ACIDOSTS IN NEPHRITIS 565 



])oi.sono(l (logs causes both ammonia ami lactic acid to disappear from the urine, 

 indicating that the ammonia is the protective sul)stance which neutralizes the 

 lactic acid, and not the reverse. likewise, lactic acid acts as a defensive mech- 

 anism when excess, of alkali is administered, appearing in the urine in slightly 

 increased amounts.*' 



Sarcolaetic acid, which is dextrorotarj-, must be distingiiished from its optical 

 isomer, the inactive lactic acid that is produced by fermentation. When this fer- 

 mentation lactic acid is formed in the stomach and enters the blood, it ordinarily, 

 like other ingested organic acids, is combined by the blood alkalies and oxidized 

 to carbonates. It is doubtful if it ever enters the urine."* 



As a general rule sarcolaetic acid is not found abundant in the urine together 

 with the acetone bodies, but is, indeed, antiketogenic. Its appearance in the 

 urine indicates that glycogen is not completely burned, and this condition is 

 usually accompanied with fatty changes in the liver, which also depend on lack of 

 oxidation. Throughout the clinical forms of acidosis, lactic acid and fatty degen- 

 eration are always associated (Ewing). To assume, as has been generally done, 

 that the lactic acid appears in the urine when hepatic alterations are marked, be- 

 cause of the loss of the liver tissue which should destroy it, is probably not warranted. 

 Rather, the liver conditions and the formation of lactic acid depend upon the same 

 cause, which is a defective oxygen supply or interchange, either general or local. *^ 



Acidosis in Nephritis. — This presents a very different urinary 

 chemistry from diabetic acidosis, in that there is no excessive excretion 

 of organic acids or ammonia, and indeed no other striking urinary 

 change to account for the acidosis which may be severe, undoubtedly 

 often terminating hfe.^^ There is a definite increase in the inorganic 

 phosphate content of the blood (Marriott and Howland^^) in nephritis 

 with acidosis, and often the urinarj' aciditj' is decreased, so the acido- 

 sis is attributed to reduced capacity of the kidney to excrete acid 

 phosphates which is one of the most important normal mechanisms for 

 maintaining the neutrality of the blood. The most marked acidosis 

 is observed in those types of nephritis that are associated with uremia, 

 i. e., advanced chronic glomerulo-nephritis and acute nephritis, but 

 not in the chronic parenchymatous types. The nocturnal hyperp- 

 noea of nephritis probably is the result of acidosis (Whitney). Acido- 

 sis generally parallels in degree the impairment in excretory capacity 

 of the kidney, and, in contrast to diabetes, it does not reach a high 

 grade so long as the excretion of acid by the kidney is comparatively 

 efficient (Sellards). While administration of sodium bicarbonate 

 corrects the acidosis it has little effect on the course of the disease, 

 or on the amount of phosphate in the blood. With this high phosphat- 

 emia there is a reduction in the blood calcium, which ma}' have an 

 unfavorable influence on the irritability of the nervous tissues. Whit- 

 ney believes that in nephritis with acidosis there is probably some 

 excessive production of acid, as a kidney with greatly impaired excre- 



" Macleod and Knapp, Ainer. Jour. Physiol., 1918 (47), 189. 



** The theory of Boix that cirrhosis of the liver may be produced bj' butyric 

 acid formed in gastric fementation could not be corroborated by Joannovics, 

 Arch. int. Pharmacodyn., 1905 (15), 241. 



83 See Macleod and Wedd (Jour. Biol. Chem., 1914 (18), 446) who found 

 that reducing the oxygen supply to the liver caused a marked rise in the lactic 

 acid content of the hepatic blood. 



9" See \Miitnev, Arch. Int. Med., 1917 (20), 931. 



91 Arch. Int. Med., 1916 (IS), 708. 



