Renal protection during surgical stress.

Abstract

It is important to analyze certain aspects of the pathophysiology of renal failure during the perioperative period, and based on the explored mechanisms, suggest particular preventive and therapeutic maneuvers. In most instances pertinent to surgery, acute renal failure is a response of the kidney to an acute ischemic insult secondary to hypotension, hypovolemia, and/or dehydration. Contraction of blood volume and cardiac failure both cause renal vasoconstriction and a decrease in renal blood flow whether there is a concomitant decrease in blood pressure or not. Renal hypoperfusion can occur despite normal or even increased cardiac output. Renal vasoconstriction apparently develops as a result of the different effects of humoral factors which may switch the available cardiac output from the kidneys to other organs. Renal Blood and Oxygen Supply. At rest, about 20% of cardiac output, or about 1 L.min-1, flows through the kidneys, although oxygen consumption usually does not exceed 10% of total body oxygen uptake. This phenomenon leads to a very low arteriovenous oxygen content difference (1.5 m102.dl.') but is confined to the cortex which receives a blood flow of about 5 ml.min".g". On the other hand, the medulla receives only 6% of total renal blood flow and has a flow rate of approximately 0.03 m1.min'I.g.' which is considerably less than any other tissue in the body. If we compare the ratio of oxygen uptake to oxygen delivery in different tissues, the lowest in the body would be in the total kidney, 1810, while the highest would be in the outer medulla, 79%.1. As a result of this heterogeneous circulation, p0, in the cortex of the kidney is around 50mmHg while in the inner medulla, it equals only 8 mmHg. There is convincing experimental evidence that the medullary thick ascending limb of Henle's loop (mTAL) is selectively vulnerable to hypoxic injury. Renal Oxygen SupplylDemand Relationship. The inhibition of cell transport activity with furosemide or an abolishing of the glomerular filtration (using a hyperoncotic non-filtering mode) can protect the mTAL in the isolated hypoperfused kidney. This and other observations suggest the concept that oxygen deprivation is related not only to its supply but also to its demand. The concept is very familiar to us since it is applied to the myocardium. The medulla may exhibit a sort of anginal syndrome in which the degree of cellular hypoxia depends on the oxygen supply/ demand relationship.' The concept of oxygen supply-demand relationship has important implications for the understanding of ischemic mTAL damage. The complete cessation of blood flow abolishes glomerular filtration and thus tends to protect the mTAL and prevent the full expression of mTAL injury that would have been produced by hypoperfusion. We can view the reduction of cortical flow during hypoperfusion as being designed to prevent medulla ischemia directly by increasing oxygen delivery and indirectly by decreasing oxygen demand for solute reabsorption as glomerular filtration rate decreases. Thus, a decreased glomerular filtration reduced the oxygen consumption of mTAL cells and might help preserve tubular integrity at the cost of retaining nitrogenous wastes.