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Abstract: TH-PO0856

Coexistence of Minimal Change Disease and Acquired Thrombotic Thrombocytopenic Purpura: A Case Report

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Alsaedi, Zainulabdeen S, New York Presbyterian Queens, Flushing, New York, United States
  • Gajre, Ashwin, Lokmanya Tilak Municipal General Hospital and Lokmanya Tilak Municipal Medical College, Mumbai, MH, India
  • Miqdad, Mohammed A., New York Presbyterian Queens, Flushing, New York, United States
  • Alatta, Lina S., New York Presbyterian Queens, Flushing, New York, United States
  • Hulwi, Hasan, New York Presbyterian Queens, Flushing, New York, United States
  • Rodriguez, Oscar, New York Presbyterian Queens, Flushing, New York, United States
  • Kuo, Sheng F., New York Presbyterian Queens, Flushing, New York, United States
Introduction

A case of coexisting minimal change disease (MCD) and acquired thrombotic thrombocytopenic purpura (TTP), highlighting a poorly understood and infrequently reported association

Case Description

A 61-year-old female presented with anasarca. Workup showed nephrotic proteinuria (PCR 6 g/g), hypoalbuminemia (1.3 g/dL), normal renal function, and normal echocardiogram. Kidney biopsy confirmed MCD. She achieved remission with steroids, tapered off over months. Weeks after stopping, she developed anuria and edema; creatinine rose to 10.3 mg/dL, requiring dialysis for 2 weeks. Prednisone 60 mg daily led to full recovery. A relapse during taper responded again to high-dose steroids. While in remission on 60 mg, she developed fever, headache, jaundice, and swelling. Labs (see table) showed anemia, schistocytosis, and thrombocytopenia. With a PLASMIC score of 6, PLEX and rituximab were initiated. ADAMTS13 activity <5% confirmed acquired TTP. Workup for autoimmune disease, infection, and malignancy was negative. She improved clinically and hematologically with treatment

Discussion

MCD and TTP are distinct immune-mediated conditions with possible overlap. MCD involves circulating factors, T cells, and possibly anti-nephrin antibodies; rituximab’s efficacy implicates B cells. TTP is caused by anti-ADAMTS13 antibodies, leading to platelet-rich microthrombi. Our patient developed TTP despite MCD remission on high-dose steroids, suggesting a steroid-resistant or separate immune pathway. She improved only with plasma exchange and rituximab. Similar reports (e.g., Tanaka et al., Cataland et al.) hint at shared mechanisms. Whether these diseases share a trigger or reflect predisposition remains unclear. This case highlights the need for vigilance even when one autoimmune process appears controlled

Digital Object Identifier (DOI)