Two Cases of Type II Membranoproliferative Glomerulonephritis.
- Author:
Jung Hoon SUNG
1
;
Mi Jung KANG
;
Eun Ah HWANG
;
Sueng Yeup HAN
;
Sung Bae PARK
;
Hyun Chul KIM
;
Kwan Kyu PARK
Author Information
1. Kidney Institute, Keimyung University, School of Medicine, Daegu, Korea. k780121@dsmc.or.kr
- Publication Type:Case Report
- Keywords:
Type II idiopathic membranoproliferative glomerulonephritis;
Dense deposit disease
- MeSH:
Basement Membrane;
Biopsy;
Capillaries;
Child;
Diagnosis;
Glomerulonephritis;
Glomerulonephritis, Membranoproliferative*;
Hematuria;
Humans;
Immunosuppressive Agents;
Korea;
Mesangial Cells;
Microscopy;
Microscopy, Electron;
Microscopy, Fluorescence;
Proteinuria;
Young Adult
- From:Korean Journal of Nephrology
2004;23(2):335-340
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The term type II membranoproliferarive glomerulonephritis (MPGN) refers to the histopathologic entity characterized by dense intramembranous deposits. It have a variable clincal courses, frequently occurs in older children and young adult. In comparison with The western, the idiopathic membranoproliferative glomerulonephritis (MPGN) has a lower frequency than secondary MPGN. Especially, of the idiopathic MPGN, the frequency of type 2 MPGN, so called dense deposit disease, is very rare in Korea. We are reporting two cases of type II MPGN, which was proven by renal biopsy. The clinical manifestations were recurrent gross hematuria in one patient and persistent nephrotic-ranged proteinuria in the other patient. The biopsy findings are characterized by diffuse wall thickening of capillary walls and focal proliferation of mesangial cell in light microscopy, and by capillary wall and granular basement membrane staining of C3 in immunofluorescence microscopy, and an irregular fusiform swelling of the lamina densa which resulting in a further thickening of basement of basement membrane in electron microscopy. Our two patients were treated conservatively without using steroid or immunosuppressive agents. One patient who had followed-up for 7 years after diagnosis remain stable in renal function, and the other patient who had followed-up for 4 years after diagnosis showed persistent nephrotic-range proteinuria.
