Abstract Introduction We present a case of a 36-year-old male with history of cocaine use who presented to the emergency department (ED) in hypertensive emergency, severe acute kidney failure, normocytic anemia, and thrombocytopenia. Kidney biopsy was ultimately performed, revealing evidence of thrombotic microangiopathy (TMA), which was attributed to cocaine use. A diagnosis of drug-induced TMA should be considered in patients presenting with microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury (AKI). Drug-induced TMA is a clinical diagnosis made in the presence of an offending agent. Hemodialysis was initiated with improvement in uremia. Case A 36-year-old male with history of hypertension, medication noncompliance, and cocaine use presented to the ED with 1 week of left flank pain and shortness of breath. He was found to have a blood pressure of 210/148 mm Hg, and his laboratory studies were notable for severe acute kidney injury (creatinine 17.52 mg/dL and BUN 148 mg/dL, from baseline creatinine 1.2 mg/dL and BUN 13 mg/dL), acute anemia (Hgb 5.7 g/dL; Hct 16.3% from baseline Hb 12 g/dL and Hct 36%), elevated total bilirubin (1.7 mg/dL), and high anion gap metabolic acidosis (anion gap 36; CO2 14 mmol/L; pH 7.31). The patient received IV sodium bicarbonate and a nicardipine infusion was initiated. Diagnostic workup revealed a low haptoglobin (10 mg/dL) with elevated LDH (871 U/L) and the peripheral blood smear showed normocytic anemia, schistocytes, and thrombocytopenia. ADAMTS13 assay revealed 50% activity, effectively ruling out thrombotic thrombocytopenic purpura (TTP). The patient underwent kidney biopsy which revealed thrombotic microangiopathy, characterized by focal intraluminal fibrin thrombi, endothelial swelling, RBC fragmentation, and extravasation involving arteries. Hemodialysis was initiated with improvement in uremia and the patient also received eculizumab for severe rapidly progressive kidney failure. Discussion Thrombotic microangiopathy is a syndrome characterized by microangiopathic hemolytic anemia due to shearing of red blood cells (RBCs) and thrombocytopenia due to platelet consumption. Cocaine is an illicit drug that can contribute to endovascular damage, thrombosis due to activation of the complement system, platelet aggregation, and vasoconstriction, leading to organ and tissue ischemia. Cocaine-induced TMA is an uncommon phenomenon that has been rarely reported in medical literature. Management involves cocaine cessation and supportive care. It is essential to exclude TTP and complement-mediated TMA. Empiric treatment with therapeutic plasma exchange and eculizumab may be considered. This abstract is funded by: None
Ahmed et al. (Fri,) studied this question.