Berl Tomas
University of Colorado at Denver and Health Sciences Center, 4200 East Ninth Avenue, Box C281, Denver, CO 80262, USA.
J Am Soc Nephrol. 2008 Jun;19(6):1076-8. doi: 10.1681/ASN.2007091042. Epub 2008 Mar 12.
It is classically taught that when renal function is normal and the secretion of antidiuretic hormone (arginine vasopressin) is fully suppressed, the human kidney has the capacity to excrete large volumes of dilute urine, allowing for a broad range of water intake. This flexibility protects against the development of hyponatremia even in the face of water intake that can approach 20 L/d. What is not as widely recognized is the impact that alterations in solute intake, and therefore excretion, have on this process. As will be illustrated here, a decrement in solute intake markedly reduces the above-mentioned flexibility and puts the individual at risk for the unexpected development of hyponatremia. In contrast, an increment in solute intake can be used therapeutically to treat this electrolyte disorder and allow those prone to it to liberalize their water intake.
传统观点认为,当肾功能正常且抗利尿激素(精氨酸加压素)的分泌被完全抑制时,人类肾脏有能力排出大量稀释尿液,从而适应广泛的水摄入量。这种灵活性可防止低钠血症的发生,即使面对每日饮水量接近20升的情况。但溶质摄入量以及排泄量的改变对这一过程的影响却未得到广泛认可。如下文所示,溶质摄入量的减少会显著降低上述灵活性,并使个体面临意外发生低钠血症的风险。相反,增加溶质摄入量可用于治疗这种电解质紊乱,并使易患低钠血症的人能够增加饮水量。