The renal excretion of hydrogen ion in renal tubular acidosis: I. Quantitative assessment of the response to ammonium chloride as an acid load

Abstract

In order to establish criteria for the quantitative assessment of the renal excretion of hydrogen ion in patients suspected of having renal tubular acidosis, or in their relatives who might have a genetically determined latent impairment of this function, a standard three day and five day ammonium chloride test was performed twenty times in eighteen normal adults. The results were analyzed and compared with similar data from five adult patients with the clinical diagnosis of renal tubular acidosis. The results show that: 1. 1. Increment indices, in which the change in hydrogen ion excretion is compared with the increment in chloride excretion or in acid load, do not always separate the patients from the normal subjects. 2. 2. A clearance index in which the absolute excretion rate of hydrogen ion is related to the total hydrogen content of the extracellular buffer systems (quantitated as the reciprocal of the serum carbon dioxide level) does separate the patients from the normal subjects under circumstances of an increased total hydrogen load. 3. 3. In these adult patients with renal tubular acidosis the primary impairment of hydrogen ion excretion appears to involve the excretion of titratable acid; the excretion of ammonium ion is somewhat less deficient relative to the degree of systemic acidosis and normal or high relative to the pH of the urine. 4. 4. Two of the patients with RTA were primarily limited in their ability to excrete acid by the amount of phosphate available in the tubular urine to accept hydrogen ions, and the other three patients with RTA were primarily limited by the capacity of the tubular cells to reabsorb bicarbonate and to transfer hydrogen ions against a concentration gradient. Thus more than one mechanism of acid excretion apparently is disturbed in renal tubular acidosis if all patients are included who have actual or potential acidosis due to “non-contractive” disease of the kidney. It is concluded that the test and data here presented provide a tool for the investigation of the pathogenesis and etiology of latent as well as overt disturbances in this renal function.