Abstract: SA-PO0102
A Cocaine Crisis: Hypertensive Emergency and Thrombotic Microangiopathy
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Bernabei, Luca L, Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
- Patel, Dhara D., Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
- Cox, Colin, Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
- Vadaparampil, Justin, Jefferson Torresdale Hospital, Philadelphia, Pennsylvania, United States
Introduction
Thrombotic microangiopathy (TMA) is a rare disease involving vascular injury of arterioles and capillaries causing microvascular thromboses. Here, we present a case of cocaine-induced hypertensive TMA.
Case Description
A 66-year-old male with PMH of HTN, cocaine & alcohol abuse presented with 1 day of epistaxis. BP was 237/120. He denied headaches, vision changes, nausea, vomiting, or urinary changes. Creatinine was 3.4 (baseline 1.0), BUN 52, hgb 9.2, and plt 96. Urine was positive for cocaine, 2+ protein, blood, RBCs, and granular casts. He was admitted for hypertensive emergency. Further workup showed low haptoglobin, elevated LDH, significantly low C3 and CH50, mildly low C4, high HCV viral load, and minimally elevated metanephrines. Direct antiglobulin test, ANCA, MPO, SPEP, anti-GBM, renin/aldosterone, antiphospholipid studies, HIV and renal ultrasound were unremarkable. Renal biopsy revealed thrombotic microangiopathy, moderate interstitial fibrosis and 10% global glomerular sclerosis. The patient ultimately required HD for worsening AKI and concern for uremia. He was discharged with additional outpatient serologic workup and HCV treatment pending.
Discussion
Our patient was diagnosed with TMA via biopsy which was likely driven by hypertension-induced endothelial injury leading to micro thromboses, capillary blockage and ischemia. His hypertension was likley a product of cocaine use and medication non-complaince. Cocaine, a known catecholamine reuptake inhibitor, increases blood pressure, decreases antioxidants and activates complement. Here the differential for TMA also includes chronic HCV infection and atypical HUS. However, his platelets and haptoglobin increased and LDH decreased once his blood pressure stabilized supporting cocaine-induced hypertensive emergency etiology for his TMA.
Angiopathy with schistocytes