90 DONALD D. VAN SLYKE 



and Myers(c) (1920) have shown that lowered plasma bicarbonate occurs 

 frequently in chronic nephritis, and consider it a grave prognostic sign. 



The states of the acid-base balance that have been observed in nephritis 

 are those of compensated alkali deficit (lowered blood bicarbonate with 

 normal pH) finally developing during the premortal coma into uncom- 

 pensated alkali deficit (very low bicarbonate and pH also lowered) ( Pea- 

 body (d)(e), 1914). The lowest blood pH observed in man according to 

 the writer's knowledge was one of 6.95 determined by Cullen in the hos- 

 pital of the Rockefeller Institute in a nephritic shortly before death in 

 uremic coma. 



The cause of acidosis in nephritis has been generally assumed to be 

 failure of the kidneys to excrete the acid products of normal metabolism. 

 There is no formation of acetone bodies or the other known organic acids. 

 Marriott and Howland(a) (1916) have found an increase in the plasma 

 PO 4 of nephritics which indicates that retention of phosphoric acid may be 

 partly responsible for the lowered alkaline reserve. In certain nephritics 

 Henderson and Palmer (1915) found the ratio (titratable acid) : (am- 

 monia) in the urine to be abnormally high. Marriott and Rowland (c] 

 (1918) have found a similar ratio after feeding acid phosphate, which is 

 further evidence of the possibility of phosphoric acid retention in nephritic 

 acidosis. That there may be in nephritis not only a retention of normal 

 acid metabolites, but also a specific acceleration of acid formation is a 

 possibility indicated by recent experimental work of Wallace (1921). 



Diagnosis. Combined blood bicarbonate and pH determination or the 

 alkali retention test, appear necessary. The indirect methods are un- 

 certain. 



Therapy. It is at present uncertain whether the moderate compensated 

 alkali deficit of chronic nephritis is of importance in accelerating the prog- 

 ress of the disease. Whether a patient in such a condition is benefited by 

 therapeutic measures to restore the alkali reserve has not yet been shown. 

 Since the acid-base balance is obviously unstable, however, and the compen- 

 sated acidosis may become uncompensated with accompanying coma and 

 death, it may possibly be desirable, in nephritics with a tendency towards 

 low blood bicarbonate, to assist the body in maintaining its alkali reserve 

 by dietary means. Such would be a diet abundant in fruits and vege- 

 tables, which produce more alkali than acid when burned in the body, 

 but sparing in meats and other protein foods, and in cereals, which 

 produce more acid than alkali when metabolized. 



In uremic coma the air-hunger can be alleviated and life prolonged, 

 perhaps, for a few days by bicarbonate administration. Its effects on 

 both clinical condition and acid-base balance are outlined in a description 

 of a case by Means, Bock, and Wood well (1921). Usually alkali therapy 

 prolongs the life of a comatose nephritic only a few days; but in an 

 instance observed by the writer (case of Dr. Edgar Stillman) such a 



