What is the most common cause of acute kidney injury?

Most Common Causes of Acute Kidney Injury

Prerenal causes are the most common etiology of acute kidney injury, accounting for more than 60% of all AKI cases, primarily due to decreased renal perfusion from hypovolemia, hypotension, or altered hemodynamics. 1, 2

Classification of AKI Etiologies

Acute kidney injury (AKI) is typically categorized into three main groups:

1. Prerenal Causes (Most Common: >60% of cases)

• Hypovolemia: Caused by hemorrhage, vomiting, diarrhea, excessive diuresis, or third-spacing of fluids (e.g., pancreatitis, peritonitis) 3, 2
• Decreased cardiac output: Heart failure, cardiogenic shock, or arrhythmias 4
• Systemic vasodilation: Sepsis, anaphylaxis, or medications causing hypotension 3
• Renal vasoconstriction: NSAIDs, calcineurin inhibitors, contrast media 5
• Impaired autoregulation: Often seen with ACE inhibitors or ARBs, especially in patients with bilateral renal artery stenosis 5

2. Intrinsic Renal Causes (35-40% of cases)

• Acute tubular necrosis (ATN): Most common intrinsic cause, resulting from ischemia or nephrotoxins 6
• Medications: Antibiotics (aminoglycosides, vancomycin), NSAIDs, chemotherapeutic agents 5
• Contrast media: Particularly in patients with pre-existing kidney disease, diabetes, or hypovolemia 1
• Glomerulonephritis: Various immune-mediated conditions 4
• Interstitial nephritis: Often medication-induced (antibiotics, NSAIDs, proton pump inhibitors) 6

3. Postrenal Causes (<5% of cases)

• Urinary tract obstruction: Prostatic hypertrophy, nephrolithiasis, tumors, or retroperitoneal fibrosis 1, 7

Risk Factors for AKI

• Age >65 years: Decreased renal reserve and increased susceptibility 3
• Pre-existing chronic kidney disease: Reduced nephron mass and compensatory ability 3
• Diabetes mellitus: Underlying vascular disease and susceptibility to nephrotoxins 3
• Heart failure: Reduced cardiac output and renal perfusion 4
• Liver disease: Altered hemodynamics and increased risk of hepatorenal syndrome 1
• Medications: NSAIDs, ACE inhibitors, ARBs, diuretics, especially when used in combination ("triple whammy") 5

Diagnostic Approach

• Laboratory findings: Rapid increase in serum creatinine (≥0.3 mg/dL within 48 hours or ≥50% increase within 7 days) 1
• BUN/creatinine ratio >20:1: Suggests prerenal etiology 3
• Urine output: Often decreased (<0.5 mL/kg/hr for 6 hours), though non-oliguric AKI can occur 1
• Urinalysis: May show muddy brown casts in ATN, RBC casts in glomerulonephritis, or WBC casts in interstitial nephritis 2
• Renal ultrasonography: Indicated to rule out obstruction, particularly in older men or when postrenal causes are suspected 2, 4

Management Principles

• Treat underlying cause: Identify and address the primary etiology 3
• Volume management: Restore euvolemia in hypovolemic states; avoid fluid overload 1
• Discontinue nephrotoxic medications: NSAIDs, certain antibiotics, and other potential nephrotoxins 5
• Adjust medication dosages: Based on estimated GFR 4
• Avoid contrast media when possible or use preventive measures in high-risk patients 1
• Consider renal replacement therapy for refractory hyperkalemia, volume overload, severe acidosis, or uremic symptoms 2

Pitfalls and Caveats

• Multiple etiologies: AKI is often multifactorial, with more than one contributing cause 6
• "Triple whammy": Concurrent use of NSAIDs, diuretics, and ACE inhibitors/ARBs significantly increases AKI risk 5
• Contrast-induced nephropathy: Risk is highest in patients with pre-existing kidney disease, diabetes, or hypovolemia 1
• Medication reconciliation: Critical at transitions of care to prevent medication-related AKI 1
• Delayed diagnosis: Can lead to irreversible kidney damage and progression to chronic kidney disease 4