Kidney Week

Abstract: FR-PO0432

A Multiple-Hit Endothelial Injury Model: Thrombotic Microangiopathy in a Patient on Carfilzomib with Concurrent COVID-19 and Influenza A

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

• Sarwat, Ahmed, Baystate Medical Center, Springfield, Massachusetts, United States

Ahmed Sarwat, MD

• Landry, Daniel L., Baystate Medical Center, Springfield, Massachusetts, United States

Daniel L. Landry, DO, FASN

Introduction

Carfilzomib-associated thrombotic microangiopathy (TMA) is a recognized complication, though diagnosis is challenging in the setting of concurrent infections that may independently trigger endothelial injury and complement activation.

Case Description

A 79-year-old man with high-risk relapsed IgG kappa multiple myeloma (1q gain, monosomy 13, t(11;14) was receiving carfilzomib, venetoclax, and dexamethasone administered on days 1, 8, and 15 of each cycle and had completed 11 cycles, with his most recent dose shortly prior to presentation. He presented with cough and fatigue, was found to have concurrent influenza A and COVID-19 infection. Paxlovid was not administered.
On admission, he was noted to have severe thrombocytopenia (platelets 3×10³ /µL, nadir 2×10³ /µL), anemia (hemoglobin 9.8 g/dL), evidence of hemolysis (Lactate dehydrogenase peaked at 1303 U/L, haptoglobin was reduced, and peripheral smear demonstrated marked schistocytosis, consistent with microangiopathic hemolytic anemia.) and acute kidney injury with creatinine 2.1 mg/dL (baseline normal), which progressed to a peak of 9.9 mg/dL
Evaluation showed a PLASMIC score of 4 and normal ADAMTS13 activity on multiple measurements, making thrombotic thrombocytopenic purpura unlikely. Coagulation studies did not support disseminated intravascular coagulation. Bone marrow biopsy demonstrated no hemophagocytic lymphohistiocytosis or active myeloma. Complement genetic testing (Factor H and I) was negative.
A diagnosis of thrombotic microangiopathy was made. Carfilzomib was discontinued, and he was treated with dexamethasone and eculizumab administered as three weekly doses with penicillin prophylaxis. Despite complement blockade, there was no immediate renal recovery, and the patient was discharged on hemodialysis via a tunneled catheter; however, over a period of 2 months, renal function gradually improved, with sufficient recovery of creatinine clearance to allow discontinuation of dialysis.

Discussion

This case highlights a “multiple-hit” model of TMA, in which carfilzomib-associated endothelial injury may be amplified by concurrent viral infections such as COVID-19 and influenza. The delayed renal recovery despite complement blockade underscores the complexity of therapeutic response in multifactorial TMA and the importance of early recognition, drug withdrawal, and supportive care.