The response of the kidney to an alkalosis during salt deficiency

Abstract

One of the functions of the kidney is unquestionably to protect the body against internal fluctuations of hydrogen ion concentration. It is well known that large doses of alkalis or a period of overbreathing lead to an alkaline urine, and the mechanism involved may be twofold. In the first place an increased amount of base may be excreted, and the way in which BH2PO4in the urine gives place to B2HPO4is an example of this. In the second place the reaction of the urine may be changed by acid radicle substitution,e.g., HCO3may be excreted instead of Cl. The latter involves no increased excretion of base. Vomiting leads to a loss of hydrochloric acid so that the urine tends to become alkaline, and persistent vomiting, which invariably causes a fall in the serum chlorides and a rise in the alkali reserve, should theoretically be accompanied by an alkaline urine—and often is so in practice (Dixon, 1924; Hoff, 1932; Glass, 1932; Katsch and Mellinghoff, 1933; Rachmilewitz, 1934; etc.). On the other hand, acid urines have repeatedly been reported even in the presence of proved alkalosis in the tissues. Thus Brown, Eusterman, Hartman, and Rowntree (1923) recorded that tetany and an acid urine might be found to coexist in the same person. Dixon (1924) described a patient with tetany whose plasma bicarbonate was 101 vols %, but who had an acid urine. GollwitzerMeier’s (1924) patient had tetany, an alkali reserve of 89 vols %, and a urine ofρh5. Similar cases have been reported by Odin (1928) and Steinitz (1928), and rather less striking ones by Achard (1930) and Meyer (1931, 1932). Several of these authors have commented on the strange anomaly, and Gamble and Ross (1924-25), Gollwitzer-Meier (1924), and Hartmann and Smyth (1926) have all made the further important observation that the urine became alkaline during recovery or after sodium chloride had been given. Few authors have attempted any explanation of their findings and Gollwitzer-Meier’s suggestions that the alkali was fixed by the tissues or that the autonomic nervous system was responsible can hardly be accepted as satisfactory. Odin (1928, quoted by Brandberg) 1929), who described a patient with alkalosis, an acid urine, and a bloodurea of 112 mg per 100 cc, regarded the inability of the patient to secrete an alkaline urine as part of the general renal failure. Such patients, however, may show an abnormally high nitrogen excretion so that the renal failure may be much less severe than the blood-urea would indicate.