Abstract
HYPERCHLOREMIC acidosis is a characteristic feature of a variety of kidney diseases that have in common impairment of urinary acidification with the excretion of an alkaline urine. These disorders, which include, prominently, renal tubular acidosis and the Fanconi syndrome, are characterized principally by minimal alterations in glomerular filtration rate, at least in early stages, and by disturbances in renal tubular function that affect not only urinary acidification but also the tubular transport of, variously, glucose, phosphate, urate, amino acids and potassium.1 2 3 The mechanisms responsible for these alterations have not been established. The loss of alkali in the urine or, alternatively, . . .