Complement plays a central role in organ ischemia/reperfusion injury (IRI) and allograft rejection. A retrospective observational study included a cohort of 73 non-diabetic deceased donor kidney allograft recipients. We collected data on donor and recipient demographic, clinical and laboratory parameters. The main outcomes of our study were delayed graft function (DGF) and kidney allograft function during five years posttransplant. Gene single nucleotide polymorphisms (SNPs) for complement components C3 (rs2230199, G_C) and FH (rs800292, G_A) were determined. The genotyping results for FH polymorphism (184G >
A) showed a distribution of GG (71.2%) and GA (28.8%) genotypes, with the AA genotype not detected in the cohort. The genotype frequencies of the C3 polymorphism (304 C >
G) were CC (71.2%), CG (26.0%) and GG (2.8%).Analysis of FH SNP demonstrated that patients with the GG genotype had a statistically higher frequency of DGF compared to those with the GA genotype (67.3% vs. 38.1%, p = 0.022). Univariate linear regression analysis confirmed that the FH GG genotype was the only significant determinant of DGF (p = 0.025). Analysis of C3 SNP showed that patients with the GC/GG genotype demonstrated significantly lower levels of creatinine clearance compared to those with the CC genotype at 1 year (p = 0.002), 3 years (p = 0.001) and 5 years (p = 0.010) posttransplant. These findings underscore the importance of genetic factors in influencing renal outcomes post-transplant.