Dietary Potassium Intake and Abdominal Aortic Calcification

Among patients with chronic kidney disease (CKD), the leading cause of mortality is cardiovascular disease. The high rate of cardiovascular disease-related mortality in that patient population is associated in part with accelerated development of arterial calcification in CKD.

Arterial calcification is an active process of mineralization and deposition of calcium-phosphate salts, and can occur in the intimal and medial layer of arteries as a consequence of aging. In patients with CKD, arterial calcification becomes more extensive. Hypertension and diabetes, as well as hyperphosphatemia and uremic toxins promote the development of arterial calcification in patients with CKD.

Results of recent animal studies have suggested that reduced dietary potassium intake promoted arterial calcification and increased arterial stiffness, while increased dietary potassium intake attenuated both arterial calcification and stiffness. There are limited data in humans on the relationship of dietary potassium and arterial clarification and stiffness.

Yuping Xie, MD, MS, and colleagues conducted cross-sectional analyses to test the hypothesis that higher dietary potassium would be associated with less abdominal aortic calcification (AAC) and lower arterial stiffness among adults in the United States. Results were reported in the Journal of Renal Nutrition.

The analyses included data on participants >40 years of age from the National Health and Nutrition Examination Survey (NHANES) 2013-2014. Dietary potassium intake was categorized into quartiles: quartile 1, <1911 mg/day; quartile 2, 1911-2461 mg/day; quartile 3, 2462-3119 mg/day; and quartile 4, >3119 mg/day.

The primary outcome of interest was AAC quantified using the Kauppila scoring system. AAC scores were categorized into no AAC (AAC=0, reference group), mild/moderate (AAC >0 to ≤6), and severe AAC (AAC >6). The secondary outcome was arterial stiffness that was examined using pulse pressure as a surrogate.

Potential cofounders included age, sex, race/ethnicity, body mass index (BMI), poverty, smoking status, hypertension, diabetes mellitus, lipid profile, kidney function, serum markers of mineral bone disease, prescription antihypertensive or antihyperlipidemic use, daily caloric intake, and level of physical activity.

Following exclusion of NHANES participants with extreme dietary potassium intake (n=49), those with missing potassium dietary intake data (n=500), and missing covariate data (n=173), the primary analysis of dietary potassium intake and AAC included data on 2418 participants. The secondary analysis of dietary potassium intake and pulse pressure included data on 2186 participants.

In the primary analysis cohort, 20% had mild/moderate calcification and 8% had severe calcification. Patient morbidities included diabetes (16.8%), hypertension (59.7%), CKD stage 1-2 (7.6%), and CKD stage 3-5 (9.1%).

Compared with participants with no AAC, those with mild/moderate or severe AAC were significantly older, less physically active, and more likely to be smokers, diabetic, or hypertensive. They were also more likely to have lower BMI, lower estimated glomerular filtration rate (eGFR), and take antihyperlipidemic medications. There were statistically significant but not clinically meaningful differences in serum phosphate levels: those with severe AAC had higher levels compared with the reference group. Mean serum potassium level was 4.0 mg/dL; there was no significant difference in serum potassium among the AAC groups.

Mean dietary potassium intake was 2654 mg/day among all participants. Mean dietary potassium intake among those in quartile 1 was 1511 mg/day; in quartile 2, 2185 mg/day; in quartile 3, 2767 mg/day; and in quartile 4, 3821 mg/day. Daily potassium intake was lower in women than in men. Participants with albuminuria were more likely to have a lower dietary potassium intake. Those with poverty, low BMI, low daily caloric intake, and low physical activity had a lower daily potassium intake. There was a positive association between serum potassium and dietary potassium intake (P<.001).

Compared with the reference group, those in the AAC groups had lower daily potassium intake; the difference did not reach statistical significance (P=.20). When examined as a continuous variable in either unadjusted or fully adjusted models, there was no association between dietary potassium intake and AAC.

When dietary potassium intake was examined within quartiles, there was a nonlinear association with AAC. In the unadjusted model, compared with quartile 1, dietary potassium intake in quartile 2 was associated with 35% lower odds of severe AAC (odds ratio, 0.65; 95% CI, 0.44-0.96; P=.01). The association remained significant in the fully adjusted model. There were no associations between dietary potassium intake and AAC in comparisons of other quartiles with the first.

In the fully adjusted model, there were significant associations between age, BMI, hypertension, diabetes, smoker, and eGFR and severe AAC. Age, sex, race-ethnicity, hypertension, diabetes, eGFR, albuminuria, and CKD did not modify the association between dietary potassium intake and AAC.

In secondary analyses, compared with participants in the reference group who had a mean pulse pressure of 50.4 mm Hg, pulse pressure was significantly higher in those with mild/moderate AAC (58.7 mm Hg) or severe AAC (69.7 mm Hg) (P for trend<.001). in the fully adjusted model, per 1000 mg higher in dietary potassium intake, pulse pressure was 1.47 mm Hg lower (95% CI, –2.47 to –0.47; P=.007).

The authors cited some limitations to the study findings, including the cross-sectional design that did not allow for inference of causation between dietary potassium intake and arterial calcification and stiffness, the small number of participants with CKD stage 4 or 5, and not differentiating the dietary potassium source (plant vs animal).

In conclusion, the researchers said, “In a population of adults over 40 years of age, there was not a linear association between dietary potassium intake and AAC. There was a negative relationship when comparing dietary potassium in quartile 2 to quartile 1, suggesting that there might be an optimal level of dietary potassium intake that is beneficial for the prevention of arterial calcification. Additionally, dietary potassium intake was negatively associated with pulse pressure. These findings support the potential important benefits of dietary potassium intake on arterial calcification and stiffness. Further large and prospective studies are needed to validate our findings.”

Takeaway Points

1. Researchers reported results of a study testing the hypothesis that higher dietary potassium intake would be associated with less abdominal aortic calcification (AAC) and lower arterial stiffness.
2. There was no linear association between dietary potassium intake and AAC. When comparing dietary potassium intake in quartiles of participants, there was an association between higher dietary potassium intake and less severe AAC
3. There was a significant association between higher dietary potassium intake and lower pulse pressure.

Source: Journal of Renal Nutrition