الفهرس 
Anatomy and PhysiologyOnly 14 pages are availabe for public view
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Abstract
Occurrence of acute oliguric renal failure in the immediate postoperative period carries important morbidity and mortality after a successful cardiac surgical procedure. Adult cardiac and aortic surgical procedures are especially prone to this complication with the incidence varying between 2% to 15% and the mortality rate as high as 40% to 60%. Some of the factors that contribute to renal failure in the postoperative period are advanced age, preexisting renal insufficiency, preoperative left ventricular dysfunction, low cardiac output in the perioperative period, and performance of operations other than isolated CABG, prolonged aortic cross-clamp, and cardiopulmonary bypass time. Factors that have potential to adversely affect renal function in the postoperative period are fluid shifts with altered hemodynamics, atheroembolic disease, angiographic dyes, and use of medications such as antihypertensives and antibiotics. Acute renal failure may also ensue despite adequate cardiac and hemodynamic function in the postoperative period. In patients with adequate cardiac output, the onset of oliguria (urine volume < 0.5 mL/kg/hour) and rising serum potassium concentration (k > 5.3 meq/L) suggests an underlying intrinsic renal dysfunction, not related to the blood flow.
Many hemodynamic, inflammatory, and nephrotoxic factors are involved in the pathogenesis of the acute postoperative renal failure.
Cardiopulmonary bypass (CPB) is a physiological extreme causing hemodynamic instability and inflammatory stimulation. Clinical studies have identified numerous risk factors involved in CPB, which induce renal injury, and have demonstrated strategies for renal protection; however, there is not any single strategy for renal protection. Similar to any other organ, the main key in renal protection is manipulating the supply/demand equation, ie, decreasing demand in parallel with increasing kidney supply.
Many investigations have studied the factors possibly contributing to supply/demand equation. Therapies aimed at avoiding renal failure post-CPB all aim at maximizing cardiac output to avoid renal hypoperfusion. Most strategies intended to maximize renal blood flow in low output states probably increase RBF by increasing overall cardiac output.The use of diuretics may fit into this category. Vasodilators may preferentially relax the renal vasculature as a form of renal protection, but there is no good evidence that either calcium channel blockers or clonidine act in a specific manner. ANP analogues, however, do have specific effects on the kidney and may prove to be of great benefit in low output states.
Diuretics administration such as mannitol during CPB allows maintenance of the glomerular capillary pressure by preventing tubular obstruction. It also reduces the plasma levels of hydrogen peroxide free oxygen radicals, lowers the ischemia-associated protein leakage from renal vasculature, and prevents renal injury.