title: Angiotensin converting enzyme gene polymorphism and development of post-transplant erythrocytosis.
abstract: BACKGROUND
  An increased activation of the renin-angiotensin system probably plays a major role in the development of post-transplant erythrocytosis (PTE). It is known that deletion type polymorphism (DD) in the angiotensin converting enzyme (ACE) gene is associated with higher circulating angiotensin II (AII) levels. The aim of this study was to investigate the effect of ACE gene polymorphism on development of PTE.
  
  
  METHODS
  86 PTE patients (male/female: 68/18, mean age: 32 +/- 10 years) and 68 consecutively transplanted non- PTE patients (male/female: 38/30, mean age: 31 +/- 10 years) were included; 140 patients (91%) had been transplanted from living donors; 92 patients (60%) had hypertension. ACE gene polymorphism was determined by polymerase chain reaction (PCR).
  
  
  RESULTS
  The mean time to appearance of PTE was 8.8 +/- 7.9 (range of 1-53) months. DD genotype was detected in 65 patients. PTE patients had a higher prevalence of hypertension (70% vs. 46%, p=0.003) and a lower frequency of DD genotype (34% vs. 54%, p=0.014) as compared to non-PTE patients [OR: 2.2 (1.14-4.25, 95% CI)]. PTE developed more frequently in male patients (68/106: 64%) than females (18/48: 38%) (p=0.002). Patients with DD genotype had a significantly longer leading time to PTE in Kaplan-Meier survival analysis with log-rank (136 +/- 15 vs. 92 +/- 13 months, p=0.015). In Cox regression analysis, hypertension (p=0.002) and recipient ACE genotype (p=0.013) were retained as independent variables for predicting PTE development.
  
  
  CONCLUSIONS
  PTE develops more frequently in male, hypertensive renal transplant recipients with good allograft function. DD-type ACE gene polymorphism seems to protect against PTE development.
authors.affiliation: Department of Internal Medicine, Istanbul School of Medicine, Istanbul University, Turkey. alaattiny@hotmail.com
authors.forename: Alaattin
authors.initials: A
authors.lastname: Yildiz
authors.forename: Halil
authors.initials: H
authors.lastname: Yazici
authors.forename: Naci
authors.initials: N
authors.lastname: Cine
authors.forename: Rumeyza
authors.initials: R
authors.lastname: Kazancioglu
authors.forename: Vakur
authors.initials: V
authors.lastname: Akkaya
authors.forename: Mehmet Sükrü
authors.initials: MS
authors.lastname: Sever
authors.forename: Ergin
authors.initials: E
authors.lastname: Ark
authors.forename: Nihan
authors.initials: N
authors.lastname: Erginel-Unaltuna
mesh_terms: D000328:Adult; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000150:complications; D015994:Incidence; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011086:Polycythemia / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D011110:Polymorphism, Genetic; D017678:Sex Distribution; D016019:Survival Analysis
chemical_list: D007703:Peptidyl-Dipeptidase A