CASE PRESENTATION A 60 year-old Caucasian female who developed chronic renal failure from focal segmental glomerulosclerosis (FSGS) received a living-related renal allograft from her 28year-old son. The patient presented initially at age 48 with signs of nephrotic syndrome (peripheral edema, hypoalbuminemia, and hypercholesterolemia) and a serum creatinine of 1.5 mg/dl (132mmol/l) (normal range 0.6–1.2 mg/dl (52.8–105.6mmol/l)). She was treated with prednisone for six months, followed by cyclosporine A, with only partial remission of proteinuria. Renal function slowly declined over the ensuing decade. At the time of initial presentation, serologic test results were negative or within normal limits for antinuclear antibody, C3 and C4 complement levels, hepatitis B surface antigen, hepatitis C antibody, and serum and urine protein electrophoreses. Her past medical history was significant for hypertension for 25 years, and hypothyroidism. She had no history of childhood urinary tract infections or urinary reflux and she denied regular intake of over-the-counter medications. The patient’s post-operative course was unremarkable and she was discharged seven days post-transplantation with a serum creatinine of 1 mg/dl. Immunosuppressive medications included FK506, mycophenolate mofetil, and prednisone. Four weeks post-transplant, the patient noted worsening lower extremity edema. A 24-hour urine collection contained 4.5 g protein (normal range 0–150 mg/day). Serum albumin was 3.6 g/dl (36 g/l) (normal range 3.5–5.0 g/dl (30–50 g/l)) and serum creatinine was 1.0 mg/ dl (88.4mmol). FK506 levels were within therapeutic range. A renal ultrasound showed no signs of urinary tract outflow obstruction and normal venous and arterial blood flow. A renal biopsy was performed. RENAL BIOPSY FINDINGS Twenty-four glomeruli were sampled for light microscopy, none of which showed segmental or global glomerulosclerosis (Figure 1). Peripheral capillary lumina were fully patent and glomerular basement membranes were uniformly normal in thickness, contour and texture. There was a minimal patchy interstitial mononuclear inflammatory cell infiltrate, involving o5% of the cortical area, with rare foci of mild tubulitis (o5 mononuclear inflammatory cells/ tubular cross-section). There was no significant tubular atrophy or interstitial fibrosis. Features of isometric tubular vacuolization or viral inclusions were not identified. Arterial vessels were unremarkable. Immunofluorescence microscopy showed no staining of peritubular capillaries for C4d and no glomerular staining for IgG, IgM, IgA, C3, C1, fibrinogen, albumin, kappa, or lambda. Electron microscopic examination of two glomeruli revealed diffuse (100%) podocyte foot process effacement and no other significant ultrastructural abnormalities (Figure 2).