402 HERMAN O. MOSENTHAL 



Monakow and Mayer). Both the amount of residual urine as well as the 

 diminution of renal function appear to be instrumental in bringing about 

 these changes (O'Conor). The actual cause of the rise of blood pressure 

 in these cases can only be surmised (Monakow and Mayer). 



It has been argued that the waste products which accumulate in the 

 blood when renal insufficiency exists may be the cause for hypertension. 

 The present methods of blood chemistry have shown very definitely, as far 

 as the non-protein nitrogenous constituents, urea, uric acid, creatinin, 

 etc,., are concerned, that this is not correct. There may be maximal ac- 

 cumulations of these substances in the blood without increase in blood pres- 

 sure and vice versa. 



In summarizing the effect of renal insufficiency upon blood pressure, 

 it must be acknowledged that diminished kidney function, whether the 

 cause resides in the kidney itself or the ureters or urethra, may at times 

 result in a hypertension but this is not a constant phenomenon. Why 

 this should be so it is impossible to state at the present time. One state- 

 ment of Janeway, which shows how wide an interest this subject has for 

 clinical medicine, is that he believes it possible that the hypertension found 

 in some instances of heart failure may be due to insufficient kidney action 

 brought on by passive congestion. 



Blood Volume and Plethora. Keith, llowntree and Geraghty found 

 that there was no causal relationship between blood volume and hyperten- 

 sion. When the total quantity of the blood increases under any circum- 

 stances, as occurs in certain states, and may be artificially brought about 

 by transfusions and infusions, in the human subject, there is no rise in 

 the blood pressure. The vasomotor control of the arteries appears to be 

 such that it can regulate the pressure of the fluid within them and main- 

 tain it at a constant level regardless of the actual volume of fluid. 



It was shown some years ago by Cohnheim and Lichtheim that plethora 

 does not increase blood pressure. Volhard believes that this statement 

 may apply to acute plethora but not to chronic. However, every case 

 of long standing edema does not exhibit an augmented blood pressure; in 

 fact the majority do not. 



Viscosity of the Blood. An increased viscosity of the blood must be 

 considered as a possible causative factor of arterial hypertension in ne- 

 phritis. The fact that such a change entails more resistance to be overcome 

 by the heart is self-evident. It must be borne in mind, however, that a dila- 

 tation of the peripheral arteries may compensate for the factors just men- 

 tioned and that the blood pressure may therefore be maintained at a nor- 

 mal level in spite of them. The finding of Lucas, that there is a hyper- 

 tension in only about thirty per cent of the cases of erythemia described 

 by him, bears this out. The whole question may be considered as set aside, 

 for the present at least, by the observations of Hirsch and Beck who showed 

 that an increased blood viscosity did not exist in nephritis. 



