Potassium bicarbonate, but not sodium bicarbonate, reduces urinary calcium excretion and improves calcium balance in healthy men

Abstract

Previous studies demonstrated that the administration of NaHCO3 or sodium citrate had either only a small effect to reduce urinary Ca excretion or no effect, but that potassium citrate significantly reduced urinary Ca excretion. In order to further evaluate and compare the effects of NaHCO3 and of KHCO3, we performed ten metabolic balances in healthy men during 18 control days, 12 days of NaHCO3, 60 mmol/day and 12 days of KHCO3, 60 mmol/day. Six subjects were fed a low Ca diet (5.2 +/- 0.7 SD mmol/day) and three of these were also given calcitriol (0.5 microgram 6-hourly). Four subjects ate a normal Ca diet (19.5 +/- 1.3 mmol/day). For all 10 subjects, KHCO3 administration reduced urinary Ca excretion from control by -0.9 +/- 0.7 mmol/day, P less than 0.001. Net intestinal Ca absorption did not change detectably so that Ca balances became less negative by a +0.9 +/- 0.9 mmol/day; P = 0.01. KHCO3 administration was also accompanied by more positive PO4 and Mg balances. NaHCO3 administration had no significant effect on urinary Ca excretion or Ca balance. NaHCO3 and KHCO3 administration were accompanied by equivalently more positive Na or K balances, respectively and equivalently more negative acid balances (HCO3 retention). Neither NaHCO3 or KHCO3 altered fasting serum HCO3 concentrations, blood pH, serum 1,25-(OH)2-D or PTH concentrations. We conclude that KHCO3 promotes more positive Ca balances by either enhancing renal Ca retention or skeletal Ca retention or both.

Acid-Base Status Determines the Renal Expression of Ca2+ and Mg2+ Transport Proteins

“…Thus, the hypocalciuria could alternatively be explained by increased passive Ca 2ϩ reabsorption. Taken together, the present data offer insight into the previously unexplained mechanism by which administration of HCO 3 Ϫ prevents nephrolithiasis in patients with recurrent kidney stones (40,41 is reabsorbed in TAL, where the Na…”

Milk Alkali Syndrome and the Dynamics of Calcium Homeostasis

“…In the studies in which the calciuric effects of metabolic acidosis were reduced with alkali treatment, urine pH increased to the 6.5 to 7 range, but plasma pH and bicarbonate values did not change (80,81,83,85). However, as shown in the two patients with the milk alkali syndrome presented in this review, urine pH values were higher than in the aforementioned studies, as were serum bicarbonate and arterial pH values.…”

“…Some studies of alkali treatment also have shown that the decrease in urine calcium excretion occurs independent of calcium regulatory hormones such as PTH and calcitriol. Whereas supplemental alkali treatment did not change plasma pH or bicarbonate levels, urine pH did increase from the 5.5 to 6 range to the 6.5 to 7.0 range (80,81,83,85). Therefore, the enhanced calcium reabsorption could be, at least in part, from an increase in luminal pH in the distal tubule.…”

“…The acid load that is produced by a high-protein diet or ingestion of ammonium chloride has been shown to increase urine calcium excretion (77)(78)(79)(80)(81)(82)(83). Alkali treatment alone or given together with a high-protein diet or ammonium chloride reduces urine calcium excretion and improves calcium balance (77,78,80 -84).…”

Alkali Therapy In Renal Tubular Acidosis

“…Nonvolatile acid is endogenously produced at a rate that can exceed the capacity of the normal kidney to excrete it (9,10), and such excessive acid is buffered by bone at the cost of its resorption and demineralization (11,12); can alkali therapy therefore prevent, delay, or reverse either metabolic bone disease or calcium-containing kidney stone formation in those with diet-induced, low-grade metabolic acidosis but neither a recognized form of RTA nor renal failure? If so is alkali therapy best provided to these patients as KHCO 3 because it: induces in normal humans a hypocalciuric effect greater than that induced by NaHCO 3 (13) and one that more than offsets the hypercalciuric effect of dietary NaCl (14); induces an improved external calcium balance in normal men (13) and women (15); occurs naturally and plentifully in precursory form in fruits and vegetables, e.g., as potassium citrate in which organate in vivo is completely converted to bicarbonate? Can realization of the therapeutic potential of alkali therapy depend on the attaining of a metabolically optimal range of plasma bicarbonate that is higher than that comprising its lower "normal" range (5,15,16)?…”