P1676LONG TERM RENAL FUNCTIONS IN LIVING KIDNEY DONORS AND ITS RELATIONSHIP WITH TRANSFORMING GROWTH FACTOR ßETA-1GENE POLYMORPISMS

Abstract

Abstract Background and Aims Renal transplantation is the optimal treatment choice for most patients with end-stage renal disease. Despite the efforts to increase cadaveric transplantation, the primary source of kidneys is still living donors. Donating a kidney is associated with lower than expected GFR especially in the presence of hypertension and proteinuria. Increased risk of ESRD and cardiovascular disease are small and controversial. TGF-β1 is an essential regulator of fibroblast phenotype and function, hence the main driver in most healthy/pathogenic fibrotic processes. TGF-β1 overexpression has been accused of poor results in chronic nephropathies. Single nucleotide polymorphisms (SNP) in the TGF-β1 gene may accelerate chronic allograft nephropathy and chronic kidney disease progression. In this study, we aimed to assess two TGF-β1 polymorphisms’ effect on long term renal function in kidney donors. Method This cross-sectional, single-center study was conducted in a tertiary referral center. Seventy-two living kidney donors who had donated between January 1999 and May 2018 were included in the study. The age, body mass index, and sex-matched control group consisted of 100 volunteers without systemic disease. GFR was calculated with CKD-EPI formula. Renal functions were compared between donors and controls. TGF-β1 gene polymorphism status of donors was evaluated with RT-PCR. Namely, +869T/C at codon 10 (rs1800470) and +915G/C at codon 25 (rs1800471) abbreviated as codon 10 SNP and 25 SNP respectively. TGF-β1 gene polymorphism effect on renal functions was assessed with a proper statistical approach. Results The study included 72 (53 female, 19 male) kidney donors, and 100 (69 female, 31 male) healthy controls. The mean age of the donor group was 50 ± 12 years, and the mean age of the control group was 47 ± 11 years.The mean creatinine levels of donors were significantly higher than the mean creatinine levels of the control group (0.96±0.2 vs. 0.72±0.2 mg/dL p <0.001). The mean GFR values of donors were markedly lower than the GFR values of the control group (76±20 vs. 107±22 mL/min). Regarding codon 10 SNP status, 34/18/20 donors had C/C, T/C, and T/T phenotypes. The preoperative and final GFR were similar between all groups. Regarding codon 25 SNP status, 61/6/5 donors had G/G, G/C, and C/C phenotypes. The preoperative GFR was statistically similar between all groups. The final GFR was highest for donors with G/G phenotype and lowest for those with C/C phenotypes (Table1). Donors with C/C phenotype were at 4.7 fold increased risk for GFR< 60 ml/min compared to those with G/G phenotype (HR:4,74 %95 CI: 1,482-15,212; p:0,009). Conclusion Kidney donation is associated with lower GFR compared to healthy individuals. The more profound decline in some cases may be explained with TGF-β1 SNP at codon 25. Our study shows C/C phenotype is associated with lower final GFR in renal transplant donors. We propose this particular finding might be useful for eligibility, especially for marginal donors after validation with studies including a higher number of participants.