262 Discussion 



Richet : In populations that are said to eat a lot of proteins, for in- 

 stance Eskimos, what is the state of the kidney? Do such people 

 often die from chronic nephritis? They are generally said to eat 5,000 

 cal./day, mostly fat and proteins. 



McCance : I think in fact the Eskimos do not eat a very high protein 

 diet, although they may eat a great deal of fat. They certainly tend to 

 die rather young, but mostly from accidents, I believe ; an old Eskimo is 

 a man of about 40-45. 



Richet: Some work has been done by Lieb (1929. J. Amer. med. Ass., 

 93, 20), by Thomas (1927. J. Amer. med. Ass., 88, 1559), and by Bischoff 

 (1932. J. Nutr., 5, 431), which seemed to demonstrate that a high protein 

 diet was absolutely harmless. 



Dr. Talbot, you mentioned the amount of protein given in cases of 

 chronic nephritis. In Paris we put some chronic nephritic patients on an 

 almost protein-free diet, about 10 g./day. Three or four patients whose 

 death was not expected died after six weeks (Hamburger, J., Serane, J., 

 and Cournot, L. (1951). Sem. Hop. Paris, 27, 2289). We therefore never 

 gave that kind of diet again to any patients for more than ten or fifteen 

 days. Also, we never give under • 5 g./kg. in chronic cases, because under 

 that amount we have a lot of trouble and the patients become so weak 

 they would never live anyway ; we prefer to have a patient with perhaps 

 a shorter life, but healthy, than the other way round. 



Fourman: Tiv. Kennedy, why did you imply a relationship between 

 catabolic reactions, adrenal hyperplasia and Selye's results with cor- 

 texone acetate? 



Kennedy : The catabolism would require over-secretion of Compound 

 F, of course. However, Hechter and Pincus (1954. Physiol. Rev., 34, 459) 

 showed that in the rat the adrenal secretes chiefly Compound B anyway, 

 and there is not in fact the contradiction there would seem to be. An 

 over-secreting adrenal could damage the rat kidney and one would, at 

 the same time, get a catabolic effect. 



Fourman: But you would not necessarily want to relate that to the 

 results with cortexone acetate? 



Kennedy: Yes, in that cortexone acetate was the particular steroid 

 which was used in most of Selye's experiments. 



Desaulles : In our laboratories Compound B has been shown to help in 

 inducing hypertension in the rat. 



Kennedy: Does it produce renal lesions? 



Desaulles: Only in enormous doses. 



Milne: The recovery lesions of potassium depletion are similar in 

 appearance to the ageing kidney, as mentioned earlier by Dr. Kennedy. 

 The histological studies reported by Dr. Desaulles seem to show the same 

 dilatation of the tubules that was seen in Dr. Kennedy's cases. We 

 repeated these experiments with dietary potassium depletion and cor- 

 texone acetate injections, but we used very young rats and were unable 

 to repeat the effects which were shown so conclusively at Cambridge. 

 Is the ageing kidney, then, more susceptible to permanent damage from 

 potassium depletion? This would tie up with Dr. Fourman's suggestions 

 regarding cortexone acetate as given by Selye. 



