Mutational Analysis of Mitochondria DNA in Children with IgA Nephropathy.
- Author:
Tae Min EOM
1
;
Chang Han JANG
;
Hyoung Kyu KIM
;
Nari KIM
;
Yun Seo CHUNG
;
Jin HAN
;
Woo Yeong CHUNG
Author Information
1. Department of Pediatrics, Busan Paik Hospital, Inje University, Busan, Korea. chungwy@chol.com
- Publication Type:Original Article
- Keywords:
IgA nephropathy;
Proteinuria;
Mitochondria DNA;
Deletions;
Children
- MeSH:
Biopsy;
Blood Platelets;
Child;
Cholesterol;
Coat Protein Complex I;
DNA;
DNA, Mitochondrial;
Follow-Up Studies;
Glomerulonephritis, IGA;
Humans;
Immunoglobulin A;
Kidney Failure, Chronic;
Mitochondria;
Nephrotic Syndrome;
Polymerase Chain Reaction;
Proteinuria;
Reference Values;
Serum Albumin
- From:Journal of the Korean Society of Pediatric Nephrology
2012;16(2):73-79
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The association of mitochondrial DNA (mtDNA) mutations, deletions and copy number with progressive changes in patients with some glomerular disease and end-stage renal disease have been reported. In this study, we performed mtDNA mutation analysis in children with IgA nephropathy to investigate its role in progressive clinical course. METHODS: Seven children with IgA nephropathy were involved in this study. MtDNA isolated from platelet was amplified by PCR and sequenced entirely. RESULTS: The mean age at renal biopsy was 11.5+/-2.2 year and the mean age at latest evaluation was 17.9+/-3.2 year. The mean follow-up period were 7.8+/-3.1 years. Patients was divided into 2 groups according to the amount of proteinuria at presenting manifestation. Group 2 patients were nephrotic syndrome. Renal function reveals within normal range in all patients. In group 2 patients, the mean serum albumin level was significantly lower than those of group 1 (3.7+/-0.6 g/dL vs. 4.7+/-0.2 g/dL, P=0.0241) and the mean total cholesterol level was significantly higher than those of group 1 (222.7+/-35.7 mg/dL vs. 148.3+/-29.1 mg/dL, P=0.0283). In Group 2 patients, total amount of protein of 24 hour collected urine also significantly higher than those of group 1 (1,466.0+/-742.5 mg vs. 122.5+/-48.1 mg, P=0.0135). Pr/Cr ratio in random urine sample was also higher in group 2 than those of group 1 but the statistical significance was not noted (1.8+/-1.6 vs. 0.2+/-0.2, P=0.0961). Deletion of mtDNA nt 8272-8281 were observed in two patients, one patient in each groups, respectively. This is non-coding lesion. No patients demonstrated the mtDNA mutations. CONCLUSIONS: We have identified a deletion of mtDNA nt 8272-8281 in two children with IgA nephropathy. Further studies are needed to clarify the role of mitochondrial function in the progressive change of IgA nephropathy.
