Abstract: TH-PO0059
Thrombotic Microangiopathy That Comes with the Job: Chemist
Session Information
- AKI: Pathogenesis and Disease Mechanisms
November 06, 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
- Lwin, Yone Mee Mee, SUNY Downstate Health Sciences University, New York, New York, United States
- Delp, Crystal, SUNY Downstate Health Sciences University, New York, New York, United States
- Suraj, Fnu, SUNY Downstate Health Sciences University, New York, New York, United States
- Soe, Thin Thin, SUNY Downstate Health Sciences University, New York, New York, United States
- Saggi, Subodh J., SUNY Downstate Health Sciences University, New York, New York, United States
- Salvatore, Steven, Weill Cornell Medicine, New York, New York, United States
- Salifu, Moro O., SUNY Downstate Health Sciences University, New York, New York, United States
Introduction
Thrombotic microangiopathy (TMA) involves microangiopathic hemolytic anemia, thrombocytopenia, and organ damage, often affecting the kidneys and brain. It can be caused by primary conditions like TTP and aHUS, or secondary causes such as infections, autoimmune diseases, malignancy, pregnancy, or drugs. Drug-induced TMA accounts for 10–13% of TMAs. Heavy metals like mercury and copper can induce TMA by damaging the endothelium and impairing renal and coagulation functions. Mercury promotes immune activation, endothelial damage, and may lead to malignant hypertension and renal tubular necrosis, which are potential contributors to secondary TMA. Copper toxicity has been associated with oxidative stress, inflammation, and a positive dose–response relationship with chronic kidney disease. We present a unique case of a young female chemist with a history of occupational mercury exposure treated with chelation, who presented with malignant hypertension, and acute kidney injury progressing to dialysis dependence.
Case Description
A 26-year-old woman with newly diagnosed hypertension and unknown kidney disease presented with dyspnea and leg swelling. She worked as a chemist in a gold mine with heavy metal exposure. A similar episode a year prior was treated with herbal medications and prednisone. On presentation, she was hypertensive and tachycardic with anemia (Hb 6.4), and renal dysfunction (Cr 9, BUN 72, eGFR 6), requiring initiation of hemodialysis. Urine studies revealed hematuria and nephrotic-range proteinuria. (>8 g/day), with pertinent workup negative. Heavy metal screening was only positive for elevated urine copper (200 µg/dL). Biopsy showed chronic and active TMA with advanced CKD. TTP, HUS, and hypercoagulable workup was unremarkable.
Discussion
While biologically plausible, clinical evidence linking heavy metals to TMA is limited. This case uniquely describes TMA associated with mercury and copper exposure in a young chemist, highlighting the need to consider toxic exposures in secondary TMA and to monitor renal and hematologic parameters in at-risk populations.