Robinson Todd W, Freedman Barry I
Wake Forest School of Medicine, Winston-Salem, North Carolina.
Methodist Debakey Cardiovasc J. 2016 Oct-Dec;12(4 Suppl):2-5. doi: 10.14797/mdcj-12-4s1-2.
Relative to those with European ancestry, African Americans have an excess incidence of nondiabetic chronic kidney disease predominantly due to two coding renal-risk variants in the apolipoprotein L1 gene (). This -kidney disease association is independent of systemic hypertension or blood pressure. Recent reports describe extra-renal effects of the G1 and G2 renal-risk variants on cardiovascular disease (CVD), subclinical atherosclerosis, lipoprotein particle concentrations, and survival. However, results have been less consistent than those seen in kidney disease, and the observed associations with CVD vary from risk to protective. This manuscript reviews the relationships between renal-risk variants and CVD, with an emphasis on study-specific factors that may have contributed to disparate observations. It is possible that renal-risk variants impact the systemic vasculature, not only the kidneys. As novel therapies for -associated nephropathy are developed, APOL1 variant protein effects on large blood vessels and risk of CVD will need to be considered.
与欧洲裔美国人相比，非裔美国人非糖尿病慢性肾脏病的发病率更高，主要是由于载脂蛋白L1基因中的两个编码肾脏风险变异（）。这种肾脏疾病关联独立于系统性高血压或血压。最近的报告描述了G1和G2肾脏风险变异对心血管疾病（CVD）、亚临床动脉粥样硬化、脂蛋白颗粒浓度和生存的肾外影响。然而，结果不如在肾脏疾病中所见的那样一致，并且观察到的与CVD的关联从风险到保护各不相同。本手稿综述了肾脏风险变异与CVD之间的关系，重点关注可能导致不同观察结果的特定研究因素。肾脏风险变异可能不仅影响肾脏，还会影响全身血管系统。随着针对相关肾病的新疗法的开发，需要考虑APOL1变异蛋白对大血管和CVD风险的影响。
