UPDATE ON RENAL ACIDIFICATION - A PHYSIOLOGICAL VIEW

The kidney plays a major role in the regulation of acid-base balance. This process is mainly dependent on H+ secretion in the tubular lumen. Two acid extruder proteins are involved: the Na+/H+ exchanger and H+- ATPase. Studies using in vivo and in vitro microperfusion and isolated membrane vesicles have clearly demonstrated that the Na+/H+ exchanger is the main mechanism regulating H+ secretion/HCO; reabsorption along the proximal nephron. Moreover, several reports indicate that this pr otein is involved in intracellular pH (pH(i)) regulation. Newer studie s using molecular biology techniques have identified at least five iso forms of the Na+/H+ exchanger: NHE-1 is the housekeeping isoform, whil e NHE-3 seems to be implicated in transepithelial acid-base transport, although other isoforms could be involved too. H+-ATPase is the major acid extruder protein along the distal nephron, but it is also expres sed along the proximal tubule, where a Na+-independent bicarbonate rea bsorption has been described. There are a few studies indicating that the proton pump participates in pH(i) regulation, particularly in the presence of a large acid load. Its absence along the distal nephron ma y be one of the causes of distal tubular acidosis.