The Excretion of Ammonia and Titratable Acid in Nephritis

As the result of past metabolic studies, especially those of Hender-son and Palmer (12) it is known that the non-volatile acids produced in excess of fixed base by human metabolism are excreted in the urine in two forms, viz., as free acids, and as ammonium salts. Since the kidney is unable to form urine with a pH much lower than 5.0, it can excrete, in significant amounts, free acids of only the weak buffer type. In this class fall acid phosphates and the various organic adds. It appears, however, that free acid excretion may assist also in elimination of strong acids, which can react with buffer salts (e.g., HC + Na2HPO4 = H(NaHPO4) + NaCl), the free buffer acid being excreted in place of the strong acid. Thus Marriott and Howland (19) found that HCl ingestion increased the output of free buffer acids. Ammonia serves to neutralize either weak or strong acids. Con-sequently both ingestion of HC1, (either as such, or as NH4Cl or CaC12) and diabetic ketosis (producing weak beta-hydroxybutyric acid) cause increase in ammonia excretion. In fact both the above con-ditions increase both ammonia and free buffer acid output, without greatly altering the NHF/acid ratio (Marriott and Howland (19), Fitz and Van Slyke (4)). Peculiarly, however, ingestion of acid phosphate was found bv Marriott and Howland to increase only the output of titratable acid, without any effect whatever on the am-monia output. Since the nature of the acid eliminated, and presumably other un-known factors, can influence the proportions excreted as ammonium salts and titratable free buffer acids respectively, it is not surprising