A case of hypocomplementemic mesangial proliferative glomerulonephritis progressing to focal membranoproliferation without aggravation of urinalysis

We reported a 14-year-old boy with hypocomplementemic mesangial proliferative glomerulonephritis progressing to focal membranoproliferation without aggravation of urinalysis. He was pointed out as having asymptomatic hematuria by a school urinalysis screening, and revealed mild hematuria and proteinuria (not nephrotic). The laboratory data showed severe hypocomplementemia and high titers of antistreptolysin 0 (ASO) and antistreptokinase (ASK). A renal biopsy specimen obtained 2 months after the onset showed diffuse mesangial proliferation, and did not display any characteristic changes in membranoproliferative glomerulonephritis by either light or electron microscopy. After eight months of observation, a second renal biopsy was performed in order to examine morphological changes, because severe hypocomplementemia, mild hematuria and proteinuria had persisted. The second biopsy specimen showed C3 deposition with a mesangiocapillary pattern detected by immunofluorescence microscopy and diffuse mesangial proliferation by light microscopy. In some glomeruli, electron microscopy showed focal mesangial interposition, which was considered to be a histological feature of focal membranoproliferative glomerulonephritis. Intravenous methylprednisolone pulse therapy and subsequent glucocorticoid administration (60 mg of prednisolone every other day) was performed . The serum complement level was elevated just after the methylprednisolone pulse therapy, but fell to the previous value within 2 months. The hypocomplementemia, even if proteinuria and hematuria were mild, indicated the existence of glomerular change in this case.