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首页> 外文期刊>Pharmacogenetics and genomics >PRKCB is associated with calcineurin inhibitor-induced renal dysfunction in heart transplant recipients
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PRKCB is associated with calcineurin inhibitor-induced renal dysfunction in heart transplant recipients

机译：PRKCB与钙调神经磷酸酶抑制剂诱发的心脏移植受者肾功能不全有关

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OBJECTIVES: Single nucleotide polymorphisms (SNPs) in the transforming growth factor-β1 gene (TGFB1) have been inconsistently associated with calcineurin inhibitor (CNI)-induced renal dysfunction following cardiac transplantation. The impact of genetic variants related to the renin-angiotensin-aldosterone system (RAAS) and natriuretic peptides, which are implicated in CNI nephrotoxicity, is unknown. The primary objective of this study was to validate the association between two common variants in TGFB1 (rs1800470, rs1800471) and postcardiac transplant renal function. The secondary objective was to investigate the effect of candidate genes related to the RAAS, natriuretic peptides, and other elements involved in the intracellular signaling of these pathways. METHODS: We conducted a retrospective cohort study of 158 heart transplant recipients treated with CNIs, and evaluated the association between select SNPs and the estimated glomerular filtration rate as calculated by the Modification of Diet in Renal Disease simplified formula. A total of 273 SNPs distributed in 44 genes were tested. RESULTS: No association was observed between TGFB1 variants and renal function. One polymorphism in the protein kinase C-β gene (PRKCB; rs11074606), which is implicated in the RAAS intracellular signaling, was significantly associated with post-transplant estimated glomerular filtration rate after adjusting for possible confounders (P=0.00049). This marker is in linkage disequilibrium with two variants located in putative regulatory regions of the gene (rs2283541, rs1013316). CONCLUSION: Our results suggest that PRKCB may be a potential predictor of CNI-induced nephrotoxicity in heart transplant recipients, and could therefore be a promising candidate to identify patients who are most susceptible to this adverse drug reaction.
机译：目的：转化生长因子-β1基因（TGFB1）中的单核苷酸多态性（SNPs）与心脏移植后钙调磷酸酶抑制剂（CNI）引起的肾功能不全不一致。与肾素-血管紧张素-醛固酮系统（RAAS）和利尿钠肽有关的遗传变异对CNI肾毒性有影响。这项研究的主要目的是验证TGFB1的两个常见变异（rs1800470，rs1800471）与明信片移植肾功能之间的关联。第二个目的是研究与这些途径的细胞内信号传导有关的RAAS，利钠肽和其他元素相关的候选基因的作用。方法：我们对158名接受CNIs治疗的心脏移植受者进行了一项回顾性队列研究，并评估了选择的SNPs与估计的肾小球滤过率之间的相关性。测试了分布在44个基因中的273个SNP。结果：TGFB1变异与肾功能之间没有相关性。调节可能的混杂因素后，蛋白激酶C-β基因（PRKCB; rs11074606）中的一种多态性与RAAS细胞内信号传导有关，与估计的移植后肾小球滤过率显着相关（P = 0.00049）。该标记与位于基因推定调控区中的两个变体处于连锁不平衡状态（rs2283541，rs1013316）。结论：我们的研究结果表明，PRKCB可能是心脏移植受者CNI诱导的肾毒性的潜在预测指标，因此可能是鉴别最容易发生这种药物不良反应的患者的有希望的候选者。

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