Contrast-induced kidney injury: Mechanisms, risk factors, and prevention

Erdmann Seeliger, Mauricio Sendeski, Charanjit S. Rihal, Pontus B. Persson

Research output: Contribution to journalReview articlepeer-review

303 Scopus citations


In general, iodinated contrast media (CM) are tolerated well, and CM use is steadily increasing. Acute kidney injury is the leading life-threatening side effect of CM. Here, we highlight endpoints used to assess CM-induced acute kidney injury (CIAKI), CM types, risk factors, and CIAKI prevention. Moreover, we put forward a unifying theory as to how CIAKI comes about; the kidney medulla's unique hyperosmolar environment concentrates CM in the tubules and vasculature. Highly concentrated CM in the tubules and vessels increases fluid viscosity. Thus, flow through medullary tubules and vessels decreases. Reducing the flow rate will increase the contact time of cytotoxic CM with the tubular epithelial cells and vascular endothelium, and thereby damage cells and generate oxygen radicals. As a result, medullary vasoconstriction takes place, causing hypoxia. Moreover, the glomerular filtration rate declines due to congestion of highly viscous tubular fluid. Effective prevention aims at reducing the medullary concentration of CM, thereby diminishing fluid viscosity. This is achieved by generous hydration using isotonic electrolyte solutions. Even forced diuresis may prove efficient if accompanied by adequate volume supplementation. Limiting the CM dose is the most effective measure to diminish fluid viscosity and to reduce cytotoxic effects.

Original languageEnglish (US)
Pages (from-to)2007-2015
Number of pages9
JournalEuropean heart journal
Issue number16
StatePublished - Aug 2012


  • Acute kidney injury
  • Iodinated contrast media
  • Pathophysiology
  • Prevention

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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