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Kidney Week

Abstract: TH-PO0527

Not All Proteinuria in Lupus Is Lupus Nephritis: IgAN in a Patient with Systemic Lupus Erythematosus and Antiphospholipid Syndrome

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Kodali, Naga Anvesh, University of Central Florida/HCA Florida Ocala Hospital, Ocala, Florida, United States
  • Gottipati, Bhavika, The Wright Center for Graduate Medical Education, Scranton, Pennsylvania, United States
  • Nalla, Akhila, University of Central Florida/HCA Florida Ocala Hospital, Ocala, Florida, United States
  • Mitra, Chandan, University of Central Florida/HCA Florida Ocala Hospital, Ocala, Florida, United States
  • Adewuyi, Joel O., University of Central Florida/HCA Florida Ocala Hospital, Ocala, Florida, United States
  • Nwakoby, Izuchukwu E., University of Central Florida/HCA Florida Ocala Hospital, Ocala, Florida, United States
  • Vaghela, Mahesh K., University of Central Florida/HCA Florida Ocala Hospital, Ocala, Florida, United States
  • Ventrapragada, Saila V., University of Central Florida/HCA Florida Ocala Hospital, Ocala, Florida, United States
Introduction

Renal disease in systemic lupus erythematosus (SLE) is often presumed to be lupus nephritis, while antiphospholipid syndrome (APS) raises concern for APS nephropathy. Although IgA nephropathy (IgAN) is common worldwide, its coexistence with SLE is uncommon and may be overlooked when proteinuria is attributed to autoimmune renal disease without tissue confirmation.

Case Description

A 37-year-old woman with SLE diagnosed after pregnancy-associated deep venous thrombosis, APS, and Raynaud phenomenon was maintained on hydroxychloroquine and warfarin. She presented with persistent microscopic hematuria and proteinuria despite preserved kidney function. Creatinine was 0.5 mg/dL, urine protein-to-creatinine ratio (UPCR) was up to 1700 mg/g, 24-hour urine protein was 1.4 g, and urine albumin-to-creatinine ratio (UACR) was 402 mg/g. C3 and C4 were normal, and repeat ANA and anti-dsDNA were negative. Kidney biopsy showed 16 glomeruli with one globally sclerosed glomerulus, segmental sclerosis, mild interstitial fibrosis/tubular atrophy, IgA-dominant mesangial staining (IgA 3+, C3 1+), and mesangial electron-dense deposits with moderate foot process effacement. Oxford score was M0E0S1T0C0. The biopsy explicitly showed no lupus nephritis and no APS nephropathy/thrombotic microangiopathy. ACE inhibitor and ARB therapy were limited by symptomatic hypotension. She was started on empagliflozin (Jardiance) for antiproteinuric renal protection and targeted-release budesonide (Tarpeyo) for IgAN-directed therapy, while hydroxychloroquine and warfarin were continued. At an early 4-week outpatient follow-up, UPCR improved to 725 mg/g and UACR to 366 mg/g; 8 weeks later, UPCR was 695 mg/g and UACR was 247 mg/g. Urinalysis improved from 2+ protein and 2+ blood to trace protein and trace blood.

Discussion

This case highlights a clinically important diagnostic pitfall: proteinuria in patients with SLE and APS should not be reflexively attributed to lupus nephritis or APS nephropathy. Discordant serologies and biopsy findings identified IgA nephropathy as a distinct glomerular disease and redirected treatment toward supportive and targeted IgAN therapy rather than escalation of lupus nephritis-directed immunosuppression. Biopsy remains decisive when autoimmune comorbidity obscures the renal diagnosis.