Associations Of Sodium And Potassium Intake With Chronic Kidney Disease in A Prospective Cohort Study: Fndings From The Hispanic Community Health Study/ Study Of Latinos, 2008–2017

Results using calibrated measures 

Using biomarker-calibrated nutrients, neither sodium, potassium, nor sodium-to-potassium ratio were statistically significantly associated with CKD (Table  3). However, the effect size for the sodium -to-potassium ratio was similar in direction and greater in magnitude to that using our 24-h recall measure of sodium -to-potassium ratio. In sensitivity analyses using our biomarker-calibrated nutrients restricted to individuals, not on diuretics or not on ACEI (Supplementary Table 2), results were largely consistent in direction and magnitude compared with our fully adjusted models, although not statistically signifcant.

Table 3 Associations between dietary sodium, potassium, and sodium (2008–2011) to potassium ratio with incident chronic kidney diseaseǂ (2014–2017), Hispanic Community Health Study/ Study of Latinos, using nutrient calibration equations 

a Incident chronic kidney disease is defned as eGFR <60ml/min/1.73m2 with >1ml/min/1.73m2 decline and/or albumin to creatinine ratio≥30mg/g. All models are adjusted for age, sex, time between visits, Hispanic/Latino heritage group, education, income, marital status, nativity/years in the US, language preference, study site, health insurance, supplement use, smoking, drinking, physical activity, body mass index, systolic blood pressure, hypertension medication, total cholesterol, and diabetes. The potassium model is adjusted for sodium intake and the sodium model is adjusted for potassium intake. b Models are additionally adjusted for overall restaurant score and fast food restaurant score

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Discussion

In a population-based cohort of diverse US Hispanics/ Latinos followed for an average of 6 years, lower potassium and higher sodium-to-potassium ratios were associated with increased risk of CKD. Additionally, the association between sodium and CKD differed by diabetes status with higher sodium associated with a greater risk of CKD among those with existing diabetes at baseline. Our results were particularly strong for sodium -to- potassium ratio which was associated with a 21% increased risk of CKD with every one-unit increment in the molar ratio. These results emphasize the importance of considering the ratio of sodium -to potassium as a dietary factor in preventing the development of CKD among healthy adults.

Consistent with prior studies [18, 27], sodium alone was not a signifcant predictor of incident CKD in our main models. For example, among young participants of the Coronary Artery Disease In Young Adults (CARDIA) study, mean 24-h sodium was not associated with the development of CKD over 20 years [17]. One potential explanation for these null results is the inability to accurately measure usual and habitual sodium intake-as diet varies over time [51]. Additionally, other research demonstrates that among persons with hypertension, a more complex nonlinear "U-shaped" relationship between dietary sodium and CKD, in which both very high or very low sodium is associated with CKD [22]. For sodium and potassium, we did not find evidence of a nonlinear relationship with risk of CKD. However, for the sodium -to-potassium ratio, we did find that the risk of CKD was lowest in the middle tertile of the sodium --to-potassium ratio suggesting the possibility of a "U-shaped" association. However, we emphasize that these findings should be interpreted with caution and warrant further investigation. In our study, we found higher sodium to be associated with the development of CKD among individuals with pre-existing diabetes, but not persons without diabetes. This finding supports dietary recommendations urging individuals with diabetes to consider further sodium restriction to intake levels below the USDA recommendations [47]. In contrast, in another study conducted among individuals with diabetes and normal kidney function, lower potassium, but not higher sodium was associated with kidney and cardiovascular outcomes [28].

