Race, Interleukin-6, TMPRSS6 Genotype, and Cardiovascular Disease in Patients With Chronic Kidney Disease.
Race, Interleukin-6, TMPRSS6 Genotype, and Cardiovascular Disease in Patients With Chronic Kidney Disease.
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DOI：
10.1161/jaha.122.025627
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发表时间：
2022-09-20
影响因子：
5.4
通讯作者：
Amdur, Richard L.
中科院分区：
文献类型：
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作者：
Barrows, Ian R.;Devalaraja, Matt;Kakkar, Rahul;Chen, Jing;Gupta, Jayanta;Rosas, Sylvia E.;Saraf, Santosh;He, Jiang;Go, Alan;Raj, Dominic S.;Amdur, Richard L.
黑人和白人慢性肾病患者死亡率和心血管疾病（CVD）的差异归因于社会文化因素、合并症、遗传和炎症。在3031名慢性肾功能不全队列研究参与者中，我们研究了种族、血浆IL - 6（白细胞介素- 6）和TMPRSS6基因型作为CVD和死亡率的决定因素的相互作用。主要结局是全因死亡率和心肌梗死、外周动脉疾病、中风和心力衰竭的综合发生率。在中位随访10年期间，与白人患者相比，患有慢性肾脏疾病的黑人患者的死亡率（34%对26%）和心血管疾病综合发生率（41%对28%）明显更高。调整后，TMPRSS6基因型与结果无关。IL - 6最高的五分位数与最低的五分位数相比，调整后的死亡率风险比（4.11 [2.48-6.80]，P<0.001）和心血管疾病综合风险比（2.52 [1.96-3.24]，P<0.001）更高。白细胞介素- 6在白人和黑人个体中每增加1五分位数调整后的死亡危险分别为1.53（1.42-1.64）和1.29 (1.20-1.38)（P<0.001）。CVD综合评分分别为1.61（1.50 ~ 1.74）和1.30 (1.22 ~ 1.39)（P<0.001）。在包含IL - 6的Cox比例风险模型中，死亡不再存在种族差异（1.01 [0.87-1.16]，P=0.92），但CVD仍存在显著的无法解释的中介作用（1.24 [1.07-1.43]；P=0.004）。包括IL - 6、糖尿病和尿白蛋白/肌酐比在内的路径模型能够识别导致死亡率和心血管疾病种族差异的变量。慢性肾病患者死亡率和心血管疾病的种族差异可以通过包括糖尿病和血浆IL - 6等中介变量的良好拟合路径模型来解释。
Differences in death rate and cardiovascular disease (CVD) between Black and White patients with chronic kidney disease is attributed to sociocultural factors, comorbidities, genetics, and inflammation. We examined the interaction of race, plasma IL‐6 (interleukin‐6), and TMPRSS6 genotype as determinants of CVD and mortality in 3031 Chronic Renal Insufficiency Cohort study participants. The primary outcomes were all‐cause mortality and a composite of incident myocardial infarction, peripheral artery disease, stroke, and heart failure. During the median follow‐up of 10 years, Black patients with chronic kidney disease experienced a significantly higher mortality (34% versus 26%) and CVD composite (41% versus 28%) compared with White patients. After adjustment, TMPRSS6 genotype did not associate with the outcomes. The adjusted hazard ratio for mortality (4.11 [2.48–6.80], P<0.001) and CVD composite (2.52 [1.96–3.24], P<0.001) were higher for the highest versus lowest IL‐6 quintile. The adjusted hazards for death per 1‐quintile increase in IL‐6 in White and Black individuals were 1.53 (1.42–1.64) versus 1.29 (1.20–1.38) (P<0.001), respectively. For CVD composite they were 1.61 (1.50–1.74) versus 1.30 (1.22–1.39) (P<0.001), respectively. In Cox proportional hazard models that included IL‐6, there was no longer a racial disparity for death (1.01 [0.87–1.16], P=0.92), but significant unexplained mediation remained for CVD (1.24 [1.07–1.43]; P=0.004). Path models that included IL‐6, diabetes, and urine albumin to creatinine ratio were able to identify variables responsible for racial disparity in mortality and CVD. Racial differences in mortality and CVD among patients with chronic kidney disease could be explained by good‐fitting path models that include selected mediator variables including diabetes and plasma IL‐6.
DOI：
10.1053/j.ajkd.2012.12.012
发表时间：
2013-08
期刊：
American journal of kidney diseases : the official journal of the National Kidney Foundation
影响因子：
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作者：
Kovesdy CP;Quarles LD;Lott EH;Lu JL;Ma JZ;Molnar MZ;Kalantar-Zadeh K
通讯作者：
Kalantar-Zadeh K