Effects of a high-sodium/low-potassium diet on renal calcium, magnesium, and phosphate handling

The distal convoluted tubule (DCT) of the kidney plays an important role in blood pressure regulation by modulating Na + reabsorption via the Na + -Cl - cotransporter (NCC). A diet containing high salt (NaCl) and low K + activates NCC, thereby causing Na + retention and a rise in blood pressure. Since high blood pressure, hypertension, is associated with changes in serum calcium (Ca 2+ ) and magnesium (Mg 2+ ) levels, we hypothesized that dietary Na + and K + intake affects Ca 2+ and Mg 2+ ransport in the DCT. Therefore, the present study aimed to investigate the effect of a high-Na + /low-K + diet on renal Ca 2+ and Mg 2+ handling. Mice were divided in four groups and fed a normal-Na + /normal-K + , normal-Na + /low-K + , high-Na + /normal-K + , or high-Na + /low-K + diet for 4 days. Serum and urine were collected for electrolyte and hormone analysis. Gene and protein expression of electrolyte transporters were assessed in kidney and intestine by qPCR and immunoblotting. Whereas Mg 2+ homeostasis was not affected, the mice had elevated urinary Ca 2+ and phosphate (P i ) excretion upon high Na + intake, as well as significantly lower serum Ca 2+ levels in the high-Na + /low-K + group. Alterations in the gene and protein expression of players involved in Ca 2+ and P i ransport indicate that reabsorption in the proximal tubular and TAL is affected, while inducing a compensatory response in the DCT. These effects may contribute to the negative health impact of a high-salt diet, including kidney stone formation, chronic kidney disease, and loss of bone mineral density.