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Introduction: Post-transplant anaemia (PTA) is a common phenomenon. The cause of PTA is multi-factorial. ACE inhibitors can contribute to PTA and their use to alleviate post transplant erythrocytosis is a well-recognised management option. However the response can be variable and the mechanism is poorly understood The angiotensin II type 1 receptor (AT1R) has an important role in determining serum erythropoietin levels. The AT1R has a single base substitution of the adenine to cytosine at position 1166 of the 3' untranslated region (A1166C). The C-allele of this single nucleotide polymorphism (SNP) has been associated with increased activity of the renin-angiotensin system (RAS) with augmented angiotensin II activity. The angiotensin converting enzyme insertion/deletion (ACE I/D) polymorphism is a 287 base pair insertion of the ACE gene. The D-allele is associated with higher serum ACE concentration. The aim of this study was to investigate associations between kidney transplant recipient AT1R A1166C and ACE I/D genotype and PTA 6 months post transplantation. We hypothesised that the presence of an AT1R C-allele and/or ACE D-allele would be associated with a reduced prevalence of PTA. Methods: This is a retrospective study. Recipients (n=163) were genotyped for the AT1R A1166C and ACE I/D polymorphisms. All recipients were older than 18 years and had a functioning graft for more than 90 days. Anaemia was defi ned using the World Health Organisation criteria as a serum haemoglobin concentration <130 g/L in men and <120g/L in women. For statistical analyses AT1R AC and CC genotypes were combined, and ACE ID and DD genotypes were combined. Results: The gene frequency of the AT1R A1166C polymorphism was 53% AA, 40% AC and 7% CC. and the frequency of the ACE I/D polymorphism was 20% II, 45% ID and 35% DD. As expected, haemoglobin concentration 6-months post-transplant was signifi cantly associated with gender, with males having a higher concentration (133g/L versus 122g/L, p<0.001). In a univariate model adjusted for gender and use of ACE inhibitors or angiotensin receptor blockers, there was no signifi cant association between haemoglobin concentration and AT1R or ACE genotype (AT1R C-allele p=0.72, ACE D-allele p=0.82). Furthermore, there was no synergistic interaction between AT1R and ACE genotypes on haemoglobin concentration after adjustment for gender, ACE inhibitor and angiotensin receptor blocker treatment and genotype main effects. In anaemic recipients, the frequency of the AT1R C-allele or ACE D-allele did not differ from non-anaemic recipients (p=0.90 and p=0.70 respectively). Conclusions: In this cohort of graft recipients, the AT1R A1166C and ACE I/D genotypes were not associated with early post transplant haemoglobin or the presence of anaemia.

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