Kidney Week

Abstract: SA-PO0320

Severe Rhabdomyolysis Mimicking Acute Liver Failure Due to Polysubstance Abuse

Session Information

• AKI: Epidemiology and Risk Factors
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

• Khan, Alina S., Liaquat National Hospital and Medical College, Karachi, Sindh, Pakistan

Alina S. Khan, MD, MBBS

• Kulkarni, Mugdha, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States

Mugdha Kulkarni, MD

• Alvi, Muhammad J., Lake Cumberland Regional Hospital, Somerset, Kentucky, United States

Muhammad J. Alvi, MD, MBBS

• Sharma, Pranav K., Montefiore Einstein Medical Center, New York, New York, United States

Pranav K. Sharma, MD, FASN

Introduction

Rhabdomyolysis is a frequent cause of acute kidney injury (AKI). In polysubstance toxicity, extensive myocyte breakdown with sarcolemmal disruption leads to marked transaminitis from muscle injury, mimicking acute liver failure (ALF) despite preserved synthetic hepatic function. Gastric pneumatosis is a rare complication indicating ischemic injury from hypotension or direct substance toxicities. We report a complex case of polysubstance-induced rhabdomyolysis presenting with AKI, ALF, and gastric pneumatosis.

Case Description

A 37-year-old male with polysubstance use presented with altered mental status, intractable nausea, vomiting, and acute renal failure. Urine toxicology was positive for cocaine, amphetamines, and cannabinoids. Labs demonstrated severe rhabdomyolysis (creatine kinase >99,000 U/L), AKI (creatinine 10.74 mg/dL, BUN 67 mg/dL), and high anion gap (18) metabolic acidosis (bicarbonate 13 mmol/L). Electrolyte abnormalities included hyperkalemia (5.6 mmol/L), hypocalcemia (7.0–7.7 mg/dL), and hypoglycemia (68–70 mg/dL). Urinalysis revealed heme positivity, consistent with myoglobinuria.Marked transaminitis was observed (AST 2,413 U/L; ALT 1,263 U/L), initially raising concern for acute liver failure. However, normal levels of total bilirubin, INR, and alkaline phosphatase supported preserved hepatic synthetic function. CT scan of the abdomen demonstrated gastric fundal pneumatosis, secondary to stimulant-induced splanchnic vasoconstriction and dehydration. The patient required hemodialysis for worsening renal failure and received intensive supportive management.

Discussion

This case highlights that extreme transaminitis in polysubstance-induced rhabdomyolysis can closely mimic acute hepatocellular failure despite preserved hepatic function, creating a significant diagnostic challenge and potentially delaying recognition of pigment-induced AKI. An AST-predominant pattern with normal INR and bilirubin helps distinguish muscle-derived enzyme release from true liver injury and avoids unnecessary evaluation. Gastric pneumatosis further complicates the presentation, likely reflecting stimulant-induced splanchnic vasoconstriction and hypoperfusion. Early recognition is essential to prevent progression to dialysis-dependent acute tubular necrosis. Aggressive volume resuscitation and timely renal replacement therapy remain the cornerstone of management in this rare toxicological phenotype.