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What is acute kidney injury (AKI)?

Acute kidney injury is one of the most common complications in hospitalized patients.

AKI is a sudden, typically reversible decline in kidney function marked by rising creatinine and/or reduced urine output. The global nonprofit organization, Kidney Disease Improving Global Outcomes (KDIGO), has identified criteria for AKI, defining it as when any of the following are present:

  • An increase in serum creatinine by > 0.3 mg/dL in a 48 hour period
  • Serum creatinine increase of > 1.5x the patient’s baseline
  • Urine output < 0.5 ml/kg/hr for six hours

Though AKI is reversible in most cases, it still carries a significant clinical impact. Not only does it increase length of stay and mortality, it can also progress to chronic kidney disease in some cases. In this article, we’ll review the key things you need to know about AKI so you can spot it early and take steps to mitigate complications and prevent further harm to your patients.

Three types of Acute Kidney Injury

There are three key subtypes of AKI – prerenal, intrarenal, and postrenal. Essentially what you’re looking at here is where the problem is originating. Is it before the kidneys, within the kidneys, or after the kidneys? 

Prerenal AKI

When the problem is before the kidneys (meaning nothing is wrong with kidney physiology itself), we call this prerenal failure or prerenal AKI. The mechanism at work here is reduced blood flow to the kidneys. Causes include:

  • Hypotension: sepsis, septic shock, cardiogenic shock, anaphylaxis
  • Hypovolemia: dehydration, vomiting, diarrhea, burns, hemorrhage, extreme diuresis
  • Decreased cardiac output: heart failure, myocardial infarction

Clinical picture: A patient with prerenal AKI will have decreased urine output and concentrated/dark yellow urine. You’ll also see signs associated with the underlying cause. For example, if the kidney injury is due to dehydration, you’ll see dry mucous membranes and poor skin turgor. Note that even short periods of hypotension (even just 10 to 20 minutes) place the patient at higher risk for developing AKI.

Labs: In prerenal AKI, BUN and creatinine increase, and you are likely to see the BUN rise disproportionately which results in a BUN:creatinine ratio greater than 20:1. Urine specific gravity is going to be increased while urine sodium is decreased (this is due to the kidneys holding on to sodium in an attempt to retain volume).

Treatment: The treatment for prerenal AKI is to address the underlying problem. For example, if the cause is hypovolemia secondary to dehydration, then renal perfusion will improve with added volume. If the cause is heart failure, medications to improve cardiac output can increase renal perfusion and alleviate prerenal AKI.

Intrarenal AKI

In intrarenal AKI, the problem is within the kidney tissue itself. Because glomerular and/or tubular function is impaired, the kidney doesn’t function properly. The most common causes are:

  • Ischemia secondary to prolonged prerenal AKI that progresses to tubular damage and acute tubular necrosis (ATN)
  • Nephrotoxic medications such as NSAIDs, contrast dye, chemotherapy medications, and some antibiotics
  • Myoglobinuria from rhabdomyolysis
  • Hemoglobinuria, which can be associated with sickle cell anemia, severe bacterial infections, transfusion reactions, and hemolytic anemia (among others)
  • Glomerulonephritis
  • Interstitial nephritis
  • Renal artery or vein occlusion

Clinical Picture: A patient with intrarenal AKI will have reduced urine output and potentially signs of fluid overload as the kidneys fail to excrete adequate amounts of urine. Urine characteristics can vary based on the underlying problem. For example, rhabdomyolysis causes dark, cola-colored urine while glomerulonephritis causes cola-colored urine that can be foamy due to excess protein.

Labs: BUN and creatinine are both elevated, with a BUN:Cr ratio in the normal range. Urine sodium will be increased since the damaged tubules aren’t able to reabsorb sodium adequately. And, urine specific gravity will be between 1.010 and 1.020, which falls within the normal range. This doesn’t mean the kidneys are healthy; in this case it indicates the kidneys are not able to concentrate the urine due to the damage that is present.

Treatment: In addition to addressing the underlying cause, patients may require electrolyte management as the kidneys lose the ability to maintain homeostasis. In severe cases, patients may require renal replacement therapy (AKA dialysis). Diuretics are typically avoided in critically ill patients, and all nephrotoxic medications should be discontinued.

Postrenal AKI

In postrenal AKI, the problem is downstream of the kidneys. Urine flow is obstructed, which increases back-pressure and reduces GFR. Common causes include: 

Clinical picture: Patients often have sudden anuria or fluctuating urine output that may be accompanied by flank pain. In addition, the bladder will be distended on palpation and show high volumes when using the bladder scanner.

Labs: BUN and creatinine may be normal or elevated depending on duration of obstruction and severity. 

Treatment: Postrenal AKI is generally the most treatable and reversible type of injury. By relieving the obstruction quickly, kidney function and urine output can be restored before prolonged damage occurs. Common treatments include catheterization, stent placement, or nephrostomy tube insertion.

