AGE AND RENAL DISEASE 



G. C. Kennedy 



Medical Research Council, Department of Experimental Medicine, 

 University of Cambridge 



Introduction 



Senescence has sometimes been described as a deteriora- 

 tion in homeostasis. Dr. Shock showed us that the deteriora- 

 tion may be due to faihng renal function, and this reopens an 

 old question of whether the kidney cells themselves are less 

 able to do their work in old people, or whether diseases of the 

 kidney become more frequent with advancing age. It seems 

 generally agreed that pathological lesions, particularly of the 

 renal vessels, are very commonly found post mortem in old 

 people in whom they were unsuspected during life. Oliver 

 (1942) reviewed the controversy as to whether these lesions 

 originate from a primary atrophy of the kidney, or are merely 

 one of the results of generalized arteriosclerosis. He decided 

 in favour of arteriosclerosis. The other view, that the kidney 

 dies piecemeal, will be re-examined here because it seems 

 possible to show that the death of some nephrons leads to 

 pathological changes in the survivors, and some indirect 

 ways in which this may happen will be suggested. 



One can raise objections to any theory of ageing. The 

 major defect of the definition in terms of homeostasis, it seems 

 to the present author, is that the newborn animal finds it just 

 as difficult to maintain a stable internal environment under 

 stress as does the senile one. An older definition by Minot 

 (1908), in more structural terms, described senescence as the 

 gradual loss by differentiated cells, throughout life, of the 

 ability to grow and to regenerate. This idea applies especially 

 well to the kidney, as we shall see. 



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