Development of IgA Nephropathy after Clinical Remission of Dense Deposit Disease / 대한신장학회지

Dense deposit disease (DDD) is a rare primary glomerulonephritis characterized by continuous band- like intramembranous dense deposits detectable on electron microscopy. We describe a case of DDD with sequential mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis, minor glomerular alterations, and a second round of mesangial proliferative glomerulonephritis during a 13-year period. Electron dense deposits were typical of DDD in the first and second biopsies taken one year apart. However, deposits dissolved and the glomerular cellularity and basement membrane normalized with clinical remission, which was achieved by a course of immunosuppressive therapy lasting seven years. The fourth biopsy was performed due to recurrence of microscopic hematuria and showed predominant mesangial IgA deposits without glomerular capillary alteration, which was interpreted as development of IgA nephropathy after remission of DDD or coexistence with nearly healed DDD in this patient.

A Case of Hypocomplementemic Henoch-Schonlein Purpura Presenting Features of Membranoproliferative Glomerulonephritis / 소아과

Henoch-Schonlein purpura (HSP) is a systemic disorder characterized by leukocytoclastic vasculitis that can affect multiple organs predominantly the skin, joints, gastrointestinal tract and kidney. Although the specific pathogenesis of HSP is not known, there are several hypotheses. Although the importance of the complement activation in glomerular injury in HSP has been suggested, the complement levels and the blood pressure in those patients are usually normal and massive proteinuria is not common. And pathologic renal changes also have been reported to show a large variety of glomerular changes. However, to our knowledge, a membranoproliferative glomerulo-nephritis (MPGN) is a rare renal clinicopathologic manifestation of HSP. We report a 6-year-old boy with HSP who developed MPGN with hypertension, massive proteinuria, and hypo-complementemia revealed activation of the classical complement pathway, although we could not exclude the possibility of other hypocomplementemic glomerulonephritis including post-streptococcal acute glomerulonephritis.