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KMID : 0811820130170020092
Journal of Korean Society of Pediatric Nephrology
2013 Volume.17 No. 2 p.92 ~ p.100
Clinicopathologic Changes in Children with Immunoglobulin A Nephritis and Henoch-Schnlein Purpura Nephritis after Cyclosporine A and Angiotensin-converting Enzyme Inhibitor Treatment
Lee Jeong-Ju

Kim Yong-Jin
Shin Jae-Il
Yim Hyun-Ee
Park Se-Jin
Abstract
Purpose: To investigate the clinicopathologic effects of cyclosporine A (CsA) in children with diseases characterized by mesangial immunoglobulin A deposits such as immunoglobulin A nephropathy (IgAN) and Henoch-SchOnlein purpura nephritis (HSPN).

Methods: We retrospectively reviewed the clinicopathologic outcomes of 54 children (IgAN, 36; HSPN, 18) treated with CsA. The starting dose of CsA was 5 mg/kg per day, and it was administered in 2 divided doses. The degree of proteinuria and pathologic changes in renal biopsies were evaluated before and after CsA treatment.

Results: The mean protein to creatinine ratio decreased from 3.7¡¾1.5 to 0.6¡¾0.4 (P <0.001), and 32 (59.2%) children achieved complete remission of proteinuria after 1-year CsA treatment. Among the 54 children, 24 maintained normal renal function and 25 exhibited microscopic hematuria or proteinuria at the end of CsA treatment. In the HSPN group, 3 children whose initial biopsies indicated class IIIb disease showed class II disease on follow-up, and the follow-up biopsies of 2 children who had class II disease indicated the same class II disease. In the IgAN group, cortical tubular atrophy occurred in 1 child, and no child with IgAN had cortical interstitial fibrosis or tubular atrophy after 1-year CsA treatment. No significant complications were found in the children treated with CsA.

Conclusion: Our findings indicate that CsA treatment is effective and beneficial in reducing massive proteinuria and preventing progression to end-stage renal failure in children with glomerular diseases characterized by IgA deposits, such as IgAN and HSPN, within 1 year of treatment.
KEYWORD
IgA deposit, IgA nephropathy, Henoch-SchOnlein purpura nephritis, cyclosporine A
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