI) occurs when kidneys suddenly lose their ability to filter waste from the blood, developing within hours or days. It replaces the term 'acute renal failure.'

The signs and symptoms of AKI can differ depending on many factors like the cause, severity, and your other health conditions. If symptoms do happen, they may include one or more of the following:

• Making less urine (pee) than usual or no urine
• Swelling in legs, ankles, and/or feet
• Fatigue or tiredness
• Shortness of breath (trouble breathing)
• Confusion or mood changes
• High blood pressure
• Decreased appetite (low desire to eat)
• Nausea
• Flank pain (pain on the side of your back - between your ribs and hips)
• Chest pain or pressure
• Seizures or coma (in severe cases)
• In some cases, AKI causes no symptoms and is only found through other tests done by your healthcare professional.

Major Causes
AKI can have many different causes. Many people get AKI when a related disease or condition puts extra stress on your kidneys. Another common cause for AKI is when your body is reacting to an urgent or emergent health concern (such as heart surgery or COVID-19 infection). Lastly, AKI can be caused by medications or other substances that you may consume. 
Usually, AKI happens because of a combination of factors. This is especially true for older adults who are at higher risk given their age.

Doctors group the causes of AKI into three main types: 
Prerenal (low blood flow): Severe dehydration, heavy blood loss, low blood pressure, or heart failure that deprives kidneys of blood.
Intrinsic (direct damage): Damage from specific medicines (like some antibiotics or NSAIDs), severe infections, or inflammation inside the kidney.
Postrenal (blockages): Kidney stones, an enlarged prostate, or tumors that block urine from leaving the body


Treatment for AKI depends on what caused it in the first place. This is why finding the cause is so important. Some most common approaches to treating AKI include:

• Stopping any medicines that may be causing or contributing to your AKI
• Giving you fluids (either by mouth or through your veins)
• Antibiotics (if AKI is caused by a bacterial infection)
• Placing a urine catheter (a thin tube used to drain your bladder, useful if AKI is caused by a blockage)
• Dialysis (depending on the severity of damage to your kidney and/or impact on your other organs)
  • In most cases, dialysis treatments are only temporary until the kidneys can recover.

Most people with AKI will need to spend some time in the hospital to be monitored while receiving treatment.
After having AKI, you have a higher risk for other health problems, such as chronic kidney disease (CKD), heart disease, or stroke). You are also at a higher risk of getting AKI again in the future. So, it is important to have regular follow-up visits with your healthcare professional and check your kidney health, starting with two simple tests (ideally within 3 months of finishing treatment for your AKI).

- National Kidney Foundation -
​- National Library of Medicine -

​The history and physical exam should focus on determining the etiology of AKI and the progression timeline. If the history points towards hypovolemia or hypotension, then the treatment is guided towards volume repletion. Providers should look for inciting events such as diarrhea, nausea, vomiting, which may have caused volume loss, or any over-the-counter drugs such as NSAIDs. Differentiating between AKI and chronic kidney disease (CKD) is essential, as CKD itself is not an uncommon risk factor for AKI. A history suggestive of CKD can include symptoms such as chronic fatigue, anorexia, nocturia, disturbed sleep-wake cycle, polyuria, and pruritis. Moreover, a careful review of past medical history may reveal comorbid conditions that can help narrow down the etiology of AKI, such as cirrhosis or a history of blood clots requiring anticoagulation. History and physical examination are essential in AKI because labs often cannot provide a clear answer as to the etiology of AKI.
The most common causes of AKI in hospitalized patients are as follows:

1. ATN, 45%
2. Prerenal disease, 21%
3. AKI superimposed on CKD, 13%
4. Urinary tract obstruction, 10% 
5. Glomerulonephritis or vasculitis, 4%
6. AIN, 2%
7. Atheroemboli, 1%

A history of urine output may give clues as to the cause of AKI. The following are some associations:

1. Oliguria favors AKI.
2. Sudden anuria suggests acute urinary tract obstruction, acute glomerulonephritis, or vascular blockage.
3. Polyuria suggests either a concentrating tubular defect, such as acute interstitial nephritis, or postobstructive nephropathy.

A detailed physical exam can provide extremely valuable information in establishing the etiology of AKI. A crucial part of the physical exam should be orthostatic vital signs, which may signify hypovolemia. Several organ systems can provide clues regarding the cause of AKI. Some of them are:

1. Skin: livedo reticularis, digital ischemia, butterfly rash, and purpuras to suggest vasculitis. A maculopapular rash may indicate drug-induced AIN. Needle marks may suggest IV drug use, which can cause endocarditis. Livedo reticularis and skin infarcts are also seen with cholesterol emboli disease. Decreased skin turgor suggests hypovolemia.
2. Eyes and ears: jaundice is present in liver disease, band keratopathy is present in multiple myeloma, diabetes mellitus can show microscopic retinopathy, and blood vessel narrowing is associated with hypertension. Keratitis, iritis, and uveitis may be present in autoimmune vasculitis. Hearing loss is associated with Alport disease. 
3. Cardiovascular system: pulse rate, blood pressure, and jugulovenous pulse can indicate volume status. Irregular rhythm may indicate electrolyte imbalance-related arrhythmias. Pericardial friction rub may be heard in uremic pericarditis, and a heart murmur is often heard in the case of endocarditis. Embolic disease can present as cyanotic extremities