The secretion of acid into the stomach is neutralized by alkaline secretions in the intestine. It follows that excessive loss of pure intestinal secretions (for example, in the presence of an enteric fistula) may lead to acidosis. A more common circumstance is the presence of an ileal conduit where the ureters are implanted into an isolated loop of intestine, which is then externalized (a 'urinary conduit'). The delivery of urine rich in chloride to the isolated intestine leads to exchange of Cl- for HCO-, and thence to excessive loss of HCO- in the conduit, resulting in metabolic acidosis.
There are also a group of conditions known as renal tubular acidosis (RTA). These are mostly inherited but may be acquired, for example, as a consequence of recurrent infection. There are two major forms - proximal and distal - reflecting the site of the tubular defect in the nephron. In distal tubular RTA (type I) H+ secretion is impaired resulting in impaired H+ excretion, whereas in proximal RTA (type I) HCO- reabsorption is impaired (usually as part of multiple tubular abnormalities) leading to net loss of bicarbonate. Both cause acido-sis, the features of which are low pH and hypokale-mia as a result of increased distal tubular H+/K+ exchange. The precise causes of these conditions is not known but is likely to reflect genetic defects on individual transporter subtypes, for example, those of the Na+/H+ exchanger (Figure 2).
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