A RARE CASE OF CONCOMITANT PRIMARY MEMBRANOUS NEPHROPATHY AND ANTI-GBM NEPHRITIS

Document Type

Conference Proceeding

Publication Date

4-1-2025

Publication Title

Am J Kidney Dis

Abstract

Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome. Crescent formation from severe glomerular damage is often associated with lupus, antineutrophil cytoplasmic antibody positive glomerulonephritis, or anti-glomerular basement membrane (GBM) nephritis. Concomitant primary membranous nephropathy and anti-GBM is rare. A 51-year-old gentleman who presented with an acute rise of creatinine along with bilateral lower extremities edema for one month. On presentation, blood pressure 154/88 mmHg, heart rate 114 bpm. He had 1+ bilateral lower extremity pitting edema. Laboratory studies showed BUN 23 mg/dL and creatinine 2 mg/dL which is doubled from his baseline creatinine of 1 mg/dL. Urinalysis showed large amount of blood and proteins. UACR 1547 mg/g, UPCR 2.6 mg/mg. Imaging showed bilateral non-obstructing nephrolithiasis with mild right hydronephrosis for which urological intervention was not indicated. Serology testing including ANA, ANCA, dsDNA, anti-Smith, C3, C4, monoclonal protein screen, HIV, and hepatitis was all negative. His creatinine continued to worsen and underwent renal biopsy which showed necrotizing and crescentic glomerulonephritis and PLA2R-positive membranous glomerulopathy. His renal function worsened and was instituted on hemodialysis. Anti GBM level resulted to 219 U which suggested moderate to strong activity despite no classic linear pattern on immunofluorescence was seen. Pulse dose steroids were initiated then transitioned to prednisone and started plasmapheresis and cyclophosphamide. MN is not often presented as RPGN. Necrotizing and crescentic glomerulonephritis with primary PLA2R membranous nephropathy has been described before but is rare and atypical. A complete serology evaluation should be carried out even in patients who do not have other apparent autoimmune diseases to minimize misdiagnosis and guide the management plan.

Volume

85

Issue

4

First Page

S39

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