title: Reversible renal concentrating defect in shock.
abstract: The loss of renal concentrating power in haemorrhagic shock is reversible upon correction of the shock state. Shock resulting from acute hypovolaemia leads to the following sequence of events: (1) diminished renal blood-flow; (2) decreased superficial cortical nephron perfusion; (3) continued juxtamedullary nephron perfusion; (4) enhanced proximal reabsorption of Na, Cl, and H23; (5) decreased delivery of these ions to the ascending limb, which results in diminished hypertonicity of the medullary interstitium. This hypotonicity is worsened by the "washout" effect on the interstitial hypertonicity caused by continued perfusion of the juxtamedullary vasa recta which results in (6) diminished renal concentrating capacity due to elimination of medullary hypertonicity. Replenishing blood-loss and correcting the hypovolaemic state "regenerates" the hypertonic renal medullary interstitium by (a) diminishing proximal reabsorption and allowing presentation of greater quantities of Na and Cl to the ascending-limb "pump", (b) restoring superficial cortical nephron perfusion, thereby decreasing juxtamedullary perfusion and in this manner eliminating medullary "washout".
mesh_terms: D000818:Animals; D001803:Blood Transfusion; D001810:Blood Volume; D002713:Chlorine / Q000378:metabolism; D004285:Dogs; D005919:Glomerular Filtration Rate; D007511:Ischemia; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology*; D007671:Kidney Concentrating Ability; D007672:Kidney Cortex / Q000098:blood supply; D009399:Nephrons / Q000503:physiopathology; D009994:Osmolar Concentration; D012039:Regional Blood Flow; D012771:Shock, Hemorrhagic / Q000150:complications / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy / Q000652:urine; D012964:Sodium / Q000378:metabolism; D014867:Water / Q000378:metabolism
chemical_list: D014867:Water; D002713:Chlorine; D012964:Sodium