Abstract: FR-PO0442
Kidney Recovery in a Patient on Hemodialysis (HD) with Thrombotic Microangiopathy After Hepatitis C Virus Eradication
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 2026 | Location: Exhibit Hall A, 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
- Abubaker, Azza, 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) caused by hepatitis C (HCV) is a rare cause of kidney failure. We present a case of renal recovery following eradication of HCV in a patient on dialysis caused by TMA.
Case Description
We previously reported a 66-yo male with a PMH of HTN and cocaine use admitted for HTN emergency ultimately requiring initiation of HD. Workup included DAAT, ANCA, MPO, SPEP, anti-GBM and antiphospholipid which were negative. He had high LDH, low haptoglobin, C3, CH50 and C4. Renal biopsy showed TMA, moderate interstitial fibrosis, 10% global glomerular sclerosis. Immunofluorescence was negative. He was found to have hepatitis C for which he declined treatment. His HTN was brought under control with multiple agents and he was discharged on HD. Following discharge, the patient remained on HD; he was non-oliguric but continued to require multiple antihypertensives. 10 months after discharge he initiated DAA (glecaprevir-pibrentasvir) for his HCV. 1 month into therapy, his creatinine began a downward trend and he required less intensive treatment for his HTN. Following completion of DAA, his creatinine stabilized at 2.4 and he came off HD. The patient remains stable off HD for 6 months at the time of this writing. His UPCR has decreased from 703 mg/g to 161 mg/g and he only requires two medications for HTN. Follow up PCR have shown undetectable HCV RNA.
Discussion
Renal recovery following treatment of HCV in patients with MPGN is well documented in the literature. Our patient did not have evidence of MPGN on microscopy and HTN was presumed to be the primary driver of his TMA. At the time of his discharge hemolysis markers were improving in conjunction with improved blood pressure control and HTN was presumed to be the primary driver of his kidney injury. TMA caused by HCV in the absence of immune complex deposition is rarely described in the literature. While renal recovery following treatment for HCV causing MPGN is well described in literature, recovery following treatment for HCV in a patient with TMA is rarely described. This case highlights the importance of HCV treatment in patients with CKD.