PMID- 31571739 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20201001 IS - 0971-4065 (Print) IS - 1998-3662 (Electronic) IS - 0971-4065 (Linking) VI - 29 IP - 5 DP - 2019 Sep-Oct TI - Impact of Angiotensin-converting Enzyme and Matrix Metalloproteinase-3 Gene Polymorphisms on Risk for Developing Vascular Access Failure in Hemodialysis Patients - A Pilot Study. PG - 329-333 LID - 10.4103/ijn.IJN_303_18 [doi] AB - For adequate hemodialysis, functional vascular access is obligatory. Neointimal hyperplasia (NIH) has a central role in stenosis and thrombosis development, which represent the most frequent causes of vascular access failure. Polymorphism of different genes that have a significant role in endothelial function may have an impact on NIH development. Therefore, the aim of our study is to determine the effect of angiotensin-converting enzyme (ACE) I/D and matrix metalloproteinase-3 (MMP3) 5A/6A polymorphism on risk for developing vascular access failure in hemodialysis patients. The study included 200 patients on regular hemodialysis at Nephrology Department, University Medical Center Zvezdara. Retrospective analysis included a collection of general and vascular access data from medical records. Genetic analysis was performed by using polymerase chain reaction-restriction fragment length polymorphism method (PCR-RFLP). Patients were divided into two groups: Group 1-patients who have never experienced vascular access failure and Group 2-patients who have at least one spontaneous vascular access failure. There was no difference in age, gender, hemodialysis vintage, main diagnosis, presence of hypertension, and diabetes mellitus between the two groups. There were no statistically significant differences in the frequencies of ACE and MMP3 genotypes between the two groups. Without statistical significance, it was found that homozygotes for I allele had two times higher risk for developing vascular access failure than homozygotes for D allele (OR 2.00; 95%CI: 0.727-5.503; P = 0.180). In addition, patients with 5A allele have 1.7 times higher risk for developing vascular access failure compared with patients without this allele (OR 1.745; 95% CI: 0.868-3.507; P = 0.118). Patients with vascular access failure do not have different genotype distribution regarding ACE gene and MMP3 gene polymorphism as compared with patients without vascular access failure. Still, homozygotes for I allele and homozygotes for 5A allele have higher risk for developing vascular access failure compared with other patients. CI - Copyright: (c) 2019 Indian Journal of Nephrology. FAU - Jankovic, Aleksandar AU - Jankovic A AD - Department of Nephrology with Dialysis, University Medical Center Zvezdara, Belgrade, Serbia. FAU - Tosic, Jelena AU - Tosic J AD - Department of Nephrology with Dialysis, University Medical Center Zvezdara, Belgrade, Serbia. FAU - Buzadzic, Ivana AU - Buzadzic I AD - Department of Human Genetics and Prenatal Diagnostics, University Medical Center Zvezdara, Belgrade, Serbia. FAU - Djuric, Petar AU - Djuric P AD - Department of Nephrology with Dialysis, University Medical Center Zvezdara, Belgrade, Serbia. FAU - Bulatovic, Ana AU - Bulatovic A AD - Department of Nephrology with Dialysis, University Medical Center Zvezdara, Belgrade, Serbia. FAU - Markovic, Dragana AU - Markovic D AD - Department of Nephrology with Dialysis, University Medical Center Zvezdara, Belgrade, Serbia. FAU - Popovic, Jovan AU - Popovic J AD - Department of Nephrology with Dialysis, University Medical Center Zvezdara, Belgrade, Serbia. FAU - Dimkovic, Nada AU - Dimkovic N AD - Department of Nephrology with Dialysis, University Medical Center Zvezdara, Belgrade, Serbia. AD - Department of Medical Faculty, University of Belgrade, Belgrade, Serbia. LA - eng PT - Journal Article PL - India TA - Indian J Nephrol JT - Indian journal of nephrology JID - 8914356 PMC - PMC6755919 OTO - NOTNLM OT - Angiotensin-converting enzyme gene polymorphism OT - failure OT - matrix metalloproteinase-3 gene polymorphism OT - vascular access COIS- There are no conflicts of interest. EDAT- 2019/10/02 06:00 MHDA- 2019/10/02 06:01 PMCR- 2019/09/01 CRDT- 2019/10/02 06:00 PHST- 2019/10/02 06:00 [entrez] PHST- 2019/10/02 06:00 [pubmed] PHST- 2019/10/02 06:01 [medline] PHST- 2019/09/01 00:00 [pmc-release] AID - IJN-29-329 [pii] AID - 10.4103/ijn.IJN_303_18 [doi] PST - ppublish SO - Indian J Nephrol. 2019 Sep-Oct;29(5):329-333. doi: 10.4103/ijn.IJN_303_18.