Abstract: SA-PO0747
Adalimumab-Associated Lupus Podocytopathy: A Rare Manifestation of Tumor Necrosis Factor-α Inhibitor-Induced Autoimmunity
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
- Al Suradi, Haya H., Johns Hopkins University, Baltimore, Maryland, United States
- Cervantes, C. Elena, Johns Hopkins University, Baltimore, Maryland, United States
- Hanouneh, Mohamad, Johns Hopkins University, Baltimore, Maryland, United States
Introduction
Tumor necrosis factor-α (TNF-α) inhibitors are well recognized to cause drug-induced lupus (DIL); however, renal involvement is uncommon, and lupus podocytopathy is an exceedingly rare manifestation. To date, no prior reports have specifically linked adalimumab to this entity. We present a case of adalimumab-induced lupus podocytopathy, highlighting its diagnostic and clinical implications.
Case Description
A 77-year-old man with hypertension and Crohn’s disease presented with worsening proteinuria while taking losartan, atorvastatin, and adalimumab started 10 months earlier. Examination revealed BP of 150/90 mmHg and lower-extremity edema. Laboratory evaluation showed serum creatinine 1.1 mg/dL and urine protein-to-creatinine ratio (UPCR) 2653 mg/g. Autoimmune serologies, previously negative, demonstrated ANA 1:320, anti–dsDNA 182 IU, and anti-histone antibody 4.3 units. Renal ultrasound was unremarkable. Kidney biopsy revealed focal global (32%) and segmental glomerulosclerosis with diffuse podocyte foot process effacement (Fig 1-A-B) without immune complex deposition on immunofluorescence. The patient was diagnosed with lupus podocytopathy (FSGS pattern). Adalimumab was discontinued, resulting in normalization of serologies and improvement of UPCR to 0.14 g/g within three months.
Discussion
TNF-α inhibitor–induced lupus differs from classic drug-induced lupus with higher rates of anti–double-stranded DNA positivity, more cutaneous manifestations, and infrequent renal involvement. Lupus podocytopathy is a distinct form of lupus nephritis characterized by nephrotic-range proteinuria, minimal change disease or focal segmental glomerulosclerosis–like patterns on light microscopy, diffuse podocyte foot process effacement on electron microscopy, and absence of significant immune complex deposition. This case represents a rare presentation of adalimumab-associated lupus podocytopathy, expanding the spectrum of TNF-α inhibitor–related renal injury. Recognition is important, as prompt discontinuation of the offending agent can result in rapid clinical and immunologic recovery.