[Normal and pathological renal aging in animals].
Ageing of the kidneys has long been associated with a fall in the number of functioning nephrons resulting in a reduction of renal blood flow and glomerular filtration. This narrow concept of age-related changes in renal function has been developed chiefly during the last few years by Brenner et al. on the basis of experimental studies conducted on rodents. According to these authors, the size and frequency of segmental and focal lesions of glomerulosclerosis increase regularly with age, and in its final phase this pathology results in occlusion of glomerular capillaries. Renal ageing, therefore, can be assimilated to the nephron reduction models obtained by surgical ablation. The hypothesis that hypofiltration in certain nephrons is compensated by hyperfiltration in healthy glomerulis, leading to a vicious circle of self-destruction, was then applied to both ageing and experimental renal impairment: the smaller the number of nephrons, the greater the filtration achieved by the remaining nephrons, a process that accelerates the probability of their destruction. Conversely, any attempt to reduce intracapillary pressure or glomerular filtration slows down the progression of renal failure. This hypothesis is supported by experiments showing that reduction of protein intake or chronic inhibition of angiotensin I-converting enzyme activity are truly capable of limiting the progression of glomerulosclerosis induced in rats by partial renal mass ablation. Similarly, prolonged food restriction increases the life expectancy of rodents and almost totally prevents the occurrence of glomerulosclerosis. The experimental finding that degenerative renal lesions do not necessarily develop with age raises the problem of normal and pathological ageing. With an adequate choice of rats' food, strain and sanitary surroundings it is possible to obtain very old animals devoid of occluded glomerular capillaries and loss of nephron. What about the functional and structural changes due to ageing and not to pathology? This question has given rise to numerous studies which concluded, on the whole, that there exists a normal ageing of the kidneys without loss of nephron and that ageing is expressed by the fact that the kidneys have difficulties in adjusting themselves to disturbances in the inner environment. As regards renal functional reserve, response to the antidiuretic hormone in case of water restriction, or stimulation of the renin-angiotensin system in response to decrease of sodium intake, it is clear that the renal cells responsible for glomerular filtration, tubular transport or synthesis and release of peptidic hormones exhibit functional alterations that are age-related. The cellular and molecular mechanisms underlying these physiological changes are little known.(ABSTRACT TRUNCATED AT 400 WORDS)
Corman
B
B
Service de Biologie Cellulaire, Centre d'Etudes de Saclay, Gif-sur-Yvette.
D000375:Aging / Q000473:pathology / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D005919:Glomerular Filtration Rate / Q000502:physiology; D005923:Glomerulosclerosis, Focal Segmental / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006869:Hydronephrosis / Q000503:physiopathology; D006961:Hyperparathyroidism / Q000209:etiology / Q000378:metabolism; D007668:Kidney / Q000473:pathology / Q000502:physiology*; D007671:Kidney Concentrating Ability / Q000502:physiology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D009399:Nephrons / Q000473:pathology; D051381:Rats; D014667:Vasopressins / Q000097:blood / Q000502:physiology
D000806:Angiotensin-Converting Enzyme Inhibitors; D014667:Vasopressins
Vieillissement rénal normal et pathologique chez l'animal.