Osorio F V, Teitelbaum I
Division of Nephrology and Hypertension, University of Colorado School of Medicine, USA.
J Nephrol. 1997 Sep-Oct;10(5):232-7.
The kidney's concentrating capacity is impaired in chronic renal failure (CRF) resulting in a relatively large rate of urine formation and nocturia. Normal renal concentrating ability depends on the maintenance of a hypertonic medullary interstitium, a structurally intact countercurrent multiplier system, and normal water permeability of the collecting tubules in response to arginine vasopressin (AVP). Each of these three components may be compromised in the setting of CRF. This review presents current knowledge regarding mechanisms of impaired renal concentrating ability in CRF, from the whole kidney level to the cellular and molecular level.
慢性肾衰竭（CRF）会损害肾脏的浓缩功能，导致尿量相对较多及夜尿症。正常的肾脏浓缩能力取决于高渗性髓质间质的维持、结构完整的逆流倍增系统以及集合管对精氨酸加压素（AVP）作出反应时的正常水通透性。在CRF情况下，这三个组成部分中的每一个都可能受到损害。本综述介绍了从全肾水平到细胞和分子水平有关CRF时肾脏浓缩能力受损机制的当前知识。
