الفهرس 
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Abstract
The kidney is a remarkable organ whose functions include maintaining fluid and electrolyte balance, excreting metabolic waste products, and controlling vascular tone. Blood flow within the kidney is very heterogeneous, which places the metabolically active medulla at high risk for ischemic injury. A number of mediators play a role in the modulation of renal blood flow, including angiotensin II, dopamine, vasopressin, prostaglandins, atrial natriuretic peptide, endothelin, and nitric oxide. Early markers of renal injury elicit strong interest, although currently there is no reliable marker available.
Surgery causes the release of catecholamines, renin- angiotensin that lead to a redistribution of renal blood flow and a decrease in GFR. Additionally, general anesthesia often results in some degree of hypotension and depressed cardiac output, which further reduces renal perfusion and potentially jeopardizes renal function. A careful anesthetic plan is imperative in the patient with renal insufficiency or failure because acute renal failure in the perioperative period is associated with a high morbidity and mortality.
Factors including advanced age, diabetes, underlying renal insufficiency, and heart failure place a patient at high risk for developing acute renal failure. It is imperative to maintain euvolemia, normotension, and cardiac output, and to avoid nephrotoxic agents to optimize renal blood flow and renal perfusion as the best prevention of renal dysfunction.
However, various pharmacological agents have been used for renal protection including: dopamine, fenoldopam, diuretics, calcium channel blockers, natriuretic peptides, prostaglandins, adenosine antagonists, antioxidants and others. Pharmacological interventions mostly consisted of different pharmaceutical agents but there had been much debate on their use (Zacharias et al., 2005).