Chapter 11

Iodinated Contrast and Acute Kidney Injury

Steven D. Weisbord

Steven D. Weisbord

Renal Section and Center for Health Equity Research and Promotion, VA Pittsburgh Healthcare System and Renal Electrolyte Division, University of Pittsburgh School of Medicine, Pittsburgh, USA

Search for more papers by this author
Martin Gallagher

Martin Gallagher

Renal & Metabolic Division The George Institute for Global Health Newtown, NSW, Australia

Search for more papers by this author
First published: 18 November 2022

Summary

Acute kidney injury (AKI) is a widely recognized complication of intravascular administration of iodinated contrast media. The primary patient-related risk factor for contrast-associated acute kidney injury (CA-AKI) is underlying kidney impairment, while absolute and effective circulating volume also increases risk. The resulting mismatch in oxygen supply and demand in an anatomical portion of the kidney with low baseline oxygen reserve leads to ischemia of tubular epithelial cells. Historically, AKI following the administration of iodinated contrast media was referred to as contrast nephropathy or contrast-induced nephropathy. Identifying patients at heightened risk for CA-AKI allows for the consideration of alternative imaging procedures that do not necessitate intravascular contrast, but that provide comparable diagnostic information. Iodinated contrast media are commonly categorized based on their osmolality. Iodinated contrast media remain largely in the extracellular space, have low protein binding, and are highly water soluble. Hence, they can be efficiently removed from the circulation by renal replacement therapies.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.