title: Angiotensin-converting enzyme gene polymorphism significantly affects renal posttransplantation erythrocytosis.
abstract: Posttransplantation erythrocytosis (PE) is a frequent problem in renal transplant patients. The pathogenesis and mechanisms of both the problem and therapy strategy are unknown. Since ACE and angiotensin 2 receptor inhibitors have been used to successfully manage PE, we speculated a relation between gene polymorphisms and this complication. Ninety-six ( 30 women, 66 men, age 34.4 +/- 11.0 years) renal transplant patients evaluated retrospectively, for gene polymorphisms of ACE, angiotensinogen, angiotensin 1 and 2 receptors (ATR1 and ATR2), as well as endothelial nitric oxide synthase (ecNOS). They were divided into two groups; patients with versus without PE, which was defined as >15 g/dL hemoglobin levels during the first year after renal transplantation. PE was found to be significantly more prevalent among D/D than I/I gene polymorphism of ACE genes (P <.04). The distribution of D/D, I/D, and I/I polymorphisms were 39.1%, 45.9%, and 7.6%, respectively. There was no difference between D/D and I/D polymorphisms. Comparing the I/D and I/I polymorphisms showed PE to be statistically more prevalent in the I/D polymorphism (P <.01). Logistic regression analysis revealed that D/D and I/D polymorphisms were significant risk factors for PE (P <.05, RR = 7.714 and P <.03, RR = 10.199, respectively). While previous studies revealed a relation between angiotensin II and PE, our study discovered the contribution of ACE gene polymorphism.
authors.affiliation: Department of Nephrology, Başkent University School of Medicine, Ankara, Turkey.
authors.forename: H
authors.initials: H
authors.lastname: Micozkadioğlu
authors.forename: T
authors.initials: T
authors.lastname: Colak
authors.forename: A
authors.initials: A
authors.lastname: Akçay
authors.forename: S
authors.initials: S
authors.lastname: Sezer
authors.forename: F B
authors.initials: FB
authors.lastname: Ataç
authors.forename: H
authors.initials: H
authors.lastname: Verdi
authors.forename: Z
authors.initials: Z
authors.lastname: Arat
authors.forename: F N
authors.initials: FN
authors.lastname: Ozemir
authors.forename: M
authors.initials: M
authors.lastname: Haberal
mesh_terms: D000328:Adult; D005260:Female; D005787:Gene Frequency; D006801:Humans; D016030:Kidney Transplantation / Q000502:physiology*; D008297:Male; D019001:Nitric Oxide Synthase / Q000235:genetics; D052250:Nitric Oxide Synthase Type III; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011086:Polycythemia / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D011183:Postoperative Complications / Q000097:blood; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics; D012189:Retrospective Studies
chemical_list: D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D007703:Peptidyl-Dipeptidase A