الفهرس 
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Abstract
Contrast Induced Nephropathy (CIN) is a feared complication of numerous radiological procedures that expose patients to contrast media (CM).
CIN is generally defined as a proportional rise of 25% in serum creatinine level or an absolute increase in serum creatinine level by 0.5 mg/dL from baseline, 48 hours after contrast exposure (Barrett and Parfrey, 1994, Barrett and Parfrey, 2006). CIN has no cure once it occurs, and treatments for the condition go mainly to supportive care. Fortunately, the timing of CM administration is often planned, which allows for the identification of patients at high risk for CIN, so that preventive measures can be undertaken. Most of the risk factors for CIN can be analyzed by pre-procedural history and physical and laboratory examination. It is known that pre-existing chronic kidney disease (CKD) is the most important risk factor for CIN, whereas pre-existing diabetes further enhancesthe risk (McCullough et al., 1997).
The overall incidence of CIN in the general population has been estimated to be as high as 16.5% (Parfrey, 2005). The figure is higher when CIN follows percutaneous coronary angiography (PCI). Not only it has been reported as a leading cause of morbidity and mortality in those patients, but CIN has also added to the costs in high risk patients undergoing PCI. In their retrospective analysis of the Mayo Clinic PCI registry, comprising 7586 patients, Rihal and colleagues found the incidence for general population undergoing PCI to be 12.8 % (Rihal et al., 2002).
Although the pathogenesis of CIN is not well understood, there is increasing evidence that it occurs as a combination of direct toxicity to the renal tubular epithelium, oxidative stress, ischemic injury, and renal tubular obstruction (Merten et al., 2004, Stacul et al., 2006). Also, increased intratubular pressure secondary to contrast-induced diuresis and increased perivascular hydrostatic pressure may lead to medullary hypoxia through lower medullary blood flow (Rudnick et al., 2006). Renal ischemia may be the result of an imbalance between vasoactive substances (Adenosine and Endothelin) and vasodilators (NO and Prostaglandins) (Recio-Mayoral et al., 2007).
Surprisingly, there is an utter paucity of studies on intra-renal hemodynamics among other risk factors for CIN. If it turns out that assessment of renal hemodynamics can contribute to stratification of risk of CIN then, this pilot investigation may pave the way to larger clinical studies that impact reducing the burden of CIN.