METABOLISM IN NEPHRITIS 365 



trated in a very simple way. If we imagine a vessel into which water 

 flows at a constant rate, escaping through an outlet at the bottom, the 

 water will seek the level in the vessel at which the pressure is such that the 

 rate of outflow is exactly equal to the intake. If we then increase or de- 

 crease the rate of inflow, the level will change to meet the new conditions. 

 The change in level of the fluid in the vessel may.be regarded as a compen- 

 satory change. Under physiological conditions fluctuations in the level of 

 blood urea compensate for changes in the rapidity of formation of urea, and 

 changes in the level of chlorid .in the plasma compensate for fluctuations 

 in chlorid intake. Under pathological conditions changes in the level of 

 urea and sodium chlorid in the blood also occur to compensate for changes 

 in the outlet, in the form of diseased kidneys. In the case of chlorids 

 the outlet of the vessel must be considered as being at some distance from 

 the bottom, and in such a case only the level of fluid above the outlet 

 would play any part in determining the rate of outflow, which would cease 

 when the level of fluid fell to the level of the outlet. Similarly, only the 

 chlorid above the threshold determines the rate of excretion, which prac- 

 tically ceases when the threshold value is reached." 



McLean, as the result of his observations, finds the chlorid threshold 

 to be of considerable value ; his reasoning concerning the underlying theory, 

 which he evidently credits with the possibility of clinical application, is as 

 follows : "It is manifestly wrong to consider the kidneys responsible for 

 the failure to excrete a certain amount of salt given by mouth, if the salt 

 is taken up by the tissues and the concentration in the plasma remains 

 low. But if the concentration of chlorids in the blood or plasma remains 

 proportionately high, and the rate of excretion proportionately low, it is 

 correct to speak of retention in the sense of a failure to excrete properly. 

 This is the condition in certain types of cardiorenal, or renal disease." 

 He observed that the plasma chlorids were high in certain forms of cardiac 

 and renal disease, and edema ; it was low in pneumonia, fever, diabetes 

 or as the result of the action of diuretics (digitalis). 



On the other hand Atchley believes from his experience with eight 

 cases of acute nephritis that : "In no case was the rate of excretion de- 

 pendent on the concentration of chlorids in the plasma. This much is 

 clear; there is no definite constant threshold for any individual nor is 

 the height of the threshold an index of the degree of impairment of chlorid 

 function. More valuable than what the formula expresses are the facts 

 that may be gathered from a determination of the plasma chlorid con- 

 centration, together with a knowledge of the daily intake and output of 

 salt. There are fairly conclusive grounds for saying that an abnormally 

 liiiih plasma chlorid on a moderate salt intake may be the only evidence 

 of a latent disturbance of chlorid metabolism." 



It is obvious that in the face of such contradictory opinions concerning 

 the value of the kidney threshold for chlorids, many more observations 



