ON THE MECHANISM OF ACIDOSIS IN CHRONIC RENAL DISEASE*

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Abstract
Balance studies have been carried out in uremic subjects after restoration of.plasma bicarbonate concentration to normal. During the phase of developing acidosis, 3 of the 4 patients with uremia were found to excrete significant quantities of bicarbonate in their urine even after plasma levels had fallen well below normal. The bicarbonate-wasting defect was not present in the 4th uremic subject nor in the majority of other uremic patients studied less completely. The other factor apparently responsible for the development of acidosis was a suppression of the excretion of ammonium and titratable acid, which appeared to be due in part to the relative alkalinity of the urine during the bicarbonate-wasting phase. There was, in addition, a delay in the acidification of the urine which occurred even when bicarbonate-wasting was absent or had ceased. However, each of the uremic patients, when severely acidotic, was ultimately able to lower urine pH below 5.5 and therefore for excrete nearly maximal amounts of titratable acid. Even in the most acid urines ammonium excretion increased only slightly. Most of the renal excretion of acid responsible for the maintenance of a low but steady plasma bicarbonate level was therefore accounted for by titratable acid. The patient with renal tubular acidosis not only wasted bicarbonate in the urine, but also continued to excrete an alkaline urine even at low plasma bicarbonate levels. It is concluded that in patients with acidosis due to renal disease, defects in the tubular reabsorption of alkali or in tubular excretion of hydrogen, or both, are at fault. The relative importance of these disorders may vary, but in general terms, all renal acidosis is "tubular" acidosis.