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 stales, 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.
Résumé
L’ischémie tubulaire rénale dans la période périopératoire peut aboutir à une insuffisance rénale aigue et un taux de mortalité élevé (60–75 pour cent). Les recherches récentes suggèrent que cette lésion tubulaire soil due à un déséquilibre de la demande et de l’apport d’oxygène dans la région médullaire des cellules du tube ascendant (mTAL). La forte demande d’oxygène est secondaire à la réabsortion active de soluté qui est augmentée dans les états d’hypovolémie. L’apport restreint en oxygène est secondaire à l’organisation du flot sanguin dans la médullaire interne. A cause de l’organisation de la vasa recta dans la médullaire interne et du contrecourant, la tension d’oxygène dans cette région peut atteindre normalement des valeurs aussi basses que 10–20 mmHg. Dans les états d’hypoperfusion, des lesions du mTAL surviennent et sont exagérées par l’hypovolémie, l’hypoxémie et l’œdème cellulaire endothélial qui réduit la perfusion de ces cellules vulnérables et mébaboliquement actives. L’anesthésiste doit prévenir on atténuer la dysfonction rénale postopératoire en identifiant les patients à haul risque en periode préopératoire, en optimalisant le volume intravasculaire et le débit cardiaque en période périopératoire et en répondant adéquatement lors des états de bas débit. Les applications thérapeutiques reliées aux conséquences pathophvsiologiques et plusieurs considérations physiologiques et pharmacologiques sont discutées.
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Byrick, R.J., Rose, D.K. Pathophysiology and prevention of acute renal failure: the role of the anaesthetist. Can J Anaesth 37, 457–467 (1990). https://doi.org/10.1007/BF03005627
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DOI: https://doi.org/10.1007/BF03005627