Biochemical and Morphological Effects of Contrast Media on the Kidney

Dobrota, Miloslav; Powell, C.J.; Holtz, E.; Wallin, Anders; Vik, Hogne

doi:10.1177/0284185195036s39924

Cited by 33 publications

(22 citation statements)

References 30 publications

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“…27 For both, GBCAs and iodine-containing contrast agents, this phenomenon was shown to be due to the transient storage of the contrast agent, and no functionally significant impairment of tubular or cellular processes was associated. 28,29 Because in the studies with gadobutrol, a clear trend to complete reversibility was observed and renal function was not affected in any study and no cytotoxic or degenerative effects in cell organelles, including cell nuclei, could be detected upon inspection with electron microscopy, the vacuolization is not regarded as adverse.…”

Section: Discussionmentioning

confidence: 80%

Toxicological Safety Evaluation of Gadobutrol

Wack¹,

Steger‐Hartmann²,

Mylecraine³

et al. 2012

Investigative Radiology

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Section: Discussionmentioning

confidence: 80%

Toxicological Safety Evaluation of Gadobutrol

Wack¹,

Steger‐Hartmann²,

Mylecraine³

et al. 2012

Investigative Radiology

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“…The observed cytoplasmic vacuolation is believed to be due to uptake and retention of ICM in the cells, and this finding is in accordance with what is previously observed in in vitro and in vivo experiments. 26,31 The morphological observations indicated that the uptake into cells could be ranked in the following decreasing order: iodixanol > iohexol > iopromide > ioversol. The osmolality appears to play a role, with the iso-osmolal ICM (IOCM) being most extensively internalized followed by the three LOCM.…”

Section: Discussionmentioning

confidence: 99%

The Effects of the Iodinated X-Ray Contrast Media Iodixanol, Iohexol, Iopromide, and Ioversol on the Rat Kidney Epithelial Cell Line NRK 52-E

et al. 2011

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Nephrotoxicity, associated with the administration of iodinated X-ray contrast media (ICM), continues to be a major side effect in a significant number of vulnerable patients undergoing diagnostic X-ray imaging procedures. The molecular mechanisms underlying these adverse effects on the kidneys are unclear despite several decades of investigation. Side effects are more common after exposure to high-osmolar compared with low-osmolar ICM, suggesting that osmolality may be an important physical-chemical property related to nephrotoxicity. This investigation in cultured NRK 52-E cells, a cell line of renal origin, compares the in vitro toxicity of the iso-osmolal ICM iodixanol with the lowosmolal ICM iohexol, iopromide, and ioversol. The cellular toxicity was evaluated with the trypan blue exclusion assay, the MTT assay, and incidences of cell death. A qualitative assessment of vacuolation of the cultured NRK 52-E cells was taken as a measure of intracellular uptake of ICM. A difference in cell death incidence was observed between the iso-osmolal iodixanol and the low-osmolal iohexol, iopromide, and ioversol contrast media, with the isoosmolal iodixanol having the least effect in each of the in vitro systems tested. The osmolality of the contrast media appeared to be the major cause for the observed in vitro toxicity.

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“…Iodine was retained in the renal cortex [44] and the RCM was abundant in vacuoles 7 days [143, 144] and was still present 28 days [143] after administration, besides normal renal function [44, 144]. Thus, CI-AKI vacuoles are a consequence of RCM reabsorption.…”

Section: Characteristic Histopathological Changes In Ci-akimentioning

confidence: 99%

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Kiss

Hamar

2016

BioMed Research International

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Contrast-induced acute kidney injury (CI-AKI) can occur in 3–25% of patients receiving radiocontrast material (RCM) despite appropriate preventive measures. Often patients with an atherosclerotic vasculature have to receive large doses of RCM. Thus, animal studies to uncover the exact pathomechanism of CI-AKI are needed. Sensitive and specific histologic end-points are lacking; thus in the present review we summarize the histologic appearance of different rodent models of CI-AKI. Single injection of RCM causes overt renal damage only in rabbits. Rats and mice need an additional insult to the kidney to establish a clinically manifest CI-AKI. In this review we demonstrate that the concentrating ability of the kidney may be responsible for species differences in sensitivity to CI-AKI. The most commonly held theory about the pathomechanism of CI-AKI is tubular cell injury due to medullary hypoxia. Thus, the most common additional insult in rats and mice is some kind of ischemia. The histologic appearance is tubular epithelial cell (TEC) damage; however severe TEC damage is only seen if RCM is combined by additional ischemia. TEC vacuolization is the first sign of CI-AKI, as it is a consequence of RCM pinocytosis and lysosomal fusion; however it is not sensitive as it does not correlate with renal function and is not specific as other forms of TEC damage also cause vacuolization. In conclusion, histopathology alone is insufficient and functional parameters and molecular biomarkers are needed to closely monitor CI-AKI in rodent experiments.

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Biochemical and Morphological Effects of Contrast Media on the Kidney

Cited by 33 publications

References 30 publications

Toxicological Safety Evaluation of Gadobutrol

Toxicological Safety Evaluation of Gadobutrol

The Effects of the Iodinated X-Ray Contrast Media Iodixanol, Iohexol, Iopromide, and Ioversol on the Rat Kidney Epithelial Cell Line NRK 52-E

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

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