Kaysen G A, Myers B D
Clin Geriatr Med. 1985 Feb;1(1):207-22.
The aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
衰老的肾脏在质量和肾小球滤过率方面都会下降。这些变化可能全部或部分归因于动脉粥样硬化和高血压，它们会减少肾血流量。除了这些过程之外，或许与肾血管疾病无关的肾实质原发性丧失有关的是肾小球损伤和退化，这是随着年龄增长肾单位数量减少时肾小球灌注压适应性增加的结果。目前可获得的数据不允许我们区分这两种肾脏衰老的潜在机制。肾小球滤过率的下降进而导致肾脏酸化功能降低以及肾脏对通常由肾脏清除的药物的清除能力下降。然而，某些肾功能的下降程度比肾小球滤过率更大。最大程度稀释尿液和最大程度浓缩尿液的能力均受血清抗利尿激素（ADH）浓度以及该激素对集合管的作用控制。老年大鼠在脱水情况下不会最大程度地分泌抗利尿激素，并且抗利尿激素对肾脏的作用也会减弱。当血清渗透压降低时，老年人也无法最大程度地抑制抗利尿激素的分泌。同样，肾素 - 血管紧张素 - 醛固酮轴在老年受试者中对容量减少的反应较差。因此，在血浆容量收缩与肾小球滤过率降低不成比例的情况下，老年人无法最大程度地保留钠。肾脏是维生素D1羟化的场所。在大鼠中，维生素D的羟化降低程度与肾小球滤过率的任何降低不成比例。目前尚无关于衰老对促红细胞生成素（红细胞生成的主要调节因子）产生影响的数据。也没有关于随着年龄增长衰老肾脏代谢各种激素（如甲状旁腺激素、胰高血糖素和胰岛素）能力可能发生变化的数据。肾脏衰老的机制以及完整的生化和生理后果仍有待充分阐明。
