Abstract
A high salt intake is harmful to diseased kidneys by several mechanisms. The acidifying salt intake effect may be one of them.
The ratio between sodium and chloride concentration is 1.4:1 in the extracellular fluid (ECF), while it is 1:1 in salt. According to the Stewart-Fencl theory, the ECF strong ion difference (SID = (Na++ K++Ca+++Mg++) – (Cl- + UA-); (UA- means routinely unidentified ions) is one of the basic variables determining the hydrogen ion concentration.
The SID decrease causes acidemia and vice versa. In the context with salt intake, we can simplify the SID equation and replace it by the difference [Na+-Cl-].
In the ECF [Na+-Cl-] difference is diminished after the salt intake and contributes to acidemia, which is signalized by [HCO3-] decrease. To maintain a physiological [Na+-Cl-] in the ECF, the kidneys must raise the NH4+ and HCO3- synthesis from glutamate.
This is associated with the increased kidney oxygen consumption. „Salt“ composed of the 2/3 of NaCl and 1/3 of NaHCO3 has [Na+-Cl-] difference in the approximately same level as it is in the ECF. Therefore this mixture does not have an acidifying effect.
Healthy kidneys cope with the chloride excess after salt ingestion easily. However, we believe that in renal patients, apart from salt intake reduction, bicarbonate should be administered early in the course of disease, sooner than pH or even [HCO3-] are reduced.
Thus, salt-elicited demand for increased bicarbonate synthesis would be suppressed early in the course of renal diseases.