Contrast media-induced nephrotoxicity--questions and answers.

Abstract

The intravascular administration of contrast media (CM) can produce acute haemodynamic changes in the kidney characterized by an increase in renal vascular resistance and a decrease in the glomerular filtration rate (GFR). These changes may lead to clinically significant reduction in renal function in patients with pre-existing risk factors such as diabetic nephropathy, congestive heart failure and dehydration. The pathophysiology of the renal haemodynamic effects of CM involves activation of the tubuloglomerular feedback (TGF) mechanism and the modulation of the intrarenal production of vasoactive mediators such as prostaglandins, nitric oxide, endothelin and adenosine. The TGF response is osmolality-dependent and accounts for about 50% of the acute functional effects of high osmolar CM on the kidney. Reduction in the synthesis of the endogenous vasodilators nitric oxide and prostaglandins increases the nephrotoxicity of CM. Endothelin and adenosine play a crucial role in mediating the acute functional effects of CM. Antagonists of these mediators attenuate the reduction in renal function induced by contrast agents. Vacuolization of the cells of the proximal tubules and necrosis of those of the medullary ascending limbs of loops of Henle are the main structural effects of CM in the kidney. The reduction in renal function induced by CM could be minimized by the use of low osmolar CM and adequate hydration. The prophylactic administration of calcium channel blockers and adenosine antagonists such as theophylline may also offer some protective effect.

Gadolinium contrast media are more nephrotoxic than a low osmolar iodine medium employing doses with equal x-ray attenuation in renal arteriography: An experimental study in pigs1

“…This may result in marked shrinkage and rigidification of red blood cells obstructing microcirculation (49 -51) and vascular endothelial injuries resulting in thrombotic occlusions (52,53). A nonosmolality-dependent release of vasoconstrictors has also been postulated (1). A direct toxic effect on tubular cells might also be possible (54).…”

“…All hypertonic solutions significantly increased elimination half-life, increasing with the osmolality of the agents. Apart from the direct exposure of red blood cells, endothelial cells, and tubular cells to the hypertonic solutions injected into the renal artery, the CM also represent an osmotic load to the kidneys with secondary diuresis and natriuresis (1,55,56). Osmotic load may activate the tubuloglomerular feedback mechanism mediating vasoconstrictive agents, increase medullary oxygen demand for active reabsorption of the increased tubular sodium load resulting in hypoxic injuries, or increase intratubular pressure with elevation of interstitial pressure and secondary vascular compression beneath the rigid renal capsula.…”

“…The risk of contrast medium nephropathy (CMN) induced by iodine contrast media (I-CM) has been recognized for many years in patients with preexisting renal insufficiency, especially in combination with diabetes mellitus (1). The use of low-osmolar instead of high-osmolar I-CM has reduced this risk (2,3).…”

New guidelines on the use of iodinated contrast media: a report on an implementation project

“…In the case of elective outpatients at risk for ICM-induced nephropathy, the test will be repeated at a date closer to the examination. Furthermore, we believe that another refresher course on the subject, scheduled for 2009 for both physicians and nurses in our area, may be more effective than sending out formal and informal reminders for them to fill in the patient history/ [27]). A tal proposito screening sheet completely (including GFR calculation).our population.…”

“…This is particularly true in the elderly (renal function decreases "physiologically" by 1 ml/min per year after the age of 20-30 years [26]) and in subjects with vascular disease or undergoing treatment with nephrotoxic agents (such as chemotherapy). On the other hand, it is important to minimise the risk of renal impairment due to the imprudent use of contrast media (ICM-induced nephrotoxicity is reported to be the third leading cause of acute renal failure in a hospital setting [27]). For these reasons, we believe the protocol should necessarily involve the nephrologist for patients at risk.…”