SPECIAL CAUSES OF EDEMA 349 



ent types of edema. In acute nephritis {e. g., in scarlatina) toxic 

 materials appear to be the chief cause, and, as Senator contends, in- 

 jure alike the capillaries of the renal glomerules and of the sub- 

 cutaneous tissues; in each case there results an increased permeability 

 which is manifested by albuminuria as a result of the injury to the 

 renal capillaries, and by edema as a result of the injury to the tissue 

 capillaries. This sort of edema is allied to that produced by peptone 

 and similar lymphag-o<iues, and we might well imagine that the 

 mechanism consisted merely in an injury to the capillaries through 

 which excessive fluid is driven by the blood pressure, were it not for 

 such observations as those of ]\Iendel and Hooker,-^^ who found that 

 postmortem flow is increased by these lymphagogues also. We can 

 hardly account for the force exhibited in postmortem lymph flow on 

 any other ground than that it is furnished b}^ osmotic pressure or 

 colloidal absorption, unless we wish to fall back upon "vital activity" 

 of the surviving cells. Hence it is probable that even in the edemas 

 of toxic conditions, such as acute nephritis, physico-chemical factors 

 play a part, the responsible substances probably being abnormal or 

 excessive metabolic products of the cells atit'ected by the poisons. An 

 interesting observation made by Bence ^- is that nephrectomized rabbits 

 develop an edema even when they are given no water at all ; this would 

 seem to indicate an increased affinity of the tissues for water when 

 the renal functions are deficient. Hydremia is always a favoring 

 factor, however, and probably important in nephritic edema,^^ while 

 nearly all students of acute experimental nephritis find evidence that 

 the resulting edema depends very much upon the changes in the vessel- 

 walls. ^"^ 



In the more common edema of chronic nephritis we have to con- 

 sider, among other factors, the blood pressure. That this is not an 

 essential or even important cause, however, is shown by the fact 

 that edema is usually much less marked in interstitial nephritis with 

 high blood pressure than it is in parenchymatous nephritis with a 

 much lower pressure. Toxic substances are, of course, also present in 

 the blood, and may alter capillary permeability ; these toxic substances 

 may account for the localized edemas and erythemas sometimes ob- 

 served in nephritis. But jirobably most important is the action of 

 the crystalloids which the kidney does not excrete, and which seem 

 to be stored up in the tissues, where they cause transudation of water 

 under the influence of their osmotic pressure. For example, Rzent- 

 kowski ^■' found that the average lowering of the freezing-point by the 

 eden:atous fluid in nephritis was 0.583°, in cardiac dropsy it was 0.548°, 



31 Amer. Jour, of Phvsiol., inn2 (7), 380. 

 32Zeit. f. klin. ]\red.,'inon (67). 0(1. 

 33Pearce, Arch. Int. Med., 1909 (.3). 422. 



34 See Schmidt and Schlaver, Deut. Arch. klin. Med.. 1911 (104). 44: Tollak, 

 Wien. klin. Woch., 1914 (27). 98. 

 35Berl. klin. Woch., 1904 (41). 227. 



