Gross hematuria and detection of nephrotic syndrome after an athletics event

Sirs, We read with great interest the article by Butani in Pediatric Nephrology [1]. The author described an infant presenting with gross hematuria (GH) at the onset of minimal-change disease nephrotic syndrome (MCNS) [1]. We recently experienced a similar case in which hematuria and nephrotic syndrome (NS) were detected in a child after an athletics, raising the question of whether the exercise induced or augmented the signs or primary renal disease. A 7-year-old Japanese girl participated in a shortdistance foot race (2 km) as a member of a selected athletics team. After completing the race, the girl was observed with prominent facial edema, GH, and proteinuria. Urinalysis showed cola-like urine with 4+ proteinuria (urine proteinto-creatinine ratio 5.49) containing numerous blood cells per high-powered field with casts. Serum total protein was 3.9 g/dl; albumin, 1.8 g/dl; total cholesterol, 410 mg/dl; creatinine, 0.3 mg/dl. Platelet counts and coagulation studies were normal. Serological tests, including those for anti-nuclear and anti-double-stranded DNA antibodies, complements C3 and C4, antistreptolysin O titers, myeloperoxidase-antineutrophil cytoplasmic antibody, and hepatitis B antigens, were all negative/normal. Renal biopsy was performed because persistent GH is unusual in MCNS. All 18 of the glomeruli obtained showed widely open patent capillary walls without mesangial proliferation. Immunofluorescence studies were negative and showed a diffuse linear staining of the alpha 5(IV)NC domain of collagen IV along the glomerular basement membrane (GBM). Electron microscopy studies revealed that the glomeruli were normal with a fusion of foot processes. The GBMs were of a normal thickness with no electrondense deposits. The profound proteinuria failed to respond to initial prednisolone therapy (dose 60 mg/m/day, orally administered each day for 4 weeks, followed by 4 weeks of the same dose on alternate days) [2]. The GH subsided 3 weeks after the athletics event concomitant with 3 weeks of oral prednisolone therapy. Weekly methylprednisolone pulse therapy combined with oral prednisolone and cyclophosphamide (2 mg/kg per day for 12 weeks) achieved an initial complete remission [3]. However, soon after prednisolone tapering, relapses accompanied with GH occurred. The manifestation of multiple relapses led to the addition of oral cyclosporin with a trough level of 80–100 ng/ml to her pharmacotherapeutic regimen. The patient continued to show frequently relapsing steroid-dependent NS even when treated with a combination of oral prednisolone and cyclosporin. Her renal function has remained normal with normotension at 6 years after diagnosis. Pediatr Nephrol (2009) 24:2463–2464 DOI 10.1007/s00467-009-1212-z