On the mechanism of acidosis in chronic renal disease.

It has been pointed out (1) that, in terms of modern acid-base chemistry, the defects reponsible for the acidosis of renal disease could be: 1) impaired renal excretion of acid in the form of ammonium and titratable acidity, 2) loss of bicarbonate (alkali) in the urine due to a failure of renal bicarbonate conservation or 3) a combination of these two defects. The two main components of urine responsible for the removal of hydrogen 1 from the body are ammonium and titratable acid. Under the stress of endogenous or exogenous acidosis the normal kidney responds by increasing the excretion of both these moieties, but the increment in ammonium usually far exceeds that in titratable acid. It has long been known that the basal excretion of ammonium is reduced in patients with renal disease, and that the capacity to increase ammonium excretion in response to acidosis is also impaired (2-7). Somewhat less attention has been directed towards the ability of the diseased kidney to excrete titratable acid, although it was demonstrated many years ago that patients with uremic acidosis can elaborate very acid urines (2, 3). In so-called "renal tubular acidosis" it is generally accepted that char-