Contrast Medium‐Induced Nephrotoxicity: Pathophysiology and Prevention

Abstract

Contrast medium-induced nephrotoxicity (CMN) is a common form of iatrogenic acute renal failure. Typically, patients experience changes in serum creatinine or creatinine clearance between 1 and 5 days after exposure to a contrast medium, but they rarely require dialysis. The mechanism for CMN is not understood, but renal insufficiency, dehydration, and congestive heart failure are risk factors. The frequency of CMN with high-osmolality versus low-osmolality media is controversial. Prophylaxis can reduce CMN. Of many different strategies, hydration with normal saline before and after exposure offers the best protection with the fewest adverse effects.

Short- and long-term renal outcomes of immediate prophylactic hemodialysis after cardiovascular catheterizations in patients with severe renal insufficiency

“…The needs and strategies for prevention of CIN have been well received and studied. Multiple measures have been used to prevent or curtail the adverse renal effects of contrast medium use [14][15][16][17][18][19]. Basically, the amount of the very contrast agent should be tailored to and minimized in every patient to avoid unnecessary exposure.…”

“…Multiple measures have been used to prevent or curtail the adverse renal effects of contrast medium use, including adequate hydration, medullary vasodilators, theophylline and antioxidants, and achieved varying success [14][15][16][17][18][19]. However, there remain occasions when pre-catheterization preparation of patients could not be optimized and/or the contrast amount could not be reduced, such as in patients with severe ischemic cardiomyopathy, making post hoc measures to minimize radiocontrast-induced renal damage mandatory and imperative.…”

Fenoldopam and N‐acetylcysteine for the Prevention of Radiographic Contrast Material—Induced Nephropathy: A Review

“…The pathophysiology of RCIN is not well understood but is thought to be a result of direct toxicity and renal medullary ischemia ( Figure 1). [16][17][18][19][20][21] The direct toxic effects of contrast media are not well established but are thought to be due to production of oxygen free radicals, with vacuolization leading to intracellular breakage and tubular cell death. 19 The role of medullary ischemia is theorized to be the result of a combination of increased metabolic demand and decreased renal blood flow.…”

“…[4][5][6][7][8][9][10][11][12][13][14][15] The clinical course of RCIN is usually benign, with serum creatinine concentrations peaking at 3-5 days after contrast material administration and returning to normal within 7-10 days. 1,2,16,17 Most cases remain nonoliguric, but some may progress to complete renal failure.…”

Delicate Percutaneous Renal Artery Stenting Minimizes Postoperative Renal Injury and Protects Kidney in Patients With Severe Atherosclerotic Renal Artery Stenosis and Impaired Renal Function

“…As more knowledge is accumulating, the issue of CIN has been reduced to a certain extent. [9][10][11] Distal protection devices have been reported to reduce major events in coronary or carotid interventions, 12,13) and protected renal interventions are showing promise. 14,15) Thus, atheroembolism to distal renal beds could be an important issue, especially in long critical lesions with voluminous atheroma load.…”