Abstract: SA-PO0700
IgM Nephropathy in Older Patients: Severe Steroid Myopathy Prompting Rituximab Rescue in an Understudied Entity
Session Information
- Glomerular Diseases: Complement-Mediated Glomerulopathies and Infection-Related GN
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Kaushal, Amit, West Virginia University, Morgantown, West Virginia, United States
- Miller, Brett Anthony, West Virginia University, Morgantown, West Virginia, United States
- Murari, Ujjwala, West Virginia University, Morgantown, West Virginia, United States
- Tomar, Ojaswi Singh, West Virginia University, Morgantown, West Virginia, United States
- Shahzad, Sheikh Raza, West Virginia University, Morgantown, West Virginia, United States
Introduction
IgM nephropathy (IgMN) is an uncommon, contested glomerular entity within the diffuse podocytopathy spectrum between minimal change disease and primary FSGS. Diagnostic criteria are unstandardized and no consensus treatment exists. Treatment decisions are particularly difficult in elderly patients with advanced chronic kidney disease (CKD), where high-dose corticosteroids carry substantial toxicity risk.
Case Description
An 82-year-old man with progressive CKD (baseline creatinine 1.9-2.2 mg/dL), type 2 diabetes, and hypertension presented with elevated creatinine (2.7 mg/dL) and nephrotic-range proteinuria (UPCR 3.9 g/g on presentation). Thorough serological work up including SPEP/UPEP/IFE, sFLC ratio, PLA2R, ANA, ANCA, hepatitis, HIV, and cryoglobulin were unremarkable. Kidney biopsy showed diffuse sclerosing glomerulopathy with 2-3+ IgM-dominant mesangial and capillary wall deposits with lambda predominance, 40% IFTA, and moderate-severe arteriosclerosis. While lambda predominance raised concern for a monoclonal process, negative serology favored a diagnosis of IgMN. Prednisone 60 mg daily was started and UPCR improved to 2.7 g/g. Four weeks later he was admitted with profound weakness, serum creatinine 5.1 mg/dL, elevated CK 2,686 U/L, consistent with steroid-induced myopathy and rhabdomyolysis-associated acute kidney injury. The course was complicated by gastrointestinal bleeding requiring blood transfusions. Steroids were tapered and two doses of rituximab (1 g IV) were administered 14 days apart. Creatinine improved to 2.0 mg/dL on discharge, and CK normalized to 40 U/L at 7 weeks.
Discussion
This case highlights an underappreciated dilemma: treating glomerular disease in elderly patients with advanced CKD when standard high-dose corticosteroid protocols carry substantial toxicity risk. Prednisone 60 mg daily for four weeks falls within reported thresholds for acute steroid myopathy with rhabdomyolysis, and our patient developed this exact complication. IgMN compounds the difficulty because it is poorly characterized, often steroid-dependent or steroid-resistant, and lacks a consensus treatment protocol. While data for rituximab in IgMN remain sparse and largely pediatric, this case suggests that earlier transition to rituximab in elderly patients at high risk of steroid toxicity may prevent significant treatment-related morbidity.