Most Common Cause of AKI in Hospitalized Patients
Prerenal causes dominate as the most common etiology of acute kidney injury in hospitalized patients, accounting for more than 60% of cases, resulting from decreased renal perfusion without initial structural kidney damage. 1, 2
Etiologic Distribution
The breakdown of AKI causes in general hospitalized patients follows a clear hierarchy:
- Prerenal causes: >60% of cases - These result from decreased renal perfusion without initial structural kidney damage 1, 2
- Intrarenal causes: ~35% of cases - Primarily acute tubular necrosis from direct parenchymal damage 1, 2
- Postrenal obstruction: <3% of cases - Urinary tract obstruction is the least common mechanism 1, 2
Key Prerenal Mechanisms in Hospitalized Patients
Volume depletion represents the dominant prerenal mechanism through multiple pathways:
- Absolute volume depletion from hemorrhage, gastrointestinal losses, burns, or excessive diuresis 1, 2
- Third-space fluid sequestration in pancreatitis or peritonitis 1, 2
- Severe hypoalbuminemia from nephrotic syndrome 1, 2
Hemodynamic compromise contributes significantly:
- Decreased cardiac output from heart failure, cardiogenic shock, or arrhythmias 1, 2
- Systemic vasodilation from sepsis, anaphylaxis, or cirrhosis 1, 2
Medication-related causes are particularly important and often overlooked:
- NSAIDs, diuretics, and ACE inhibitors/ARBs represent the "triple whammy" combination that dramatically increases AKI risk 1, 2
- Each additional nephrotoxin increases AKI odds by 53%, and three or more nephrotoxins more than doubles the risk 2
Special Population Considerations
In patients with decompensated cirrhosis, prerenal AKI accounts for approximately 68% of cases, with the most common precipitating factors being:
- Infections (most common precipitant) 1
- Diuretic-induced excessive diuresis 1
- Gastrointestinal bleeding 1
- Therapeutic paracentesis without adequate volume expansion 1
- Nephrotoxic drugs 1
Critical Diagnostic Approach
Fluid challenge with albumin at 1 g/kg (maximum 100 g/day) differentiates prerenal from intrinsic causes:
- Hypovolemic (prerenal) AKI shows reduction in serum creatinine to within 0.3 mg/dL of baseline 1, 2
- Patients with intrinsic AKI do not respond to fluid challenge alone 1
Common Pitfalls to Avoid
Don't assume traditional categories are discrete - Prerenal and intrinsic mechanisms frequently coexist and evolve dynamically, especially in septic patients 3
Don't overlook medication combinations - Electronic health record systems identifying patients exposed to three or more nephrotoxic drugs have led to sustained decreases in AKI incidence 2
Don't discharge without stopping diuretics - All diuretics should be discontinued irrespective of AKI stage when prerenal AKI is diagnosed 1, 2
Don't forget infection screening - Infection is the most common precipitant of hepatorenal syndrome and should be treated immediately 1