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The Impact of MYH9 Polymorphic Variant rs5756168 on Kidney Allograft Function

J. Pazik,1 M. Oldak,2 Z. Lewandowski,3 D. Ozieblo,4 K. Michalska,5 E. Sitarek,1 A. Sadowska,1 M. Nowaczyk,5 T. Grochowiecki,6 J. Malejczyk,4 M. Durlik.1

1Department of Nephrology and Transplantation Medicine, Medical University of Warsaw, Warsaw, Poland
2Institute of Physiology and Pathology of Hearing, Warsaw, Poland
3Department of Epidemiology, Medical University of Warsaw, Warsaw, Poland
4Department of Histology and Embryology, Medical University of Warsaw, Warsaw, Poland
5Department of Clinical Immunology, Medical University of Warsaw, Warsaw, Poland
6General, Vascular and Transplant Surgery, Medical University of Warsaw, Warsaw, Poland.

Meeting: 2015 American Transplant Congress

Abstract number: B98

Keywords: Gene polymorphism, Graft function, Kidney transplantation, Proteinuria

Session Information

Session Name: Poster Session B: Kidney Complications: Late Graft Failure

Session Type: Poster Session

Date: Sunday, May 3, 2015

Session Time: 5:30pm-6:30pm

 Presentation Time: 5:30pm-6:30pm

Location: Exhibit Hall E

The MYH9 gene was identified as a susceptibility locus associated with diminished filtration rate in the course of chronic nephropathies: primary focal segmental glomerulosclerosis (FSGS), lupus nephritis, IgA nephropathy. Nevertheless, there is no data regarding its impact on the kidney allograft function.

In the prospective cohort study performed in 296 deceased donor kidney recipients (transplantation between 2007 and 2012) eight SNPs previously shown to be associated with kidneys function (rs4821480, rs4821481, rs2032487, rs3752462, rs11089788, rs5756168, and rs2239784) were genotyped.

Minor allelic variant of rs5756168 (NC_000022.11:g.36378767T>C) was associated with increased incidence of FSGS as a primary disease: 9.5% (4/42) in allele C carriers and 2.5% (7/248) in TT homozygotes (p<0.058), as well as excessive risk of delayed graft function (p<0.010).

Kidneys from donors with TT genotype were prone to moderately diminished but stable eGFR (p<0.012) with excessive risk for proteinuria since sixth post-transplant months (OR 1.91 95%CI: 1.00-3.64; p<0.050). Recipients carrying two T alleles experienced higher eGFR starting from the sixth post-transplant month (p<0.038) and their risk of proteinuria was halved until third (p<0.010) and after sixth (p<0.044) post-transplant months.

There was a complex interplay between donor and recipient rs5756168 genotypes that resulted in eGFR stratification. Allele C carriers, who received a kidney transplant also carrying an allele C experienced significantly diminished filtration rate which persisted over 4 years of observation (p<0.008). Genotyping for MYH9 may be useful in identifying patients and organs of excessive risk for graft dysfunction.

The study was supported by grant from the National Science Centre N N402 5668 40.

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To cite this abstract in AMA style:

Pazik J, Oldak M, Lewandowski Z, Ozieblo D, Michalska K, Sitarek E, Sadowska A, Nowaczyk M, Grochowiecki T, Malejczyk J, Durlik M. The Impact of MYH9 Polymorphic Variant rs5756168 on Kidney Allograft Function [abstract]. Am J Transplant. 2015; 15 (suppl 3). https://atcmeetingabstracts.com/abstract/the-impact-of-myh9-polymorphic-variant-rs5756168-on-kidney-allograft-function/. Accessed May 31, 2025.

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