Contrast-Induced nephropathy: Pathophysiology, risk factors, and prevention

Abstract

Contrast-induced acute kidney injury is a common iatrogenic complication associated with increased health resource utilization and adverse outcomes, including short- and long-term mortality and accelerated progression of preexisting renal insufficiency. The incidence of contrast-induced nephropathy (CIN) has been reported to range from 0% to 24%. This wide range reported by the studies is due to differences in definition, background risk factors, type and dose of contrast medium used, and the frequency of other coexisting potential causes of acute renal failure. CIN is usually transient, with serum creatinine levels peaking at 2-3 days after administration of contrast medium and returning to baseline within 7-10 days after administration. Multiple studies have been conducted using variety of therapeutic interventions in an attempt to prevent CIN. Of these, careful selection of patients, using newer radiocontrast agents, maintenance of hydration status, and avoiding nephrotoxic agents pre- and post-procedure are the most effective interventions to protect against CIN. This review focuses on the basic concepts of CIN and summarizes our recent understanding of its pathophysiology. In addition, this article provides practical recommendations with respect to CIN prevention and management.

Meta-analysis on allopurinol preventive intervention on contrast-induced acute kidney injury with random controlled trials

“…Patients undergoing a contrast procedure, especially those with risk factors such as chronic kidney disease, accompanying with hypotension, contrast medium volume, congestive heart failure, aging, diabetes mellitus, and cardiovascular disease would be risky to develop mild to serious complications. [21,22] In this meta-analysis, it was found that the administration of periprocedural allopurinol could cause reduction in the incidence of CI-AKI in patients undergoing interventional procedures (RR 0.39, 95% confidence interval[CI] 0.20,0.74, P = .004; Fig. 3) which leading to a significantly lower level of Scr and BUN (SMD -0.50, 95% CI −0.79,−0.21, P = .0009; SMD −0.40, 95% CI −0.60,−0.20, P < .0001; respectively).…”

Prophylaxis of Contrast-Induced Nephropathy in Intravascular Contrast Computed Tomography Procedures by Use of Low Osmolality Contrast Media and Good Hydration

“…The post-CT oral hydration can easily be done at home and monitored by the patient's family. Third, previous studies [28][29][30] investigated CIN by estimated glomerular filtration rate (eGFR), whereas the current study could not test the eGFR pre-and post-CT. Thus, further studies of outpatients and high-risk groups in Gaza Strip-Palestine are necessary.…”

Comparison of acute kidney injury with radial vs. femoral access for patients undergoing coronary catheterization: An updated meta‑analysis of 46,816&nbsp;patients

“…Patient characteristics, including old age, hypotension, diabetes mellitus, pre-existing renal impairment, history of renal transplantation, anemia and use of nephrotoxic drugs are known to significantly increase the risk of post-procedural AKI. Similarly, procedural factors, including contrast media properties, contrast media volume and number of procedures within 72 h also influence the probability of AKI ( 2 , 3 ).…”

“…The incidence of AKI following the use of contrast media has been reported to be 0-24% ( 2 ). Although in most cases, AKI is transient, irreversible renal injury may occur in a proportion of patients, leading to progressive kidney damage, which may require prolonged hospitalization and result in long-term adverse effects ( 4 ).…”