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Eur Heart J. 2012 Aug;33(16):2007-15. doi: 10.1093/eurheartj/ehr494. Epub 2012 Jan 19.

Contrast-induced kidney injury: mechanisms, risk factors, and prevention.

Author information

1
Institute of Physiology, Center for Cardiovascular Research, Charité-Universitätsmedizin Berlin, CCM, Hessische Str. 3-4, Berlin D-10115, Germany. erdmann.seeliger@charite.de

Abstract

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.

PMID:
22267241
DOI:
10.1093/eurheartj/ehr494
[Indexed for MEDLINE]

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