Rs10887800 renalase gene polymorphism is associated with an increased risk of coronary artery disease in hemodialyzed patients

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Abstract

Purpose

Coronary artery disease (CAD) is common in patients with end-stage renal disease (ESRD). Recent studies have suggested that renalase, a novel FAD-dependent amine oxidase, may play an important role in the pathogenesis of cardiovascular complications in ESRD patients. The aim of the study was to investigate the association between renalase gene polymorphisms and a risk of CAD in patients on hemodialysis.

Methods

In a case–control study, a total of 309 hemodialyzed patients (107 with and 202 without CAD) were genotyped for two SNPs in the renalase gene (rs10887800 and rs2576178) using the PCR–RFLP method.

Results

By multivariate logistic regression analysis, we found that rs10887800GG genotype was associated with an increased risk of CAD under the codominant model [GG vs AA; adjusted OR 2.66 (95 % CI, 1.19–5.94), p = .017] and under the recessive model [GG vs AG + AA; adjusted OR 2.10 (95 % CI, 1.10–4.02), p = .025]. The rs2576178 polymorphism did not influence the risk of CAD.

Conclusion

The study suggested for the first time that the rs10887800 renalase gene polymorphism may be involved in the pathogenesis of CAD in hemodialyzed patients and thus could be considered a new genetic risk factor for CAD in this population.

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Most cited references 22

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Renalase is a novel, soluble monoamine oxidase that regulates cardiac function and blood pressure.

Guoyong Li, Susan P. Crowley, Gary V. Desir … (2005)

The kidney not only regulates fluid and electrolyte balance but also functions as an endocrine organ. For instance, it is the major source of circulating erythropoietin and renin. Despite currently available therapies, there is a marked increase in cardiovascular morbidity and mortality among patients suffering from end-stage renal disease. We hypothesized that the current understanding of the endocrine function of the kidney was incomplete and that the organ might secrete additional proteins with important biological roles. Here we report the identification of a novel flavin adenine dinucleotide-dependent amine oxidase (renalase) that is secreted into the blood by the kidney and metabolizes catecholamines in vitro (renalase metabolizes dopamine most efficiently, followed by epinephrine, and then norepinephrine). In humans, renalase gene expression is highest in the kidney but is also detectable in the heart, skeletal muscle, and the small intestine. The plasma concentration of renalase is markedly reduced in patients with end-stage renal disease, as compared with healthy subjects. Renalase infusion in rats caused a decrease in cardiac contractility, heart rate, and blood pressure and prevented a compensatory increase in peripheral vascular tone. These results identify renalase as what we believe to be a novel amine oxidase that is secreted by the kidney, circulates in blood, and modulates cardiac function and systemic blood pressure.

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Cardiovascular mortality in end-stage renal disease.

Allan J Collins (2003)

Cardiovascular disease accounts for more than 50% of end-stage renal disease (ESRD) deaths. The reported cardiovascular death rates in patients receiving dialysis are substantially higher than in the general population. Cardiovascular mortality in ESRD is particularly high after acute myocardial infarction, but it is also elevated in ESRD patients with other forms of atherosclerotic vascular disease (eg, chronic coronary artery disease, strokes, transient ischemic attacks, and peripheral arterial disease). Left ventricular hypertrophy and dilation are associated with increased cardiovascular mortality, as is congestive heart failure. One of the major reasons for such high cardiovascular mortality in ESRD is the large burden of cardiovascular disease present in patients with chronic artery disease before renal replacement therapy. These observations mandate not only aggressive diagnosis and treatment of cardiovascular disease in patients with ESRD, but also active screening, diagnosis, and treatment in those with chronic kidney disease before renal replacement therapy.

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Renalase deficiency aggravates ischemic myocardial damage.

Guoyong Li, Gary V. Desir, Manuel Pestana … (2011)

Chronic kidney disease (CKD) leads to an 18-fold increase in cardiovascular complications not fully explained by traditional risk factors. Levels of renalase, a recently discovered oxidase that metabolizes catecholamines, are decreased in CKD. Here we show that renalase deficiency in a mouse knockout model causes increased plasma catecholamine levels and hypertension. Plasma blood urea nitrogen, creatinine, and aldosterone were unaffected. However, knockout mice had normal systolic function and mild ventricular hypertrophy but tolerated cardiac ischemia poorly and developed myocardial necrosis threefold more severe than that found in wild-type mice. Treatment with recombinant renalase completely rescued the cardiac phenotype. To gain insight into the mechanisms mediating this cardioprotective effect, we tested if gene deletion affected nitrate and glutathione metabolism, but found no differences between hearts of knockout and wild-type mice. The ratio of oxidized (NAD) to reduced (NADH) nicotinamide adenine dinucleotide in cardiac tissue, however, was significantly decreased in the hearts of renalase knockout mice, as was plasma NADH oxidase activity. In vitro studies confirmed that renalase metabolizes NADH and catecholamines. Thus, renalase plays an important role in cardiovascular pathology and its replacement may reduce cardiac complications in renalase-deficient states such as CKD. © 2011 International Society of Nephrology

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Author and article information

Contributors

Anna Stec: +48 (81) 724 47 04 , annastec@poczta.onet.pl

Journal

Journal ID (nlm-ta): Int Urol Nephrol

Journal ID (iso-abbrev): Int Urol Nephrol

Title: International Urology and Nephrology

Publisher: Springer Netherlands (Dordrecht )

ISSN (Print): 0301-1623

ISSN (Electronic): 1573-2584

Publication date (Electronic): 29 March 2016

Publication date PMC-release: 29 March 2016

Publication date (Print): 2016

Volume: 48

Pages: 871-876

Affiliations

Department of Nephrology, Medical University of Lublin, Jaczewskiego Street 8, 20954 Lublin, Poland

Article

Publisher ID: 1270

DOI: 10.1007/s11255-016-1270-7

PMC ID: 4894921

PubMed ID: 27023477

SO-VID: 00493a9a-b64e-4cb6-aa79-246308bfde1d

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

History

Date received : 17 December 2015

Date accepted : 13 March 2016

Funding

Funded by: Medical University of Lublin, Poland

Award ID: DS383

Award Recipient : Andrzej Ksiazek

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ScienceOpen disciplines: Nephrology

Keywords: renalase gene,end-stage renal disease,hemodialysis,coronary artery disease

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ScienceOpen disciplines: Nephrology

Keywords: renalase gene, end-stage renal disease, hemodialysis, coronary artery disease

Rs10887800 renalase gene polymorphism is associated with an increased risk of coronary artery disease in hemodialyzed patients

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Karger: Cardiovascular System

Most cited references 22

Renalase is a novel, soluble monoamine oxidase that regulates cardiac function and blood pressure.

Cardiovascular mortality in end-stage renal disease.

Renalase deficiency aggravates ischemic myocardial damage.

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