Mechanisms of defective hydroosmotic response in chronic renal failure

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.