Clinicopathologic Changes in Children with Immunoglobulin A Nephritis and Henoch-Schonlein Purpura Nephritis after Cyclosporine A and Angiotensin-converting Enzyme Inhibitor Treatment.
- Author:
Jeong Ju LEE
1
;
Yong Jin KIM
;
Jae Il SHIN
;
Hyunee YIM
;
Se Jin PARK
Author Information
1. Department of Pediatrics, Ajou University Hospital, Ajou Universtiy School of Medicine, Suwon, Korea. fli018@hanmail.net
- Publication Type:Original Article
- Keywords:
IgA deposit;
IgA nephropathy;
Henoch-Schonlein purpura nephritis;
cyclosporine A
- MeSH:
Atrophy;
Biopsy;
Child*;
Creatinine;
Cyclosporine*;
Fibrosis;
Follow-Up Studies;
Glomerulonephritis, IGA;
Hematuria;
Humans;
Immunoglobulin A*;
Immunoglobulins*;
Kidney Failure, Chronic;
Nephritis*;
Proteinuria;
Purpura, Schoenlein-Henoch*;
Retrospective Studies
- From:Journal of the Korean Society of Pediatric Nephrology
2013;17(2):92-100
- CountryRepublic of Korea
- Language:English
-
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+/-1.5 to 0.6+/-0.4 (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.
