THE INTERNAL SECRETION OF THE KIDNEY 443 



had been confirmed by various authors (Riva-Rocci, Vincent and 

 Sheen, Batty Shaw), who believe that the tonic internal secretion 

 of the kidney forms the connecting link between renal disease on 

 the one hand, and arterial hypertension and cardiac hypertrophy 

 on the other. Seeing, however, that the hypertensive effect of 

 renal extract is not specific but is the property of extracts obtained 

 from a large number of other organs, it can hardly be regarded 

 as proof of an internal secretion on the part of the kidney, and 

 still less as a satisfactory explanation of the cardiac ^hypertrophy 

 of renal disease. 



Rautenberg recently described marked cardiac hypertrophy 

 and sclerotic changes in the vessels of rabbits after temporary 

 ligature of the ureter. 



The formation of what are known as " autonephrotoxins," 

 has been regarded as a further argument in favour of the passage 

 of the renal substance into the blood-stieam. Lindemann was 

 the first to show that, after the repeated injection of the expressed 

 juice of the kidney, an active poison, heteronephrotoxin, is 

 formed in the serum of immunized animals, which has a specific 

 and very injurious effect upon the kidney in animals of the same 

 species as that from which the expressed juice was obtained. 

 Nefediew next showed that blood taken from animals after ligature 

 of the ureters or of the renal artery, produced diffuse nephritis 

 when injected into animals of the same species. Lindemann 's 

 experiments showing that the blood of rabbits with chromian- 

 nephritis produced a parenchymatous nephritis in other rabbits, 

 provided further evidence in favour of the existence of auto- or 

 iso-nephrolysins. 



As in the case of the other cytotoxic sera, however, these 

 autonephrolysins do not represent physiological processes ; they 

 represent the toxic activities of substances formed under conditions 

 of immunization, and are probably not even organ-specific. 



Timofeew, a pupil of Lindemann's, has recently endeavoured 

 to prove that nephritic oedema is chiefly the outcome of the 

 presence in the blood-stream of decomposed constituents of the 

 renal cells. These substances, which he calls " nephroblaptins," 

 act in a manner similar to that of Heidenhain's lymphagogues 

 of the first class. According to Timofeew, the suppression of 

 renal activity which accompanies lesions of the renal parenchyma, 

 produces disturbance of the osmotic interbalance between the 

 organic fluids, and this leads to the retention in the tissues of an 

 excess of water. The substances which pass from the diseased 

 kidney into the blood-stream bring about changes in the blood 

 similar to those produced by lymphagogues of the first class; 

 and the consequent venous and capillary engorgement increases 

 the permeability of the vessel walls. The excess of fluid in the 

 organism, in combination with the increasing permeability of 

 the vessel walls, produces oedema. 



