Key result
ACE DD genotype linked to ~37% lower risk and delayed onset of post-transplant erythrocytosis.
Why the study?
Renin-angiotensin system activation may drive post-transplant erythrocytosis, and the ACE gene DD polymorphism yields higher angiotensin II levels, prompting investigation into whether ACE gene polymorphism affects development of post-transplant erythrocytosis.
Does the DD genotype of the ACE gene protect against the development of post-transplant erythrocytosis in renal transplant recipients?
Does the DD genotype of the ACE gene protect against the development of post-transplant erythrocytosis in renal transplant recipients?
The DD-type ACE gene polymorphism appears to be protective against the development of post-transplant erythrocytosis in renal transplant recipients.
May support DD genotype as protective against post-transplant erythrocytosis; hypothesis-generating and requires prospective validation before clinical use.
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 hada 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. Conclusion: 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.
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Yildiz et al. (2003) studied this question. DD genotype of ACE gene is associated with a lower risk of post-transplant erythrocytosis (34% vs. 54%, p=0.014) and delayed onset (136 vs. 92 months, p=0.015).
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