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Relationship and Interaction between Sodium and Potassium

R. Curtis Morris, Jr., MD, Olga Schmidlin, MD, Lynda A. Frassetto, MD and Anthony Sebastian, MD

Department of Medicine, Division of Nephrology, University of California, San Francisco, San Francisco, California


Figure 1
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  		Fig. 1. Hypothesized relationships between certain dietary inorganic electrolytes and bicarbonate, the kidney, essential hypertension, kidney stones, and osteoporosis: the modern diet’s excessive dietary sodium and chloride and deficient dietary potassium and bicarbonate precursors as determinants of salt-sensitive blood pressure, low-grade metabolic acidosis and hypercalciuria and thereby hypertension, kidney stones and osteoporosis. As formulated, the acidosis can be amplified by impaired renal acidification that occurs as part of the "incomplete syndrome of renal tubular acidosis" (iRTA), an age-related decline in renal function ("age"), or both. The underlined dietary determinants and pathogenic events are those originally hypothesized and depicted. In this scheme, the word "osteoporosis" replaces the term "bone mineralization" specified in the depiction of the original formulation. (Modified from MacGregor and Cappuccio [30] by Morris RC et al. [8].)

 

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  		Fig. 2. Dietary KHCO3 dose-dependently suppresses and ultimately abolishes hypercalciuria otherwise induced by dietary NaCl-loading in normal men.

 

Figure 3
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  		Fig. 3. Effect of potassium intake on frequency of salt-sensitivity in non-hypertensive African-American men (solid bar) and white men (cross-hatched bar). No white men were tested with 4.7 g/day (120 mmol/day) of potassium. Throughout an initial 7-day period of salt loading in all study subjects, potassium intake as potassium bicarbonate was set at 1.2 g/day (30 mmol/day), then increased to a total of either 2.7 or 4.7 g/day (70 or 120 mmol/day) for a subsequent 7-day period of salt loading.

 




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