OBJECTIVE: Arachidonic acid metabolism by cytochrome P450 (CYP) epoxygenases 
leads to epoxyeicosatrienoic acids (EETs), which are eicosanoids with 
vasodilator and anti-inflammatory properties. We aim to determine whether 
genetic variability in these routes may contribute to cardiovascular (CV) risk 
in renal transplant recipients.
METHODS: In a cohort of 355 patients, we determined the presence of two 
polymorphisms, CYP2C8*3 and CYP2J2*7, known to affect eicosanoid levels. 
Associations with CV mortality, CV event-free long-term survival and graft 
survival were retrospectively investigated by logistic regression models.
RESULTS: CYP2J2*7 showed a statistical trend towards higher CV mortality 
(p = .06) and lower cardiac or cerebral event-free long-term survival (p = .05), 
whilst CYP2C8*3 displayed a significant inverse association with the risk of CV 
event (hazard ratio [HR] = 0.34 [0.15-0.78], p = .01). The association of 
CYP2J2*7 with CV mortality became significant when the analysis was restrained 
to 316 patients without a history of CV events prior to transplantation 
(HR = 15.72 [2.83-91.94], p = .005). In this subgroup of patients both single 
nucleotide polymorphisms (SNPs) were significantly associated with event-free 
survival. HR values were 5.44 (1.60-18.51), p = .007 and 0.26 (0.09-0.75), 
p = .012 for CYP2J2*7 and CYP2C8*3, respectively.
CONCLUSIONS: Our results show, for the first time to our knowledge, that two 
SNPs in CYP2C8 and CYP2J2, which synthesize EETs, may modify CV outcomes in 
renal transplant recipients, a population that is already at a high risk of 
suffering these events.