Background: Post-transplant erythrocytosis (PTE) is estimated at 5-20%. Angiotensin II generated by angiotensin I-converting enzyme (ACE) stimulates erythropoiesis. The highest activity of ACE is observed in DD genotype. The question arises if ACE gene polymorphism influences PTE.
Methods: One-year prospective study included 89 kidney recipients (28 women and 61 men).
Results: Thirty-four (38%) recipients proved to be DD genotype, 36 (40%) ID, and 19 (22%) II genotype. Absolute PTE [hematocrit level (HCT) >50% and RBC > 5.5 mln/mm(3)] was found in 14 (19%) patients. PTE developed 6-12 months after kidney Tx. There were no significant differences in genotype distribution between patients with and without PTE. ANOVA showed that the most significant predictor of PTE development was the time since kidney Tx (p < 0.0001). Analysis of logistic regression showed that male sex was the most important factor in PTE development 12 months after kidney Tx (OR = 13.6: 95% CI 1.2-150.9, p < 0.05). D allele increased the PTE risk (OR = 3.3 for each allele: 95% CI 1.1-10.4, p < 0.05), the use of angiotensin-converting enzyme inhibitors (ACEI) decreased the PTE risk (OR = 0.15: 95% CI 0.03-0.85, p < 0.05). In patients with DD genotype, there was a correlation between hemoglobin, RBC and HCT concentration, 12 months after Tx and panel of reactive antibody value before Tx (Rs = +0.43, p < 0.05).
Conclusions: Male sex and D allele presence increase the risk of PTE development, especially in highly immunized patients. The use of ACEI decreases the risk of PTE development.