In our study, low potassium intake was associated with the development of CKD. This finding corroborates results from black and white young adult participants of the CARDIA study that showed that every 1 g increment of 24-h urinary potassium excretion was associated with a 29% reduction in risk of albuminuria in the subsequent 25 years [18]. However, in our calibrated models, we did not find an association between potassium and CKD. We propose that this may be explained by the variability added to the measured values through the calibration modeling process. Tough our calibrated estimate for the association between potassium and CKD was stronger than our estimate using 24-h recall potassium (IDR=1.20 vs IDR=1.09), it did not achieve statistical significance due to the high variance (depicted with the wide confidence bands). Further examination of this important research question with more objective and repeated measurements may be required to fully elucidate the association between potassium and kidney function. For example, in research conducted in a population-based sample in Switzerland, high sodium and high sodium -to- potassium ratio but not low potassium was associated with a greater decline in eGFR [19]. This is in contrast to our findings which did not show any independent associations between sodium, potassium, or the sodium-to-potassium ratio with decreased eGFR, though we caution against over-interpretation of these diferences. We note that our study was conducted in a US Hispanic/Latino population with unique characteristics and with different measures of each nutrient of interest. Finally, we highlight that our general findings showing that higher sodium higher sodium -to potassium ratio, and lower potassium are associated with a worsening of kidney function are consistent with other studies conducted in population-based samples [18, 19]. Further, among individuals with CKD, there are a number of studies showing mixed findings with respect to the relationship between potassium intake and continued eGFR decline [20, 21]. For example, research from a clinic-based retrospective cohort study of CKD patients in Japan showed that high potassium intake was associated with CKD progression [21]. However, research from the Chronic Renal Insufficiency Cohort (CRIC) study in the United States showed that among individuals with CKD, higher potassium intake was associated with slower eGFR decline [20]. We emphasize that our study was conducted in a population-based sample free from CKD, and our findings are therefore most relevant for the prevention of CKD rather than the management of CKD.

To our knowledge, this is the frst study to demonstrate associations between the ratio of dietary sodium -to potassium intake and CKD in a population of Hispanics/Latinos who are relatively free from multiple comorbid conditions. Our research builds on previous evidence suggesting that the ratio of sodium -to- potassium intake may be an important predictor of CKD [8, 17, 18], eGFR decline [19], and other chronic diseases [52] in addition to dietary sodium [18, 19, 22] or potassium [17, 27] intake alone. Our results build on these findings by demonstrating this association with CKD among a population with most participants free of comorbid conditions. Our results are also consistent with a larger body of research demonstrating the importance of the sodium-to-potassium ratio with other chronic disease outcomes, such as hypertension [52, 53] and general CVD outcomes [54, 55]. Our results emphasize that diets such as the Dietary Approaches to Stop Hypertension Diet (DASH) [56], which have been demonstrated to reduce risk for CKD [57], continue to be important for CKD prevention because these diets simultaneously emphasize decreased sodium and increased potassium intake.

There are several mechanistic pathways by which low dietary potassium and high dietary sodium-to-potassium ratio may lead to decreased kidney function. Higher sodium intake is a risk factor for elevated blood pressure [58], and hypertension is in turn a risk factor for CKD [59]. Diets higher in potassium are thought to reduce vascular resistance [60, 61], lowering the risk of hypertension and also directly lowering the risk of kidney dysfunction by increasing eGFR [61, 62]. Diets high in potassium intake may also directly improve kidney function through increased kallikrein expression which has been demonstrated to reduce kidney injury in animal models [63].

This study is not without limitations. First, our primary dietary exposure measures were ascertained using two 24-h dietary recalls, which may be inaccurate [64]. However, we were able to collect two dietary recall surveys on 94% of participants, accounting for within-person variability. Studies that have compared 24-h dietary recall to 24-hour urine collection (the gold-standard assessment of sodium) [65] have found sodium to be underreported, particularly among those with higher BMI [64]. To address this limitation, we also included calibrated measures of sodium and potassium intake, which were designed to correct this measurement error using data from 24-hour urinary sodium and potassium excretion measurements taken from a subsample of HCHS/SOL participants [36]. In this analysis, we found an effect size similar in direction and stronger in magnitude to that of our primary measure for sodium -to-potassium ratio. However, these results were not signifcant, possibly due to the variability that calibration added to our models. Finally, our use of the composite CKD outcome makes it difficult to examine the relationships between each nutrient and incident decreased eGFR (< 60 ml/min/1.73 m2 with > 1 ml/ min/1.73 m2 decline) or incident albuminuria (albumin to creatinine ratio ≥ 30 mg/g) independently. Our sensitivity analysis as seen in Supplementary Table 4 suggests that greater sodium, lower potassium, and greater sodium-to-potassium ratio are associated with albuminuria (albumin to creatinine ratio ≥ 30 mg/g) but not incident decreased eGFR (< 60 ml/min/1.73 m2 with > 1 ml/min/1.73 m2 decline). Tough Surprisingly, these results are consistent with other findings showing that sodium or potassium is associated with albuminuria but not decreased eGFR [18].

