Abstract: FR-PO0726
Collapsing FSGS as a Complication of Sjogren Syndrome: The Importance of Testing for Proteinuria
Session Information
- Glomerular Diseases: Membranous Nephropathy, FSGS, and Podocytopathies
October 23, 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
- Dean, Emily, Medical University of South Carolina, Charleston, South Carolina, United States
- Obimdike, Faith, Medical University of South Carolina, Charleston, South Carolina, United States
- Hargous, Emily Rose, Medical University of South Carolina, Charleston, South Carolina, United States
- Hendrix, Curtis Anthony, Medical University of South Carolina, Charleston, South Carolina, United States
- McMahon, Blaithin A., Medical University of South Carolina, Charleston, South Carolina, United States
Introduction
Collapsing Focal Segmental Glomerulosclerosis (cFSGS) is associated with a high rate of dialysis dependence that progresses to end-stage renal disease. Causes include APOL1 risk allele, select medications, viral infections, severe ischemia, and autoimmune conditions.
Case Description
This case presents a 39-year-old black male with a past medical history of appendicitis and myositis-related Sjogren Syndrome versus Antisynthetase syndrome since 2024. He presented to an outside hospital with hypoxia after an influenza B infection. A CTA chest showed right subsegmental pulmonary emboli without right heart strain, diffuse lung nodules with cavitation, and bilateral lower lobe consolidations. He was treated with piperacillin-tazobactam and vancomycin for presumed pneumonia. Significant labs: CK 3242 U/L, ANA 1:1280 (speckled pattern), SSA >8 AI, Jo Ag IgG 7.8 AI, UPCR 4.86g/g (UA showed 300mg/dL proteinuria one year previously during a rheumatology clinic visit). Serum creatinine increased from 0.75 to 4.23 mg/dL in 1st 24 hours. Vancomycin trough was 57 mcg/dL. He was started on dialysis after failing a diuretic challenge.
He had no improvement in oxygenation and was started on pulse dose steroids for a possible interstitial lung disease flare. Renal biopsy obtained 1 week later showed cFSGS (17/32 segmental, 2/32 global), mild-moderate interstitial fibrosis with tubular atrophy, and acute tubular injury with scattered calcium phosphate crystals. He required dialysis on discharge and continued steroids with azathioprine, with subjective improvement in symptoms.
Discussion
It was believed that the patient had been dealing with mixed connective tissue disease with myositis since 2024. This likely caused a predisposition for cFSGS in the setting of vancomycin toxicity, with ATN in the biopsy. This case illustrates how rheumatological disease can act as a possible first step for cFSGS and shows the necessity for follow-up and quantification for all screening urinalyses.