Andreucci V E, Russo D, Cianciaruso B, Andreucci M
Chair of Nephrology, Faculty of Medicine, University Federico II of Naples, Italy.
Nephrol Dial Transplant. 1996;11 Suppl 9:9-17. doi: 10.1093/ndt/11.supp9.9.
Creatinine clearance decreases with age by 1 ml/min/year after 40 years of age, although serum creatinine remains constant because of reduction of muscle mass. Reduction of water intake may occur in the elderly because of a reduced sensation of thirst; this is associated with a tendency to lose water with urine. The capacity to respond to sodium load is impaired in aged kidneys, thereby leading to ECV expansion and hypertension. But there is also, in the elderly, a reduced capacity for retaining sodium (FENa is higher than in young subjects), making old subjects sensitive to salt depletion and ECV contraction. Hypernatraemia (Nas > 150 mmol/l) is not infrequent in the elderly (1%) and is usually due to water deficiency (old subjects should be forced to drink), and rarely to iatrogenic excess of sodium. It is the abrupt occurrence of severe hypernatraemia that causes neurological symptoms due to dehydration and brain shrinking, which may lead to cerebral haemorrhage and death. Hyponatraemia (Nas < 130 mmol/l) is frequent among the elderly (7-11%) and is mainly due to water overload, which is usually iatrogenic. Hypovolaemic hyponatraemia occurs when salt depletion causes ECV contraction > 10%, and is due to water retention in an attempt to normalize ECV. Hypervolaemic hyponatraemia is due to ADH hypersecretion because of a decrease in 'effective' circulating blood volume. 'Pseudohyponatraemia' may occur because of hyperlipidaemia or hyperproteinaemia. It is the abrupt occurrence of severe hyponatraemia that causes neurological symptoms (water intoxication), secondary to the oedomatous swelling of the brain within the skull. While rapidly occurring hyponatraemia may be lethal, slowly occurring hyponatraemia is usually asymptomatic. Rapid correction of hyponatraemia may cause cerebral dehydration and 'osmotic demyelination syndrome' ('central pontine myelinosis'). Decrease (e.g. by diuretics) or increase (e.g. by ACE-inhibitors, non-steroidal anti-inflammatory drugs, beta-blockers) or serum potassium may occur in the elderly. Diuretics should be used with caution in elderly subjects to avoid salt depletion, hypotension and renal function impairment.
40岁以后,肌酐清除率随年龄增长每年下降1ml/分钟,尽管由于肌肉量减少血清肌酐保持不变。老年人可能因口渴感降低而减少水的摄入量;这与尿液失水倾向有关。老年肾脏对钠负荷的反应能力受损,从而导致有效循环血量增加和高血压。但老年人保留钠的能力也下降(老年受试者的滤过钠排泄分数高于年轻受试者),使老年受试者对盐缺乏和有效循环血量减少敏感。高钠血症(血钠>150mmol/L)在老年人中并不少见(1%),通常是由于缺水(应强迫老年受试者饮水),很少是医源性钠摄入过多。严重高钠血症的突然发生会因脱水和脑萎缩导致神经症状,这可能导致脑出血和死亡。低钠血症(血钠<130mmol/L)在老年人中很常见(7-11%),主要是由于水负荷过多,通常是医源性的。当盐缺乏导致有效循环血量减少>10%时发生低血容量性低钠血症,这是由于机体试图通过水潴留使有效循环血量正常化。高血容量性低钠血症是由于“有效”循环血量减少导致抗利尿激素分泌过多。“假性低钠血症”可能由于高脂血症或高蛋白血症而发生。严重低钠血症的突然发生会导致神经症状(水中毒),继发于颅骨内脑的水肿性肿胀。虽然快速发生的低钠血症可能致命,但缓慢发生的低钠血症通常无症状。快速纠正低钠血症可能导致脑脱水和“渗透性脱髓鞘综合征”(“中枢性脑桥髓鞘溶解症”)。老年人的血清钾可能降低(如使用利尿剂)或升高(如使用血管紧张素转换酶抑制剂、非甾体抗炎药、β受体阻滞剂)。在老年受试者中应谨慎使用利尿剂,以避免盐缺乏、低血压和肾功能损害。