Abstract: SA-PO0805
A Wolf in Minimal Change Clothing: A Case of Lupus Podocytopathy
Session Information
- Glomerular Diseases: Lupus Nephritis, Monoclonal Gammopathy-Related Disease, and Transplantation
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
- Burgos Guntin, Eusebio Felipe, NYC Health + Hospitals / Elmhurst, Icahn School of Medicine at Mount Sinai, Queens, New York, United States
- Raman, Shakthi, NYC Health + Hospitals / Elmhurst, Icahn School of Medicine at Mount Sinai, Queens, New York, United States
- Stern, Aaron S., NYC Health + Hospitals / Elmhurst, Icahn School of Medicine at Mount Sinai, Queens, New York, United States
Introduction
Lupus podocytopathy (LP) is a rare manifestation of lupus nephritis (LN) that causes nephrotic syndrome (NS) via podocyte foot process effacement (FPE) in the absence of subendothelial or subepithelial deposits.
Case Description
A 29-year-old woman with Systemic Lupus Erythematosus (SLE) complicated by recurrent Warm Autoimmune Hemolytic Anemia (WAHA) was admitted for WAHA recurrence and incidentally found to have new proteinuria. She was normotensive and without edema.
Labs showed Cr of 0.88 mg/dL (at baseline) and a urine protein-to-creatinine ratio (UPCR) of 20, with serum albumin 1.9 g/dL and LDL 135 mg/dL. Complement was markedly depressed (C3 34 mg/dL, C4 <4 mg/dL, CH50 <10 U/mL), and hemoglobin was 3.7g/dL. Urinalysis showed moderate blood without RBCs.
She was treated with high dose prednisone for the WAHA, after which repeat UPCR improved to 4.28 g. Renal biopsy revealed minimal mesangial expansion, no endocapillary hypercellularity, and mild to moderate interstitial fibrosis and tubular atrophy on light microscopy. Immunofluorescence revealed rare mesangial deposits without subepithelial or subendothelial deposits. Electron microscopy revealed extensive FPE, consistent with LP.
Discussion
LP represents ~1% of LN biopsies and mimics minimal change disease (MCD) or primary focal segmental glomerulosclerosis (FSGS). In our patient, heme-positive urine without RBCs was attributable to hemoglobinuria from WAHA rather than glomerular hematuria, a finding rare in LP (18%). Low C3 is frequently noted in LP (68%), while low C4 is less common (28%). Notably, both were depressed in this case.
This patient fulfilled LP diagnostic criteria (NS in SLE, diffuse FPE, absence of subendothelial/subepithelial deposits), though notably without overt edema. LP can be subclassified as MCD or FSGS subtypes, with the latter portending worse outcomes, higher rates of AKI (78% of LP AKI), HTN at presentation, and more severe tubulointerstitial injury on biopsy. In this patient, the preserved renal function, normal blood pressure, and only mild-to-moderate tubulointerstitial changes on biopsy favored the MCD subtype. The pathogenesis of LP is thought to be driven by cytokine or lymphokine release and T-cell dysfunction rather than immune complex deposition - a mechanism shared with primary MCD that helps explain the robust response to glucocorticoids observed in both conditions, as seen in this patient.