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Apolipoprotein L1 Genotypes and the Association of Urinary Potassium Excretion with CKD Progression

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机构： [1]Section of Nephrology, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts Tilori1@bu.edu. [2]Renal Division, Kidney Research Institute, West China Hospital of Sichuan University, Chengdu, China. [3]Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah, Salt Lake City, Utah. [4]Molecular Medicine Program, University of Utah, Salt Lake City, Utah. [5]Medical Service, Veterans Affairs Salt Lake City Health Care System, Salt Lake City, Utah. [6]Section of Nephrology, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts. [7]Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana. [8]Basic Research Program, Frederick National Laboratory for Cancer Research and the Cancer Innovation Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, Maryland. [9]Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. [10]Department of Public Health, Herbert Wertheim School of Public Health and Human Longevity Science, University of California San Diego, La Jolla, California.

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Progressive CKD in Black individuals is strongly associated with polymorphisms in the APOL1 gene, but it is unknown whether dietary risk factors for CKD progression vary in high- versus low-risk APOL1 genotypes. We investigated if APOL1 genotypes modify associations of dietary potassium and sodium with CKD progression and death.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 APOL1 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 APOL1 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 APOL1 genotypes and urinary potassium excretion with CKD progression and CKD progression or death (P=0.003 and P=0.03, respectively). In those with high-risk APOL1 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 APOL1 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 APOL1 genotypes and urinary sodium excretion with CKD outcomes.Higher urinary potassium excretion was associated with lower versus higher risk of CKD progression in APOL1 high-risk and low-risk genotypes, respectively.Copyright © 2022 by the American Society of Nephrology.

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大类 | 1 区

医学

小类 | 1 区泌尿学与肾脏学

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大类 | 1 区

医学

小类 | 1 区泌尿学与肾脏学

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第一作者机构： [1]Section of Nephrology, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts Tilori1@bu.edu.

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