Can alcohol cause prerenal or intrinsic (acute kidney injury) acutely?

Alcohol's Impact on Acute Kidney Injury

Alcohol can cause both prerenal and intrinsic acute kidney injury through multiple mechanisms including volume depletion, hemodynamic alterations, and direct nephrotoxicity. 1

Mechanisms of Prerenal Injury

• Alcohol causes volume depletion through diuresis, vomiting, and reduced fluid intake, leading to hypovolemic prerenal AKI 1
• Systemic hemodynamic effects of alcohol decrease renal perfusion pressure, which can compromise kidney function 1
• The combination of alcohol-induced volume depletion and altered renal hemodynamics creates a state of renal hypoperfusion 1
• In patients with alcoholic hepatitis, the hemodynamic consequences of portal hypertension overlap with systemic inflammatory responses, placing them at high risk for AKI due to hepatorenal syndrome 2

Mechanisms of Intrinsic Injury

• Prolonged or severe alcohol consumption can progress from prerenal injury to intrinsic renal damage through ischemic acute tubular necrosis 1
• Direct nephrotoxicity from alcohol metabolites can damage renal tubular cells 1
• Alcohol-induced rhabdomyolysis can lead to myoglobinuric acute kidney injury 1
• At-risk drinking is independently associated with stages 2-3 acute kidney injury in critically ill patients, even after adjustment for other risk factors 3

Risk Factors for Alcohol-Induced AKI

• Pre-existing liver disease, especially cirrhosis, significantly increases the risk of developing AKI 1
• Concurrent use of nephrotoxic medications with alcohol creates a "triple whammy" effect, particularly when combined with diuretics and renin-angiotensin system inhibitors 1, 4
• Dehydration from alcohol's diuretic effect combined with reduced fluid intake during drinking episodes 1
• Systemic inflammatory response syndrome (SIRS) associated with alcoholic hepatitis increases AKI risk 2

Diagnostic Considerations

• In patients with suspected alcohol-induced AKI, assessment should include evaluation of volume status, urinalysis, and calculation of fractional excretion of sodium (FENa) and urea (FEUrea) 1
• A FENa <1% suggests prerenal causes including alcohol-induced AKI 1
• AKI is defined as an increase in serum creatinine by ≥0.3 mg/dL within 48 hours or a 50% increase over baseline 5
• Renal ultrasound should be performed to rule out obstruction as a cause of AKI 6

Management Approach

• Immediate fluid resuscitation is essential for treating prerenal AKI caused by alcohol 1
• Discontinuation of all nephrotoxic medications and adjustment of diuretics is crucial 1
• In patients with alcoholic hepatitis and AKI with serum creatinine >2.5 mg/dL, corticosteroid treatment is contraindicated 2
• Careful surveillance of AKI allows for early treatment with intravenous albumin and vasoconstrictors when appropriate 2
• Multidisciplinary care involving specialists in hepatology, critical care, infectious disease, and nephrology should be provided for patients with alcohol-related AKI 2

Prevention Strategies

• Complete avoidance of alcohol use, especially in patients with underlying liver or kidney disease 1
• Avoiding concurrent use of nephrotoxic medications in patients who consume alcohol 1
• Careful monitoring for infection, which can precipitate AKI and worsen outcomes 1
• Strategies to preserve renal function include avoiding nephrotoxins like intravenous contrast, aminoglycosides, and nonsteroidal anti-inflammatory drugs 2

Prognosis

• Even one episode of AKI increases the risk of cardiovascular disease, chronic kidney disease, and death 5
• Among patients with severe alcohol-associated hepatitis requiring renal replacement therapy, those with pre-RRT MELD-Na <35 had better 6-month survival (50% vs 18%) 7
• AKI is seen in approximately 30% of patients with severe alcohol-associated hepatitis and is associated with increased mortality 7