The relatively short six-year follow-up time in this cohort presents another limitation. CKD develops over decades throughout the life course and diet varies over time as well, due to changes in individual preferences in diet and secular changes in food availability [66]. We recommend that future studies examine this association in cohorts with repeated measures of dietary exposure and more follow-up time. We were unable to examine the associations between sodium and potassium with CKD according to clinically relevant cut points of sodium and potassium, making it harder to detect nonlinear relationships. Only 21.3 and 0.6% of HCHS/SOL participants met recommendations for sodium and potassium respectively [30]. Given this, sample sizes for individuals who met dietary recommendations were too small for meaningful comparisons. This limitation may be difficult to address in other US cohorts given that most of the US population fails to meet dietary guidelines for sodium or potassium [67]. Finally, there are some medications that can interfere with the urinary excretion of sodium and potassium, thus contributing bias to our calibrated measures. To address these potential biases, we also conducted our sensitivity analyses among persons not taking diuretics or ACEI. In these analyses, our results were consistent in magnitude and direction with our main analyses, however, they were not statistically signifcant.

Our study also includes notable strengths. To our knowledge, associations between dietary intake of sodium, potassium, and CKD have not been demonstrated in a large sample of Hispanics/Latinos, so our findings have important implications for generalization to an understudied ethnic minority population. The large sample size of the HCHS/SOL study and the diversity of countries of origin strengthened our ability to detect associations that are both statistically signifcant and clinically meaningful. While previous research demonstrated the importance of the sodium -to- potassium-ratio for CKD among obese persons [8], and in a European population [19], our study builds on those findings by demonstrating this association among Hispanic persons living in the US with and without comorbid conditions.

In conclusion, our findings support dietary approaches to the prevention of CKD that focus simultaneously on limiting sodium and increasing potassium intake, rather than more simplistic approaches focused on individual nutrients. Potassium is a known marker of diets high in fruits and vegetables [68], so we believe our results further underscore the importance of diets high in fruits and vegetables in the prevention of chronic disease.

References 

1. Coresh J, Selvin E, Stevens LA, et al. Prevalence of chronic kidney disease in the United States. JAMA. 2007;298(17):2038–47. https://doi.org/10. 1001/jama.298.17.2038. 

2. Bowe B, Xie Y, Li T, et al. Changes in the US burden of chronic kidney disease from 2002 to 2016: an analysis of the global burden of disease study. JAMA Netw Open. 2018;1(7):e184412. https://doi.org/10.1001/ jamanetworkopen.2018.4412. 

3. Ricardo AC, Flessner MF, Eckfeldt JH, et al. Prevalence and correlates of CKD in Hispanics/Latinos in the United States. Clin J Am Soc Nephrol. 2015;10(10):1757–66. 

4. Sarnak MJ, Levey AS, Schoolwerth AC, et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association councils on kidney in cardiovascular disease, high blood pressure research, clinical cardiology, and epidemiology and prevention. Hypertension. 2003;42(5):1050–65. https://doi.org/10.1161/ 01.HYP.0000102971.85504.7c. 

5. Khan S, Amedia CA, Jr. Economic burden of chronic kidney disease. J Eval Clin Pract Jun 2008;14(3):422–434. https://doi.org/10.1111/j.1365-2753. 2007.00883.x. 

6. Brück K, Stel VS, Fraser S, et al. Translational research in nephrology: chronic kidney disease prevention and public health. Clin Kidney J. 2015;8(6):647–55. https://doi.org/10.1093/ckj/sfv082. 

7. Han SY, Hong JW, Noh JH, Kim DJ. Association of the estimated 24-h urinary sodium excretion with albuminuria in adult Koreans: the 2011 Korea National Health and Nutrition Examination survey. PLoS One. 2014;9(10):e109073. https://doi.org/10.1371/journal.pone.0109073.

 8. Aaron KJ, Campbell RC, Judd SE, Sanders PW, Muntner P. Association of dietary sodium and potassium intakes with albuminuria in normalweight, overweight, and obese participants in the reasons for geo-graphic and racial diferences in stroke (REGARDS) study. Am J Clin Nutr. 2011;94(4):1071–8. https://doi.org/10.3945/ajcn.111.013094. 

9. Verhave JC, Hillege HL, Burgerhof JG, et al. Sodium intake affects urinary albumin excretion, especially in overweight subjects. J Intern Med. 2004;256(4):324–30.

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