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Published on: April 18, 2013
Hemodynamic and tubular changes induced by contrast media
Antonella Caiazza1, Luigi Russo1, Massimo Sabbatini1
1Department of Surgery and Nephrology, University of Naples "Federico II", Via Sergio Pansini 5, 80131 Naples, Italy.
Insights
Contrast media can cause kidney injury (CI-AKI) through hemodynamic changes and tubular cell damage. Using low-osmolar contrast media is recommended, especially for high-risk patients, to mitigate CI-AKI risks.
Area of Science:
- Nephrology
- Radiology
- Pharmacology
Background:
- Contrast media administration is a frequent cause of acute kidney injury (AKI) in hospitalized patients.
- Contrast-induced AKI (CI-AKI) results from complex interactions affecting renal hemodynamics and tubular cell function.
- Understanding these mechanisms is crucial for preventing CI-AKI.
Purpose of the Study:
- To elucidate the pathophysiological mechanisms underlying contrast-induced acute kidney injury (CI-AKI).
- To highlight the role of contrast media properties and patient risk factors in CI-AKI development.
- To emphasize current guidelines for CI-AKI prevention.
Main Methods:
- Review of existing literature on contrast media nephrotoxicity.
- Analysis of the interplay between hemodynamic alterations and cellular damage.
- Examination of the impact of contrast media physicochemical properties.
Main Results:
- Contrast media induce intrarenal vasoconstriction, leading to ischemia and reduced glomerular filtration.
- Direct cytotoxicity causes tubular cell apoptosis, cast formation, and exacerbates ischemia.
- Renin-angiotensin system activation and reactive oxygen species (ROS) production intensify hypoxia and endothelial dysfunction.
Conclusions:
- Physiochemical properties of contrast media significantly influence CI-AKI incidence.
- Guidelines recommend iso-osmolar or low-osmolar contrast media over high-osmolar agents.
- Patient factors like age, comorbidities, and concomitant medications increase CI-AKI risk.
Abstract:
The incidence of acute kidney injury induced by contrast media (CI-AKI) is the third cause of AKI in hospitalized patients. Contrast media cause relevant alterations both in renal hemodynamics and in renal tubular cell function that lead to CI-AKI. The vasoconstriction of intrarenal vasculature is the main hemodynamic change induced by contrast media; the vasoconstriction is accompanied by a cascade of events leading to ischemia and reduction of glomerular filtration rate. Cytotoxicity of contrast media causes apoptosis of tubular cells with consequent formation of casts and worsening of ischemia. There is an interplay between the negative effects of contrast media on renal hemodynamics and on tubular cell function that leads to activation of renin-angiotensin system and increased production of reactive oxygen species (ROS) within the kidney. Production of ROS intensifies cellular hypoxia through endothelial dysfunction and alteration of mechanisms regulating tubular cells transport. The physiochemical characteristics of contrast media play a critical role in the incidence of CI-AKI. Guidelines suggest the use of either isoosmolar or low-osmolar contrast media rather than high-osmolar contrast media particularly in patients at increased risk of CI-AKI. Older age, presence of atherosclerosis, congestive heart failure, chronic renal disease, nephrotoxic drugs, and diuretics may multiply the risk of CI-AKI.
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