METABOLISM IN NEPHRITIS 401 



creased arterial pressure, but that increased arterial pressure may result 

 in an arteriosclerotic, contracted kidney. 



The Cause of Increased Arterial Pressure in Nephritis 



The exciting cause of increased arterial pressure is unknown with the 

 exception of the fact that lead poisoning is frequently associated with a 

 hypertension. The classification of the theoretical possibilities, that may 

 be responsible for a rise of blood pressure, has often been attempted, and 

 the material subdivided under the heads of chemical, mechanical, etc., 

 factors. This is an extemely artificial arrangement and it is preferable 

 simply to state the facts as they have been developed thus far without 

 forcing the material into an orderly but unnatural and illogical sequence. 



One probability has been almost completely lost sight of. This is that 

 there is almost assuredly more than one cause for hypertension. It would 

 be very strange if the raised level of blood pressure in acute nephritis, lead 

 poisoning, essential hypertension, toxemia of pregnancy, etc., were all due 

 to the same pathological physiological disturbance and yet this is not uncom- 

 monly assumed to be true. 



Insufficient Renal Function. It has been previously mentioned that 

 in some cases of bichlorid of mercury poisoning, associated with anuria, 

 the blood pressure may rise slightly. This is not true in all instances 

 of this sort; why it should occur in some cases and not in others is not 

 clear. 



A reduction of kidney substance in experimental animals results in a 

 rise of arterial pressure (Passler and Heinecke, Janeway (c) ). In addition 

 such animals showed a marked polyuria (Bradford). Janeway found 

 that the blood pressure in a patient rose to 180 when the only remaining 

 kidney was excised. On the other hand in animals, extirpation of both 

 kidneys causes no notable changes in the arterial tension. 



A partial obstruction of both ureters may bring about an increased 

 blood pressure. Cohnheim demonstrated this many years ago. However, 

 there are cases in which the blood pressure does not change. When such 

 an obstruction becomes complete the pressure may rise markedly, as high 

 as 210 on the third day of anuria ( Passler (Z>), Brasch). A temporary 

 ligature of the ureters produces a contracted kidney and a hypertension 

 (Beckman, Strauss, Rautenberg). 



It is curious that the marked renal insufficiency so commonly seen in 

 congenital polycystic kidneys is not necessarily associated with a blood pres- 

 sure above the normal (Means and Rogers). The author has seen a similar 

 patient, observed for about two years. 



Prostatic obstruction apparently may be responsible for an increase 

 in blood pressure, which has a tendency to subside as the conditions are 

 restored to normal, by retention catheters or operative means (O'Conor, 