Priority nursing assessments

Regardless of the subtype of AKI, your nursing assessments focus on monitoring for progression of the condition and any potential complications. 

Urine output: The frequency of urine output monitoring will vary based on the patient’s acuity. In the ICU, output is assessed every one to two hours. On a med surg unit, output monitoring isn’t as strict but should still be top of mind so you can notice any changes as they occur. As a reminder, the KDIGO criteria for AKI is urine output less than 0.5ml/kg/hr for six hours, which means you’re assessing output at least every six hours.

Fluid volume status: Assess your patient for signs of volume depletion such as dry mucous membranes, decreased skin turgor, tachycardia, hypotension, and orthostatic hypotension. It’s equally important to also monitor your patient for signs of fluid volume overload. This includes adventitious lung sounds (crackles) indicating pulmonary edema, sudden weight gain, hypertension, and peripheral edema.

Daily weights: Weighing your patient daily is a highly sensitive way to monitor for fluid volume overload (or less). One kilogram is equal to approximately one liter of fluid.

Vital signs: BP and HR are the key ones here, while tachypnea can occur in cases of severe AKI where metabolic acidosis develops.

Neurological status: Uremia (a buildup of waste products in the blood) can cause confusion, lethargy and altered mental status.

Cardiovascular: Severe AKI can lead to hyperkalemia which can cause dangerous cardiac arrhythmias.

Respiratory: Monitor your patient’s respiratory status for signs of pulmonary edema secondary to fluid overload. These include crackles upon auscultation, SOB, tachypnea, and decreased SpO2.

Skin: Assess for peripheral edema, noting the location and severity. 

Important labs to understand in AKI

When caring for a patient with AKI, you’ll be monitoring both blood and urine lab results. 

Creatinine: Creatinine is the most specific marker of renal function. As GFR falls, creatinine rises. 

BUN: Blood urea nitrogen (BUN) rises with reduced GFR, but also rises with GI bleeding and high protein intake. As such, it is less specific to renal injury but is still a useful lab to follow.

Ratio: The BUN:Cr ratio is highly informative and tells you more than either result all on its own. A ratio greater than 20:1 suggests prerenal AKI, while a ratio between 10:1 and 15:1 is associated with intrarenal AKI. In postrenal AKI, the ratio often elevates initially then drops.

Potassium: Because damaged kidneys can’t balance potassium adequately, hyperkalemia is a serious concern. Watch this value closely as dangerous cardiac arrhythmias can occur.

Bicarbonate/Co2: In serious cases, metabolic acidosis can develop as the kidneys lose the ability to excrete hydrogen ions effectively. This shows as low bicarb/CO2 values.

Phosphorus and calcium: These two labs have an inverse relationship…when one is elevated the other is low. In AKI, phosphorus rises and calcium falls.

Urine sodium: Values less than 20 are associated with prerenal AKI due to the kidneys holding on to sodium in an attempt to increase fluid volume. Values greater than 40 suggest intrinsic damage to the kidneys themselves.

Urine specific gravity: Concentrated urine is associated with prerenal AKI (values greater than 1.020) as the body attempts to hold on to fluid. Values around 1.010 are associated with intrarenal AKI as the kidneys aren’t able to concentrate urine as effectively.

Urinalysis: Urinalysis can show abnormalities such as blood, protein, casts, and WBCs.

Complications of AKI

The consequences of AKI are not restricted to just the kidneys themselves, multiple organ systems can be affected. 

Cardiovascular: Cardiac complications include arrhythmias from electrolyte imbalances (especially hyperkalemia) and heart failure can result from fluid overload when the kidneys aren’t able to excrete urine adequately.

Pulmonary edema: Oliguric kidneys cannot excrete excess fluid, which leads to pulmonary edema.

Uremia: The accumulation of waste products manifests as neurological changes, nausea, vomiting, anorexia, and possibly even uremic pericarditis and encephalopathy. 

Metabolic acidosis: When injured, the kidneys are not able to excrete hydrogen ions or regenerate bicarbonate adequately. The result is metabolic acidosis which can manifest as decreased LOC and Kussmaul respirations (these are deep, rapid respirations that occur as the body attempts to blow off excess CO2).

Progression to chronic kidney disease (CKD): When AKI is severe and prolonged, it can progress to a chronic condition.

Then you might want to dive into some other articles covering the renal system

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References:

Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. “KDIGO Clinical Practice Guideline for Acute Kidney Injury.” Kidney International Supplements, vol. 2, no. Supplement, 2012, pp. 1–138, https://kdigo.org/guidelines/.

Manzoor, Hassan, and Harshil Bhatt. “Prerenal Kidney Failure.” StatPearls, StatPearls Publishing, 2026. PubMed, http://www.ncbi.nlm.nih.gov/books/NBK560678/.

Moses, Scott. “Acute Kidney Injury.” Family Practice Notebook, 2019, https://mobile.fpnotebook.com/Renal/Failure/ActKdnyInjry.htm.

Last Updated on August 29, 2026 by Maureen Osuna, MSN, RN