METABOLISM IN NEPHRITIS 345 



to the presence of an increased amount of epinephrin. This theory, 

 as do all those that postulate a hypersecretion of the suprarenal glands, 

 awaits confirmation. Pierce and Keith offered some experimental evi- 

 dence that ordinarily sugar did not appear in the urine because the kid- 

 ney utilizes sugar as presented to it. While these authors did not attempt 

 to explain the high blood glucose of nephritis in this way, their work 

 is suggestive of the possibility that a damaged kidney will not consume 

 the usual amount of sugar and that, consequently, it may accumulate in 

 the blood. 



The most valuable explanation thus far offered is that of Myers and 

 Killian(a) (1917). They showed that many cases of nephritis have an ab- 

 normally high figure for diastatic activity of the blood ; the patients with 

 an increased blood diastase are the ones that have a high blood sugar. 

 Renal insufficiency is supposed to be responsible for the high blood dias- 

 tase. The latter mobilizes glucose from the liver and muscle glycogen, thus 

 making the series of events complete. Previously an increase of diastase 

 in the body and diminution of liver glycogen had been demonstrated in 

 various forms of renal injury (Griinwald, Orkin). Recently Lewis and 

 Mason expressed the view that the diastase of the blood in nephritis showed 

 no direct relation to the type of renal lesion, to the degree of kidney in- 

 volvement or the progress of the disease. This observation does not neces- 

 sarily impair the soundness of Myers and Killian's theories. O'Hare(c) 

 (d)(1920) has suggested that sclerosis of the arteries of the pancreas di- 

 minishes the functional efficiency of that organ and that certain cases of 

 hypertension may therefore be regarded as potential cases of diabetes 

 mellitus. This undoubtedly is true in some instances of essential hyperten- 

 sion and nephritis; however, it is certain that this explanation will not 

 suffice to account for all the cases of hyperglycemia occurring in nephritis. 

 The problem of the cause of the rise of blood sugar in nephritis awaits a 

 final solution. 



The renal threshold to the glucose of the blood presents some very in- 

 teresting facts. The normal threshold is at a level of about 0.17 per cent 

 (Hamman and Hirschman). It may be considerably raised in acute or 

 chronic nephritis (Mason, Neubauer (1910)). Neubauer had one case 

 in which the blood glucose rose to 0.36 per cent without glycosuria. In 

 this connection, as with many of the other phases of nephritis, there are 

 discrepancies that make it certain that other conditions can interfere 

 with renal function and that lesions of the kidney do not involve the 

 whole organ in uniform fashion. Thus, in some cases of diabetes mellitus 

 in which the kidneys gave no evidences of nephritis, the blood sugar was 

 as high as 0.32 per cent, while the urine remained sugar free, and in 

 one patient, suffering with nephritis and a considerable impairment of 

 renal function, the glucose threshold was less than 0.10 per cent (Mosen- 

 thal and Lewis(fe), 1917). 



