Renal protective effect of metabolic therapy in patients with coronary artery disease and diabetes: from bench to bed side.
Coronary artery disease (CAD) is due to subintimal deposition of atheromatous plaques in large and medium-sized coronary arteries. Different risk factors have been identified such as hypertension, hypercholesterolemia, diabetes and smoking. Both hypertension and diabetes mellitus affect the same major target organs. The common hypertensive/diabetic target is the vascular tree, hence renal function is particularly exposed in these patients and often reduced by vascular injury. Consequently, renal protection is a major concern for patients with CAD and/or diabetes who are facing vascular or abdominal surgery, potential nephrotoxic treatment or contrast agents-induced nephropathy. Ischemia reperfusion injury (IRI) is also a common and important clinical cause of renal disease such as renal transplantation and following shock from any cause. Acute renal failure and chronic renal insufficiency are significant complications associated with prolonged warm ischemia (WI). The WI duration remains the most important factor governing the return of postoperative renal function in surgical procedure in which renal blood flow is interrupted. Beside traditional therapy, metabolic therapy is another approach for the treatment of myocardial ischemia at the cellular level itself, with agents that have the capacity to exert their action on the cell without affecting the hemodynamic condition. Such therapies could also be of major interest in the prevention of renal damage and limitation of long term effect of renal IRI, particularly for patients with reduced functional nephron mass. The absence of hemodynamic effect is useful in situations such as shock.
Thuillier
Raphael
R
Inserm, U927 Poitiers, Poitiers cedex, France.
Tillement
Jean Paul
JP
Hauet
Thierry
T
D058186:Acute Kidney Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D003324:Coronary Artery Disease / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000037:antagonists & inhibitors / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000098:blood supply / Q000378:metabolism; D018384:Oxidative Stress; D020011:Protective Agents / Q000627:therapeutic use*; D051436:Renal Insufficiency, Chronic / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D015427:Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D012307:Risk Factors; D014665:Vasodilator Agents / Q000627:therapeutic use*; D052096:Warm Ischemia / Q000009:adverse effects
D005230:Fatty Acids, Nonesterified; D020011:Protective Agents; D014665:Vasodilator Agents