Untitled

Abstract

An increasing number of diagnostic imaging procedures requires the use of intravenous radiographic contrast agents, which has led to a parallel increase in the incidence of contrast-induced nephropathy. Risk factors for development of contrast-induced nephropathy include pre-existing renal dysfunction (especially diabetic nephropathy and multiple myeloma-associated nephropathy), dehydration, congestive heart failure and use of concurrent nephrotoxic medication (including aminoglycosides and amphotericin B). Because contrast-induced nephropathy accounts for a significant increase in hospital-acquired renal failure, several strategies to prevent contrast-induced nephropathy are currently advocated, including use of alternative imaging techniques (for which contrast media are not needed), use of (the lowest possible amount of) isoosmolar or low-osmolar contrast agents (instead of high-osmolar contrast agents), hyperhydration and forced diuresis. Administration of N-acetylcysteine, theophylline, or fenoldopam, sodium bicarbonate infusion, and periprocedural haemofiltration/haemodialysis have been investigated as preventive measures in recent years. This review addresses the literature on these newer strategies. Since only one (nonrandomized) study has been performed in intensive care unit patients, at present it is difficult to draw firm conclusions about preventive measures for contrast-induced nephropathy in the critically ill. Further studies are needed to determine the true role of these preventive measures in this group of patients who are at risk for contrast-induced nephropathy. Based on the available evidence, we advise administration of Nacetylcysteine, preferentially orally, or theophylline intravenously, next to hydration with bicarbonate solutions.

Differential Effects of N-Acetylcysteine, Theophylline or Bicarbonate on Contrast-Induced Rat Renal Vasoconstriction

“…direct application of vasodilators such as dopamine, ANP or ET1 antagonists, failed to exert appreciable renoprotective effects [23], thus calling for the search of alternative ways to ameliorate CIN. In a number of studies, augmentation of adenosine formation, and consequent excretion in urine evident after the CM administration, has been implicated in inducing sustained vasoconstriction of afferent arterioles and vasodilation of efferent arterioles, thus reducing renal glomerular filtration rate and developing renal ischemia [24,25,26,27]. Studies involving theophylline, a direct selective renal adenosine antagonist, demonstrated controversial results with respect to the renoprotective vasodilatory properties of the latter [25,26,27].…”