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J Korean Soc Pediatr Nephrol. 2013 Oct;17(2):92-100. English. Original Article.
Lee JJ , Kim YJ , Shin JI , Yim H , Park SJ .
Department of Pediatrics, Ajou University Hospital, Ajou Universtiy School of Medicine, Suwon, Korea. fli018@hanmail.net
Department of Pathology, Yeungnam University College of Medicine, Daegu, Korea.
Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Korea.
Department of Pathology, Ajou University Hospital, Ajou Universtiy School of Medicine, Suwon, Korea.
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.

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