Abstract: PUB546
Overlapping Features of Membranous Glomerulonephritis and Focal Segmental Glomerulosclerosis in a Patient with Nephrotic Syndrome
Session Information
Category: Trainee Case Report
- 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix
Authors
- Jensen, Colton, University of Iowa, Waukee, Iowa, United States
- Holanda, Danniele Gomes, University of Iowa Hospitals and Clinics, Iowa City, Iowa, United States
- Swee, Melissa L., University of Iowa, Waukee, Iowa, United States
Introduction
Nephrotic syndrome may be classified into different histopathologic patterns, including membranous glomerulonephritis (MGN) and focal segmental glomerulosclerosis (FSGS). While MGN may be secondary to drug exposure, FSGS is more commonly seen due to obesity, uncontrolled hypertension, and HIV. Overlap between these two conditions is rare and, when coexisting, tends to clinically resemble primary MGN. We present a case with overlapping features of NSAID-induced MGN and FSGS.
Case Description
A 37-year old Caucasian male with chronic daily headaches on ibuprofen daily presented for elevated creatinine (2.4 mg/dL, compared to 0.8 mg/dL 3 years prior). Vital signs were notable for hypertension (219/107 mmHg), and physical examination was notable for 2+ pedal edema.
Urinalysis showed 3+ protein and no blood. His UPC was 7.5. C3 and C4 levels, hepatitis B and C, HIV, ANA, dsDNA, RNP, Smith, SSA, SSB, and Histone serologies were within normal limits.
Renal biopsy demonstrated MGN with negative PLA2R and THSD7A staining, global sclerosis in 3/23 glomeruli, segmental sclerosis in 3/23 glomeruli, and moderate tubular atrophy and interstitial fibrosis.
He was advised to stop all NSAID use and was started on amlodipine, carvedilol, lisinopril, and spironolactone. At 2-week followup, his blood pressure was 110/72 mmHg, creatinine was 2.3 mg/dL, and UPC was 2.5.
Discussion
The coexistence of MGN and FSGS is a rare phenomenon, but may occur in patients who share risk factors like chronic NSAID use, uncontrolled hypertension, and obesity. Although the pathogenesis is unclear, MGN injury may contribute to FSGS since subepithelial deposits may hinder podocyte adhesion, and FSGS-mediated podocyte damage may lead to local antigen exposure and subepithelial immune complex formation.