What are the common prerenal causes of acute kidney injury?

Prerenal Causes of Acute Kidney Injury

Prerenal AKI results from decreased renal perfusion without initial structural kidney damage and accounts for more than 60% of all AKI cases, making it the most common type you will encounter. 1, 2

Volume Depletion (Absolute Hypovolemia)

The most straightforward prerenal causes involve true fluid loss:

• Hemorrhage from any source reduces circulating blood volume and renal perfusion 1, 2
• Gastrointestinal losses including vomiting, diarrhea, or nasogastric suction deplete intravascular volume 1, 2
• Excessive diuresis from overaggressive diuretic therapy or osmotic diuresis causes volume depletion 1, 2
• Burns result in massive fluid shifts and evaporative losses 1, 2
• Third-space sequestration in pancreatitis, peritonitis, or bowel obstruction reduces effective circulating volume despite total body fluid overload 1, 2

Decreased Effective Circulating Volume

Even with normal or increased total body fluid, effective arterial blood volume can be inadequate:

• Heart failure, cardiogenic shock, or arrhythmias reduce cardiac output and forward flow to kidneys 1, 2
• Severe hypoalbuminemia from nephrotic syndrome decreases oncotic pressure, reducing effective circulating volume 1, 2
• Systemic vasodilation from sepsis, anaphylaxis, or cirrhosis causes relative hypovolemia despite adequate total volume 1, 2

Renal Vasoconstriction and Impaired Autoregulation

Medications and disease states can directly impair renal blood flow:

• NSAIDs inhibit prostaglandin synthesis, eliminating compensatory afferent arteriolar vasodilation 1, 2
• ACE inhibitors and ARBs dilate efferent arterioles, impairing glomerular filtration pressure—though creatinine increases up to 30% from baseline should NOT be confused with true AKI and do not require discontinuation absent volume depletion 2
• The "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs dramatically increases AKI risk through combined hemodynamic effects 1
• Hepatorenal syndrome in cirrhosis involves splanchnic vasodilation with compensatory renal vasoconstriction 3, 2
• Renal artery thrombosis or embolism directly occludes arterial supply 1

High-Risk Clinical Scenarios

Recognize these situations where prerenal AKI is particularly likely:

• Decompensated cirrhosis where prerenal causes account for approximately 68% of AKI cases, most commonly triggered by infections, diuretic-induced excessive diuresis, GI bleeding, therapeutic paracentesis without albumin replacement, and nephrotoxic drugs 3, 4
• Community-acquired AKI where approximately 70% of cases are prerenal 5
• Patients receiving three or more nephrotoxic medications where each additional nephrotoxin increases AKI odds by 53% 1

Critical Diagnostic Maneuver

Withdraw all diuretics regardless of AKI stage and administer albumin 1 g/kg (maximum 100 g/day) as a fluid challenge—response with serum creatinine reduction to within 0.3 mg/dL of baseline confirms prerenal (hypovolemic) AKI, while lack of response suggests intrinsic kidney disease or hepatorenal syndrome. 3, 1, 4

Common Pitfalls to Avoid

• Do not rely solely on FENa <1% to diagnose prerenal AKI in cirrhosis—it has only 14% specificity in this population 1
• Do not discontinue ACE inhibitors/ARBs for creatinine increases <30% without evidence of volume depletion, as this represents expected hemodynamic effect rather than true AKI 2
• Do not assume prerenal AKI is completely reversible—even "functional" prerenal states can cause mild tubular injury detectable by biomarkers, and prolonged prerenal insults progress to acute tubular necrosis 6
• Do not overlook increased intra-abdominal pressure from tense ascites as a postrenal/prerenal hybrid cause in cirrhotic patients 2