Presentation Summary

Written by Jasna Trbojevic-Stankovic
Reviewed by Sandro Mazzaferro

Potassium is the most abundant intracellular cation. Its homeostasis is achieved by matching intake with excretion and by ensuring adequate distribution between extra- and intracellular fluid compartments. Potassium is primarily removed by the kidneys and, to a much lesser extent, by the colon. Dietary reference intakes (DRI) for potassium differ among the general population and chronic kidney disease (CKD) patients (1). The level of restriction for CKD patients depends on residual diuresis, but it does not seem difficult to achieve since the estimated average potassium intake in modern diets is even lower than DRI for CKD patients (2-4). The World Health Organization guideline suggests a potassium intake of at least 90mmol/day (3150mg/day) for individuals ≥16 years of age (5). A low potassium diet is associated with higher blood pressure and risk of stroke, thus adequate intake is mandatory, provided that there is no predisposition to hyperkalemia and CKD progression (5).

The mechanism by which potassium affects blood pressure is uncertain, however, there is a known relationship between dietary potassium deficiency and sodium retention secondary to the activation of the thiazide-sensitive NaCl cotransporter (NCC) (6). Even in the setting of high salt intake, insufficient potassium intake modulates distal convoluted tubule cells membrane voltage activating the NCC and limiting potassium loss, even at the expense of increased blood pressure. (Figure 1). This finding is supported by the fact that in the general population urinary potassium excretion is inversely associated with the risk of developing hypertension (7).

Figure 1. The effect of dietary potassium intake on kaliuresis, natriuresis, and blood pressure (6, 8)

Based on these facts, the latest suggested strategy to improve blood pressure control relies on measuring sodium and potassium concentrations in urine and adjusting the diet to achieve the urine Na/K ratio close to 1 (9). However, high potassium intake may be risky and sometimes even dangerous in hypertensive patients with CKD stages 3-5, especially those with diabetes. Furthermore, even though increasing potassium in the diet may be beneficial for hypertension, its effect on CKD progression is less clear. Some analyses suggest that high urinary sodium and potassium excretion are associated with increased risk of CKD progression, while others found a completely inverse relationship (10, 11). Nevertheless, the prevalence rates of hyperkalemia and hypokalemia in CKD patients are similar, and both are associated with equally high mortality risk. Moreover, even serum potassium levels in the low normal range are associated with higher mortality rates in CKD patients (12). The content of the diet also seems to be relevant in preserving the glomerular filtration rate (GFR). A diet rich in fruits and vegetables mitigates further GFR decline in patients with CKD stage 3, probably related to its alkalizing effect (13). Such conflicting evidence precludes the definitive recommendations on whether to restrict or liberate potassium intake in CKD patients and call for further research in this area (14).

The DRI for phosphorus in the general population and CKD patients is equivalent. However, unlike for potassium, the estimated average phosphorus intake is more than double the DRI (4, 15). This is especially alarming since for phosphorus there is a tolerable upper intake level compatible with life. On the other hand, many inaccuracies, plus hidden phosphate preservatives, make dietary counseling of a low-phosphate diet challenging, and dietary adherence by patients nearly impossible (16).

Serum phosphorus level is independently associated with renal failure and mortality in non-dialysis dependent CKD patients (17). Thus, it might seem that restricting dietary phosphorus intake should slow down CKD progression. However, this relationship is not that simple. In CKD stages 3 to 5 phosphate intake is not tightly associated with serum phosphate concentrations and there is no evidence that higher phosphate intake, assessed by 24-h phosphate excretion, is associated with end-stage renal disease or all-cause mortality (18). Hence, factors other than dietary intake may affect serum phosphate concentrations calling for additional investigation.
There is indirect evidence of the renoprotective effect of dietary phosphorus restriction. While high phosphate levels attenuate nephroprotection through angiotensin-converting enzyme inhibition, reducing phosphate burden decreases proteinuria and mitigates the progression of renal disease in CKD patients (19). Dietary phosphorus originates from protein-rich foods, thus the protein source of the phosphate may also be important. Even with the same overall protein intake, serum phosphorus levels were lower with vegetarian than with a meat-based diet, thus emphasizing the significance of protein source (16).

Based on all this evidence, the KDIGO guidelines suggest that limiting dietary phosphorus intake should only be undertaken as a measure to control hyperphosphatemia in CKD patients stage 3 to 5D and with careful consideration of phosphate source (20). However, randomized controlled trials are necessary to further evaluate the impact of dietary phosphorus on disease progression and outcomes.

The DRI for magnesium in the CKD population is lacking, but it is established that the estimated average intake in the general population is somewhat lower than the DRI (4, 21). The recommended daily intake for magnesium is at least 10 mmol (240mg), and preferred sources include nuts, grains, fish, vegetables, and legumes. Low serum magnesium is associated with inflammation, atherogenesis, endothelial dysfunction, and vascular calcification, while a higher intake of this element is related to lower blood pressure. Furthermore, it appears that both lower dietary magnesium intake and low serum magnesium levels are associated with greater odds of rapid kidney function decline and progression to end-stage renal disease (22, 23).

Based on all these data it seems that a vegetable-based diet carries numerous advantages in CKD patients. It improves gut microbiota, provides fibers to promote intestinal transit, contributes to serum alkalization, decreases phosphate and increases magnesium serum levels, and, last but not least, increases urinary potassium thus contributing to better blood pressure control (Figure 2). It is thus reasonable to propose a reconsideration of the current practice and encourage a more liberal intake of vegetables in CKD patients.

Figure 2. The benefits of vegetable-based diets in CKD patients (8, 24)


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