A 34-year-old man was seen in renal clinic for proteinuria and microscopic hematuria that were found incidentally on routine labs 2 years earlier. He fractured his leg during military training 3 years earlier and had a prolonged recovery period. During that time, he took naproxen almost daily for at least 1 year after the injury. He is also obese, weighing 150 kg with BMI of 39 kg/m2. Laboratory studies showed persistent proteinuria for the last 2 years although decreasing in quantity. He is otherwise doing well. Current medications include losartan (started after findings of proteinuria) and omeprazole for acid reflux symptoms. Physical examination is unremarkable. Blood pressure is well controlled at 123/70 mm Hg on losartan 100 mg daily.
Laboratory findings at disease onset 2 years earlier:
- Urine albumin/creatinine ratio (ACR): 4500 mg/g
- Urinalysis (UA): 300 protein, no blood
- Serum creatinine (SCr): 0.9 mg/dL
Laboratory findings now:
- Urine ACR 195 mg/g
- UA: 30 protein, no blood
- SCr 1.02 mg/dL
- Phospholipase A2 receptor (PLA2r) antibody: negative
- Complement C3: 135 mg/dL (normal 82-185 mg/dL)
- Complement C4: 36 mg/dL (normal 15-53 mg/dL)
- Anti-nuclear antibody (ANA): negative
- Testing for HIV, hepatitis B, hepatitis C and syphilis are all negative
A kidney biopsy was performed. Results were consistent with membranous nephropathy. Light microscopy (LM) showed thickened glomerular basement membranes (GBM) with spikes and intramembranous lucencies seen on silver stain. Electron-dense deposits were found in the glomerular subepithelial spaces. There were no tubuloreticular structures in the glomerular endothelial cells. Immunofluorescence studies showed diffuse global granular capillary wall staining with IgG (3+), IgA (trace), C1q (0-trace), C3 (0-trace). Staining for phospholipase A2 receptor (PLA2R), thrombospondin type-1 domain-containing 7A (THSD7A), Semaphorin 3B, and neural epidermal growth factor-like 1 (NELL-1) were all negative.”
