854 HAEOLD BAILEY 



19 the increase in the urea to 22 mg. together with the high uric acid 

 would indicate that there is a secondary functional renal disturbance. 



Changes of the Urea Nitrogen in the Blood 



In studying the urea variations it is well to remember that in 

 eclampsia it represents to a large extent the endogenous metabolism, 

 for at the time that the bloods were collected little or no food was taken 

 and in all the toxemic cases protein was eliminated from the diet. 

 While urea is a very diffusable substance, passing rapidly through such 

 an organ as the placenta, it is probable that there is a limitation on the 

 part of the kidneys as to the amount that can be excreted. The substance 

 itself, however, is a diuretic and has even been used as such by Pinard. 

 It is easily proven that it does not produce convulsions, at least 

 in any ordinary amount. Hewlett and Wickett have recently found 

 that when 100 to 125 mg. of urea is given to normal men they develop 

 symptoms similar to asthenic uremia, which appear only when the urea 

 retention reaches 160 to 245 mg. per 100 c.c. 



urea 

 In the non-pregnant renal efficiency is evidenced by a of 0.50. 



Mosenthal and Hiller have shown that any functional disturbance 

 leads to an increase of the urea and consequently to a rise in the co- 

 efficient. 



Lyle's figures for the urea nitrogen in the blood in 5,000 women show 

 18 mg. or less but in the pregnant state it averages, in his cases, 11.5 mg. 

 Folin found that it ran as low as 5 to 9 mg. In the non-pregnant, Folin 

 and Denis placed the normal from 12 to 17 mg. and Gettler and Baker 

 in a series of 30 cases found 15 to 25 mg. per 100 c.c. 



In the 8 cases of eclampsia that recovered in Caldwell and Lyle's chart, 

 there are only 2 cases that surpass these normal figures of the non-pregnant 

 and of the 4 fatal cases (9, 10, 11 and 12 of Table VII) there were 2 

 that were higher. 



When we come to compare Caldwell and Lyle's eclamptic cases with 

 those of Killian from the standpoint of urea-non-protein nitrogen co- 

 efficient, their cases (N"os. 1, 3, and possibly 12) would fall into the class 

 called hepatic toxemias by Killian and the remainder under the caption 

 of hepatic toxemias accompanied by renal insufficiency. In hepatic 

 toxemias the urea is not only low and considerably lower than in 

 the normal individual but in a few instances it is lower than the average 

 in pregnancy. The explanation for this low figure, taking into considera- 

 tion the increased non-protein nitrogen must be that there is a failure 

 on the part of the liver to respond to a flux of nitrogenous bodies with an 

 increased urea synthesis. It is unfortunate that these more recent observ- 



