The effect of contrast media on the aortic endothelium of rats.

Gospos, Christian; Freudenberg, Nikolaus; Staubesand, J.; Mathias, K; Papacharlampos, X

doi:10.1148/radiology.147.3.6844605

Cited by 32 publications

(14 citation statements)

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“…The use of LOCM rather than HOCM reduces nephrotoxicity in patients with renal failure. Therefore, HOCM are used less frequently 2,3…”

Section: Iodinated Contrast Drugsmentioning

confidence: 99%

“…The damage to endothelial cells has been studied by scanning electron microscopy that allowed visualization of cell shrinkage, fenestration of the endothelial layer, and formation of microvilli (blebbing) on the cell membrane, nuclear protrusion, and cellular apoptosis 2. Damaged and apoptotic endothelial cells reduce the release of NO in the medullary vasa recta 54,56,57…”

Section: Contrast-induced Acute Kidney Injurymentioning

confidence: 99%

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Update on the renal toxicity of iodinated contrast drugs used in clinical medicine

Andreucci¹,

Faga²,

Serra

et al. 2017

DHPS

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An important side effect of diagnostic contrast drugs is contrast-induced acute kidney injury (CI-AKI; a sudden decrease in renal function) occurring 48–72 hours after injection of a contrast drug that cannot be attributed to other causes. Its existence has recently been challenged, because of some retrospective studies in which the incidence of AKI was not different between subjects who received a contrast drug and those who did not, even using propensity score matching to prevent selection bias. For some authors, only patients with estimated glomerular filtration rate <30 mL/min/1.73 m2 are at significant risk of CI-AKI. Most agree that when renal function is normal, there is no CI-AKI risk. Many experimental studies, however, are in favor of the existence of CI-AKI. Contrast drugs have been shown to cause the following changes: renal vasoconstriction, resulting in a rise in intrarenal resistance (decrease in renal blood flow and glomerular filtration rate and medullary hypoxia); epithelial vacuolization and dilatation and necrosis of proximal tubules; potentiation of angiotensin II effects, reducing nitric oxide (NO) and causing direct constriction of descending vasa recta, leading to formation of reactive oxygen species in isolated descending vasa recta of rats microperfused with a solution of iodixanol; increasing active sodium reabsorption in the thick ascending limbs of Henle’s loop (increasing O2 demand and consequently medullary hypoxia); direct cytotoxic effects on endothelial and tubular epithelial cells (decrease in release of NO in vasa recta); and reducing cell survival, due to decreased activation of Akt and ERK1/2, kinases involved in cell survival/proliferation. Prevention is mainly based on extracellular volume expansion, statins, and N-acetylcysteine; conflicting results have been obtained with nebivolol, furosemide, calcium-channel blockers, theophylline, and hemodialysis.

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“…The use of LOCM rather than HOCM reduces nephrotoxicity in patients with renal failure. Therefore, HOCM are used less frequently 2,3…”

Section: Iodinated Contrast Drugsmentioning

confidence: 99%

Section: Contrast-induced Acute Kidney Injurymentioning

confidence: 99%

Update on the renal toxicity of iodinated contrast drugs used in clinical medicine

Andreucci¹,

Faga²,

Serra

et al. 2017

DHPS

View full text Add to dashboard Cite

show abstract

“…The endothelial cells are the first to come in contact with intravenously injected RCM [25]. Direct endothelial cell damage was observed by electron microscopy in rat aortic endothelial cells [153]. Endothelial damage in peritubular capillaries by RCM directly or through ROS can be an important driving force of the medullary hypoxia.…”

Section: Further Pathological Markers Of 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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“…Endothelial damage, including nuclear protrusion, cell shrinkage, fenestration of the endothelial layer, and formation of microvilli (“blebbing”) on the cell membrane, and cellular apoptosis have been observed by scanning electron microscopy [38]. Endothelial damage may also release endothelin and hence lead to vasoconstriction.…”

Section: Pathogenesismentioning

confidence: 99%

Acute Kidney Injury by Radiographic Contrast Media: Pathogenesis and Prevention

Andreucci

Faga

Pisani

et al. 2014

BioMed Research International

107

112

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It is well known that iodinated radiographic contrast media may cause kidney dysfunction, particularly in patients with preexisting renal impairment associated with diabetes. This dysfunction, when severe, will cause acute renal failure (ARF). We may define contrast-induced Acute Kidney Injury (AKI) as ARF occurring within 24–72 hrs after the intravascular injection of iodinated radiographic contrast media that cannot be attributed to other causes. The mechanisms underlying contrast media nephrotoxicity have not been fully elucidated and may be due to several factors, including renal ischaemia, particularly in the renal medulla, the formation of reactive oxygen species (ROS), reduction of nitric oxide (NO) production, and tubular epithelial and vascular endothelial injury. However, contrast-induced AKI can be prevented, but in order to do so, we need to know the risk factors. We have reviewed the risk factors for contrast-induced AKI and measures for its prevention, providing a long list of references enabling readers to deeply evaluate them both.

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The effect of contrast media on the aortic endothelium of rats.

Cited by 32 publications

References 0 publications

Update on the renal toxicity of iodinated contrast drugs used in clinical medicine

Update on the renal toxicity of iodinated contrast drugs used in clinical medicine

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Acute Kidney Injury by Radiographic Contrast Media: Pathogenesis and Prevention

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