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DISCUSSION 



Swyer: You said that this renal damage in the obese rat might be a 

 question of protein overloading. Did you try feeding these rats on an 

 isocaloric diet, but with half the protein content? 



Kennedy: I have tried it as a short-term experiment but I did not 

 carry it to its logical conclusion. There was no renotrophic effect. 



Sivyer : Over- feeding is itself a stressful activity in the Selyeian sense 

 and that alone might lead to adrenal over-activity. Certainly there is 

 clinical evidence that it may. Obese people who give evidence of in- 

 creased adrenal steroid production may cease to do so after they have 

 been put on a diet and have had their weight brought down to normal. 



Kennedy : To answer that I must challenge the question of whether in 

 fact stress ever produces renal lesions in the rat. I can do that quickly 

 by quoting some recent work by Crane, Baker and Ingle (1958. Endo- 

 crinology, 62, 216; and Crane and Ingle, Endocrinology, 62, 474), who 

 have studied a large number of so-called stresses which sound quite 

 barbaric, and have found that the only one which produces what Selye 

 calls the stressed kidney is exposure to cold. Selye has always said 

 that this is the most effective, and these workers now say that it is the 

 only effective stress. Under those circumstances the rats eat twice as 

 much food. If they are then fed isocalorically, as you suggest, with a 

 high caloric diet made up with carbohydrate and fat, they do not 

 develop lesions. These workers attribute renal lesions to overloading 

 with salt; I choose protein. 



Talbot: Will you take this as evidence in favour of restricting the 

 protein intake of patients with handicapped renal function? 



Kennedy: I can see that it would be a dangerous thing to press a 

 trophic stimulus like a high protein intake too far in an attempt to get 

 recovery. Are you thinking of chronic renal disease, or a recovery from 

 acute damage? 



Talbot: Both. 



Kennedy : Purely from my own findings I would have said that I could 

 see no point in producing additional renal growth in trying to help 

 recovery of the kidney by giving a high protein diet; if the object was 

 simply to replace protein lost from the body then my results, of course, 

 are not relevant. I think the problem of a high protein intake has to be 

 studied from this point of view on the human, and we cannot answer 

 from the work on the rat. Moreover, there may be a totally different 

 limitation to the structural renal reserve in the rat, which has a kidney 

 of completely different anatomical character. 



Borst: We treat all patients with a kidney function of less than 10 per 

 cent of normal with a diet adequate in calories but very poor in protein 



