Abstract Introduction Cocaine is a recreational drug with euphoric, addictive, and vasoconstrictive properties due to inhibition of norepinephrine, dopamine, and serotonin reuptake. (1,11) It has a half-life of 40-90 minutes, with metabolites detectable for up to 96 hours. (12) Short-term effects include tachycardia, hypertension, and seizures; chronic use may cause neurodegeneration, depression, and vascular injury. (11) Cocaine is also associated with renal failure (RF), often secondary to rhabdomyolysis, which causes muscle breakdown and myoglobin release, leading to acute RF with azotemia, elevated creatine kinase, and electrolyte disturbances. (1, 2, 4, 5, 9, 11, 13, 14) Cocaine-induced rhabdomyolysis (CIR) may result from hyperthermia, vasoconstriction, or oxidative stress. (2,24) Although cocaine-related hepatic injury (HI) is recognized, concurrent rhabdomyolysis, RF requiring renal replacement therapy (RRT), and HI are rarely documented together. (5, 7, 8, 9, 10) Case A 42-year-old man with major depressive disorder and polysubstance abuse presented with dark urine, flank and back pain, and hematuria. He reported recent substance use and a possible seizure the day prior. On admission, he was hemodynamically stable but had abdominal and costovertebral tenderness. Labs showed acute RF, markedly elevated creatine kinase, and transaminases. Urinalysis confirmed a urinary tract infection, and toxicology was positive for cocaine. Imaging revealed hepatic steatosis and mild hepatomegaly. The patient received intravenous fluids, pain control, and antibiotics and was admitted to the ICU for rhabdomyolysis, RF, and hepatic injury. His renal function deteriorated, necessitating RRT, including nine sessions of hemodialysis and a brief period of continuous RRT. He subsequently improved, no longer required RRT, and was discharged with ongoing renal recovery on outpatient follow-up. Discussion No prior reports describe concurrent acute HI, rhabdomyolysis, and RF requiring RRT due solely to cocaine use. The mechanism of cocaine-induced HI remains uncertain but may involve toxic metabolites disrupting mitochondrial glutathione or ischemia from vasoconstriction leading to hepatic and muscular hypoxia. Elevated AST and an AST:ALT ratio 1 may reflect skeletal muscle damage contributing to this pattern. RRT likely facilitated clearance of myoglobin, cocaine, and its metabolites, promoting renal and hepatic recovery. The patient’s course supports cocaine as the primary etiology. Following KDIGO guidelines and investigating N-acetylcysteine use for acute HI may enhance outcomes and drug clearance in similar cases. Conclusion This case highlights severe concurrent RF, HI, and rhabdomyolysis from isolated cocaine toxicity. RRT may offer therapeutic benefit for both renal and hepatic recovery in such cases, warranting further study. This abstract is funded by: None
Uhlen et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: