Abstract: PO1546
Primary Membranous Nephropathy Concurrent with ANCA-Positive Crescentic Glomerulopathy in a Hispanic Man
Session Information
- Glomerular Diseases: Clinical Features and Outcomes in Nephrotic Syndromes and Complement-Mediated Diseases
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Pozo Garcia, Leonardo, The University of Texas Rio Grande Valley School of Medicine, Edinburg, Texas, United States
- Varela, Daniel, The University of Texas Rio Grande Valley School of Medicine, Edinburg, Texas, United States
- Sathiyaraj, Steffi, The University of Texas Rio Grande Valley School of Medicine, Edinburg, Texas, United States
- Alsabbagh, Mourad, DHR Health, Edinburg, Texas, United States
- Trevino Manllo, Sergio A., South Texas Kidney Specialists, McAllen, Texas, United States
- Manllo, John, South Texas Kidney Specialists, McAllen, Texas, United States
Introduction
Primary membranous nephropathy (MN) is a common cause of glomerular disease in adults usually presenting with nephrotic syndrome. Crescents are an unusual finding in MN, its presence suggests a concomitant disease process, such as pauci-immune anti-neutrophil cytoplasmic antibody-related (ANCA) glomerulonephritis (GN).
Case Description
A 36-year-old Hispanic man presented with a 1-week history of worsening lethargy.
Examination revealed an obese Hispanic man with rales on lung auscultation and lower-extremity edema. Laboratory results showed a serum creatinine (sCr) 8.8 mg/dL, BUN of 54 mg/dL. Urinalysis revealed 4+ protein, 25-50 red blood cells per hpf. Spot urine protein creatinine ratio (UPCR) was 19 g/g, p-ANCA titer 1:640. Urine toxicology screen was positive for cocaine. Other serologies and imaging were unremarkable. Renal biopsy showed MN with PLA2R positive staining as well as necrotizing and crescentic glomerulonephritis. Interstitial fibrosis and tubular atrophy were seen only in 10% of the sample.
Management was initiated with a pulse of steroids followed by a taper, and renally dosed oral cyclophosphamide. The patient was initiated on hemodialysis due to uremic symptoms and volume overload. Three months after initiation of therapy, urine output significantly improved. Laboratory data showed: a 24 hours urine creatinine clearance of 31 ml/min, sCr 2.9 mg/dL, and UPCR 5.3 g/g. Patient was euvolemic. Hemodialysis was discontinued.
Discussion
MN and ANCA GN are distinct manifestations of renal injury with different clinical, laboratory, and pathology findings. Our case highlights an individual with both entities. We hypothesize that the patient's renal findings of p-ANCA and crescentic GN were likely associated with levamisole adulterated cocaine in the background of primary MN. The patient discontinued cocaine use after our discussions. We decided to treat the patient’s MN with immunosuppressive therapy. Fortunately, the patient has responded favorably to our management with significant improvement in renal function.