Kujawa-Szewieczek A, Kolonko A, Kocierz M, Szotowska M, Trusolt W, Karkoszka H, Gumprecht J, Chudek J, Więcek A
Department of Nephrology, Endocrinology and Metabolic Diseases, Medical University of Silesia, Katowice, Poland.
Transplant Proc. 2011 Oct;43(8):2957-63. doi: 10.1016/j.transproceed.2011.07.016.
Genetic predisposition, including polymorphisms of the renin-angiotensin system (RAS) genes, are among the potential factors that may affect the occurrence of hypertension, anemia, or erythrocytosis as well as transplanted kidney function. However, the association of the RAS genes polymorphism and the kidney transplant outcomes is controversial. The aim of this study was to analyze the association between polymorphic variants of the angiotensin-converting enzyme (insertion/deletion [I/D]), angiotensinogen (M235T), and angiotensin II receptor type 1 (A1166C) genes, and the early and long-term kidney graft outcomes, as well as the prevalence of hypertension, anemia and erythrocytosis after kidney transplantation.
We included 331 consecutive kidney transplant patients performed between 1998 and 2003. Of the total, 87.9% of patients completed a 5-year follow-up. Subjects were genotyped for the I/D, M235T, and A1166C polymorphisms.
None of the examined polymorphism affected early or long-term graft function or was associated with hypertension before or after kidney transplantation. There was no significant difference in genotype distribution between patients with and without posttransplant erythrocytosis. However, posttransplant anemia (PTA) seemed to be significantly more common among kidney recipients with TT and MT than MM angiotensinogen genotypes (35.7% vs 20.7%; P=.03). The T allele was associated with the risk of development of PTA (odds ratio, 2.12; 95% confidence interval, 1.12-3.99; P=.02).
Our results do not support the hypothesis that polymorphism of the genes coding RAS components may by an independent risk factor for the development of interstitial fibrosis/tubular atrophy, posttransplant hypertension, or PTE. Further studies are necessary to investigate the association between angiotensinogen M235T genotypes and PTA.
遗传易感性，包括肾素 - 血管紧张素系统（RAS）基因的多态性，是可能影响高血压、贫血或红细胞增多症的发生以及移植肾功能的潜在因素之一。然而，RAS基因多态性与肾移植结局之间的关联存在争议。本研究的目的是分析血管紧张素转换酶（插入/缺失[I/D]）、血管紧张素原（M235T）和血管紧张素II 1型受体（A1166C）基因的多态性变体与肾移植早期和长期结局，以及肾移植后高血压、贫血和红细胞增多症的患病率之间的关联。
我们纳入了1998年至2003年间连续进行肾移植的331例患者。其中，87.9%的患者完成了5年随访。对受试者进行I/D、M235T和A1166C多态性的基因分型。
所检测的多态性均未影响早期或长期移植肾功能，也与肾移植前后的高血压无关。移植后有红细胞增多症和无红细胞增多症的患者之间基因型分布无显著差异。然而，肾移植受者中，血管紧张素原基因型为TT和MT的患者移植后贫血（PTA）似乎比MM基因型更为常见（35.7%对20.7%；P = 0.03）。T等位基因与PTA发生风险相关（优势比，2.12；95%置信区间，1.12 - 3.99；P = 0.02）。
我们的结果不支持以下假设，即编码RAS成分的基因多态性可能是间质纤维化/肾小管萎缩、移植后高血压或PTE发生的独立危险因素。有必要进一步研究血管紧张素原M235T基因型与PTA之间的关联。
