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.

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