Abstract: PUB017
A Toast Too Far: The Unseen Renal Consequences of Binge Drinking
Session Information
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Lorenzo Capps, Maria Jose, RWJBarnabas Health, Toms River, New Jersey, United States
- Vega Batista, Franklyn, RWJBarnabas Health, Toms River, New Jersey, United States
- Rajendran, Jackson, RWJBarnabas Health, Toms River, New Jersey, United States
- Jain, Keshani, RWJBarnabas Health, Toms River, New Jersey, United States
Introduction
Acute alcoholic myopathy can occur after excessive alcohol consumption, leading to rhabdomyolysis and acute kidney injury. Rhabdomyolysis results from muscle necrosis, releasing intracellular components like creatine kinase (CK) into circulation. Patients with chronic alcohol consumption are at higher risk for acute myopathy following binge drinking.
Case Description
A 49-year-old male with alcohol use disorder, presented to the emergency department with shortness of breath and generalized body aches following significant cognac consumption at a family gathering. Symptoms began the morning after drinking, with chills and diffuse body aches progressively worsening over two days. He denied trauma, statin use, or supplements. Physical examination was unremarkable. Laboratory tests showed elevated creatinine (2.0 mg/dL), BUN (16 mg/dL), AST (229 U/L), ALT (1387 U/L), elevated CK (49,643 U/L), and troponin T (2471). Urinalysis showed blood without RBCs, proteinuria (300 mg/dL), and granular casts.
Discussion
The patient received aggressive intravenous hydration and urine alkalinization with sodium bicarbonate. Despite decreasing CK levels, kidney function deteriorated with oliguria, necessitating renal replacement therapy. Autoimmune markers (anti-SRP and MI-2) were negative. Due to slow improvement in kidney function, persistent proteinuria, and mild hypocomplementemia (low C3, normal C4), kidney biopsy was performed, revealing acute tubular necrosis in a resolving phase. After three hemodialysis sessions, renal function progressively improved, allowing discontinuation of dialysis. This case highlights that severe rhabdomyolysis following alcohol binge drinking can lead to significant acute kidney injury requiring temporary dialysis. The risk of kidney injury in rhabdomyolysis is directly associated with volume depletion, acidosis, and CK levels, causing renal tubular obstruction from heme pigment casts and tubular injury from free chelatable iron. Early recognition and aggressive fluid resuscitation are crucial first-line treatments, but when myoglobin has already caused acute tubular necrosis, prompt initiation of hemodialysis can facilitate myoglobin clearance and expedite recovery of kidney function. Clinicians should maintain high suspicion for rhabdomyolysis in patients presenting with myalgia after binge drinking, even in the absence of trauma.