Angiotensin-converting enzyme gene polymorphism significantly affects renal posttransplantation erythrocytosis

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.