Pathophysiology and prevention of acute renal failure: the role of the anaesthetist

Abstract

Ischaemic renal tubular damage in the perioperative period can lead to acute renal failure (ARF) with a very high mortality rate (60-75 per cent). Recent research suggests that this tubular injury is caused by an imbalance of the oxygen supply and demand of medullary thick ascending limb (mTAL) tubular cells. High oxygen demand is secondary to active reabsorption of solute which is increased in states of intravascular volume depletion. The restricted supply of oxygen is secondary to the organization of blood flow to the inner medulla. Because the vasa recta loop into the inner medulla and a countercurrent exchange process for oxygen is established, the oxygen tension in this area may normally be as low as 10-20 mmHg. In hypoperfusion states, mTAL injury occurs and is exacerbated by intravascular volume depletion, hypoxaemia and endothelial cell swelling which reduces perfusion of these vulnerable and metabolically active mTAL cells. The anaesthetist must prevent or attenuate postoperative renal dysfunction by identifying high-risk patients preoperatively, optimizing intravascular volume status and cardiac output in the perioperative period, as well as responding appropriately to hypoperfusion states. Therapeutic implications relate to this pathophysiological sequence and several physiological and pharmacological considerations are discussed.