Section of Nephrology, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts.
Renal Division, Kidney Research Institute, West China Hospital of Sichuan University, Chengdu, China.
Clin J Am Soc Nephrol. 2022 Oct;17(10):1477-1486. doi: 10.2215/CJN.02680322. Epub 2022 Aug 31.
Progressive CKD in Black individuals is strongly associated with polymorphisms in the gene, but it is unknown whether dietary risk factors for CKD progression vary in high- versus low-risk genotypes. We investigated if genotypes modify associations of dietary potassium and sodium with CKD progression and death.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We analyzed 1399 self-identified Black participants enrolled in the Chronic Renal Insufficiency Cohort from April 2003 to September 2008. Exposures were calibrated 24-hour urine potassium and sodium excretion. The primary outcome was CKD progression defined as the time to 50% decline in eGFR or kidney failure. The secondary outcome was CKD progression or death. We tested for an interaction between urinary potassium and sodium excretion and genotypes.
Median 24-hour urinary sodium and potassium excretions in Black participants were 150 mmol (interquartile range, 118-188) and 43 mmol (interquartile range, 35-54), respectively. Individuals with high- and low-risk genotypes numbered 276 (20%) and 1104 (79%), respectively. After a median follow-up of 5.23 years, CKD progression events equaled 605, and after 7.29 years, CKD progression and death events equaled 868. There was significant interaction between genotypes and urinary potassium excretion with CKD progression and CKD progression or death (=0.003 and =0.03, respectively). In those with high-risk genotypes, higher urinary potassium excretion was associated with a lower risk of CKD progression (quartiles 2-4 versus 1: hazard ratio, 0.83; 95% confidence interval, 0.50 to 1.39; hazard ratio, 0.54; 95% confidence interval, 0.31 to 0.93; and hazard ratio, 0.50; 95% confidence interval, 0.27 to 0.93, respectively). In the low-risk genotypes, higher urinary potassium excretion was associated with a higher risk of CKD progression (quartiles 2-4 versus 1: hazard ratio, 1.01; 95% confidence interval, 0.75 to 1.36; hazard ratio, 1.23; 95% confidence interval, 0.91 to 1.66; and hazard ratio, 1.53; 95% confidence interval, 1.12 to 2.09, respectively). We found no interaction between genotypes and urinary sodium excretion with CKD outcomes.
Higher urinary potassium excretion was associated with lower versus higher risk of CKD progression in high-risk and low-risk genotypes, respectively.
黑人个体的进行性 CKD 与 基因的多态性密切相关，但尚不清楚 CKD 进展的饮食风险因素在高风险和低风险 基因型中是否存在差异。我们研究了 基因型是否会改变饮食钾和钠与 CKD 进展和死亡的关系。
设计、地点、参与者和测量：我们分析了 2003 年 4 月至 2008 年 9 月期间参加慢性肾功能不全队列的 1399 名自我认定的黑人参与者。暴露于经校准的 24 小时尿钾和钠排泄量。主要结局为 CKD 进展，定义为 eGFR 下降 50%或肾功能衰竭的时间。次要结局为 CKD 进展或死亡。我们检测了尿钾和钠排泄与 基因型之间的相互作用。
黑人参与者的 24 小时尿钠和钾排泄中位数分别为 150mmol（四分位距，118-188）和 43mmol（四分位距，35-54）。高风险和低风险 基因型的个体分别为 276 名（20%）和 1104 名（79%）。中位随访 5.23 年后，发生了 605 例 CKD 进展事件，随访 7.29 年后，发生了 868 例 CKD 进展和死亡事件。 基因型与尿钾排泄与 CKD 进展和 CKD 进展或死亡之间存在显著的相互作用（=0.003 和 =0.03）。在高风险 基因型的个体中，较高的尿钾排泄与较低的 CKD 进展风险相关（四分位距 2-4 与 1：风险比，0.83；95%置信区间，0.50 至 1.39；风险比，0.54；95%置信区间，0.31 至 0.93；风险比，0.50；95%置信区间，0.27 至 0.93）。在低风险 基因型的个体中，较高的尿钾排泄与 CKD 进展的风险增加相关（四分位距 2-4 与 1：风险比，1.01；95%置信区间，0.75 至 1.36；风险比，1.23；95%置信区间，0.91 至 1.66；风险比，1.53；95%置信区间，1.12 至 2.09）。我们未发现 基因型与尿钠排泄与 CKD 结局之间存在相互作用。
高风险和低风险 基因型中，较高的尿钾排泄与 CKD 进展的风险降低与升高相关。
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