Date: Sunday, May 3, 2015
Session Time: 5:30pm-6:30pm
Presentation Time: 5:30pm-6:30pm
Location: Exhibit Hall E
MYH9 encoding a non-muscle myosin heavy chain IIA is expressed in podocytes, mesangial, tubular, capillary endothelial cells and vascular wall. Intronic variants of MYH9 associate with a variety of kidney diseases and diminished glomerular filtration rate. Histologic features include segmental/global glomerular sclerosis, mesangial proliferation and tubulointerstitial injury.
This study aims to evaluate the associations between MYH9 risk alleles and chronic transplanted kidney abnormalities graded according to Banff'07criteria. Genotyping for MYH9 SNPs associated with native kidneys function (rs4821480, rs4821481, rs2032487, rs3752462, rs11089788, rs5756168, and rs2239784) was performed in recipients (n=296) and their deceased donors (n= 222). Patients with at least one transplant biopsy, after obtaining graft function were included in the study (n=184). Transplantation took place in 2007-2012. The study endpoint was the occurrence of chronic graft lesions in follow-up period, with a median observation time of 3.6 yrs (range 0.33- 7.4). Of kidneys carrying allele C 43% presented with at least grade I chronic interstitial (ci) and chronic tubular (ct) lesions in opposition to 68% of TT homozygotes (p<0.012). Diminished incidence of ct/ci in rs 5756168 C kidneys was confirmed in donors below 60 years of age (p<0.008). In recipients carrying allele T of rs3752462 vs CC diminished risk of chronic vascular (cv) lesions (61% vs 79%, p<0.010) was found. No associations were found between chronic glomerular (cg) lesions and arteriolar hyalinosis (ah) and analyzed SNPs. Since chronic lesions present in sites typical for non-muscle myosin heavy chain II A expression and they coincide with MYH9 SNPs shown to increase chronic kidney disease risk, they may be of relevance for renal allograft functioning. These results corroborate with our other study, showing the impact of rs5756168 donor and recipient matching on transplanted kidney function.
The study was supported by grant from the National Science Center N N402 5668 40.
To cite this abstract in AMA style:Pazik J, Oldak M, Lewandowski Z, Ozieblo D, Michalska K, Ptasińska APerkowska, Sadowska A, Nowaczyk M, Malejczyk J, Durlik M. MYH9 Polymorphic Variants and Chronic Lesions in Transplanted Kidney Biopsy [abstract]. Am J Transplant. 2015; 15 (suppl 3). https://atcmeetingabstracts.com/abstract/myh9-polymorphic-variants-and-chronic-lesions-in-transplanted-kidney-biopsy/. Accessed April 15, 2021.
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