Contrast Medium–induced Nephrotoxicity: Which Pathway?

Katzberg, Richard W.

doi:10.1148/radiol.2353041865

Cited by 73 publications

(49 citation statements)

References 37 publications

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“…Recently, studies have shown that renal ischemia, direct toxicity to renal tubular epithelium cells, oxidative stress, and tubular obstruction are considerably linked to the pathogenesis of CIN. 8,9 Changes in renal hemodynamics are implicated in animal models due to the effects of contrast media on the action of many substances, including dopamine-1, adenosine, angiotensin II (Ang II), nitric oxide, and endothelin. [10][11][12][13] Our previous studies have indicated that serum ACE is a sensitive parameter for the early assessment of CIN, and renal Ang II might play a role in renal tubular cell apoptosis induced by contrast media.…”

Section: Introductionmentioning

confidence: 99%

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

et al. 2012

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Objective: The objective of this study is to evaluate the effect and mechanism of aging on iodinated-contrast-mediainduced nephropathy in male rats. Methods: Twenty-four healthy male rats were initially divided into 12-month-old and 24-month-old age groups (adult and older age groups, respectively; n ¼ 12/group); subsequently, each age group was randomly divided into saline control (NS) and contrast media (CM) groups (n ¼ 6/group). CM (76% diatrizoate, 10 mL/kg b.w.) was given through the caudal vein. Urinary creatinine (Ucr) and serum creatinine (Scr) were detected by an automatic biochemical analyzer. The activities of renal malondialdehyde (MDA), superoxide dismutase (SOD), angiotensinconverting enzyme (ACE), angiotensin II (Ang II), and reduced form of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) were determined by spectrophotometric assays with commercially available kits according to the manufacturers' protocols. Renal histological changes were observed by hematoxylin and eosin staining and scored semiquantitatively. Results: In diatrizoate-injected aged rats, Scr, the activities of ACE, Ang II, MDA, and NADPH oxidase in renal tissues were significantly increased (p < 0.01). The histologic scores were higher in the aged animals with CM treatment than those of control or adult rats (p < 0.01). There was an increasing trend but no significant statistical difference in renal ACE, Ang II, MDA, and NADPH oxidase or histologic scores in adult CM-injected rats compared with control animals (p > 0.05). Conclusions: Older age is an aggravating factor of iodinated-contrast-media-induced nephropathy in male rats. Oxidative stress and the renin-angiotensin system (RAS) may play an important role in nephrotoxicity induced by iodinated contrast media, especially in aged male rats.

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Section: Introductionmentioning

confidence: 99%

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

et al. 2012

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“…Therefore, the early diagnosis of CI-AKI is critical for prevention (13). It is generally accepted that the pivotal reason for causing CI-AKI is renal medulla hypoxic (14), which is initiated by three different ways: Contrast agent-induced hemodynamic changes, oxygen free radical damage and a direct toxic effect to renal tubular disease (15). KIM-1 is a transmembrane glycoprotein located in the membrane of renal proximal tubule epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Urinary kidney injury molecule-1 as an early indicator to predict contrast-induced acute kidney injury in patients with diabetes mellitus undergoing percutaneous coronary intervention

et al. 2015

Biomedical Reports

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Abstract. With the improvement of the skill level of coronary intervention, contrast agents are used more widely. As a result, contrast-induced acute kidney injury (CI-AKI) is currently the third leading cause of hospital-acquired AKI. Traditionally, AKI is defined by measuring an increase of the serum creatinine concentration (Scr). CI-AKI indicates impairment in renal function, which is diagnosed as an elevation in the SCr levels following intravascular injection of the contrast media. However, Scr is an insensitive indicator for detecting CI-AKI. The present study was designed to investigate whether human urinary kidney injury molecule-1 (KIM-1) is an early marker to predict CI-AKI in patients with diabetes mellitus undergoing percutaneous coronary intervention (PCI). The present study includes the general clinical data of 145 patients with diabetes mellitus who underwent PCI between March 1, 2013 and December 31, 2013. A non-ionic, low osmolarity contrast agent was used during the present study. The Scr levels and estimated glomerular filtration rate were measured prior to and within 24 and 48 h after the injection of contrast agents. Urinary samples were collected prior to and within 2, 6, 12, 24 and 48 h after the coronary interventional procedure. Simultaneously, the urinary KIM-1 values were measured using an ELISA kit. CI-AKI was diagnosed as an increase of ≥0.5 mg/dl or ≥25% in Scr concentration over baseline, 24-48 h after the procedure. In total, 19 of 145 (13.1%) patients exhibited CI-AKI. There was a significant difference (P<0.05) between the urinary KIM-1 levels measured 2, 6, 12, 24 and 48 h after the procedure and those prior to the procedure in the CI-AKI group. There was no significant difference between the Scr values measured 24 h after the procedure and those prior to the procedure. Evidently, using KIM-1 values to predict CI-AKI was <24 h earlier compared to using Scr values. The area under the receiver operating characteristic curve of KIM-1 24 h after the procedure was 0.856 and the 95% confidence interval of the corresponding area was 0.782-0.929. When the pivotal point of CI-AKI diagnosis was 6,327.755 pg/ml, the specificity was 85.7% and the sensitivity was 73.7%. Univariate analysis showed that the Scr concentration was positively correlated with the urinary KIM-1 level during the time prior to the procedure and 24 and 48 h after the procedure. In conclusion, the urinary KIM-1 may be a potential indicator for the early diagnosis of CI-AKI.

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“…The accepted aetiologic factors comprise three different but potentially interacting pathways: the haemodynamic effects of CM; the effects of reactive oxygen species (ROS); and direct tubular cellular toxicity by CM molecules. (7,15) Renal-related adverse effects of intravenous contrast media in computed tomography …”

Section: Pathophysiology Of Cinmentioning

confidence: 99%

“…(7) These ROS include superoxide (O 2 − ), hydroxyl radicals (OH − ) and less aggressive reacting molecules such as hydrogen peroxide (H 2 O 2 ). (15,16) Once exceeding the scavenging capabilities of antioxidants, these ROS cause oxidative stress and lead to ischaemia reperfusion injury at the cellular level. (7) ROS also triggers and increases angiotensin II-and endothelin I-induced vasoconstriction, and decreases the bioavailabilty of vasodilative nitric oxide (NO), thus compromising the ischaemic state of the outer medulla.…”

Section: Haemodynamic Effectsmentioning

confidence: 99%

Renal-related adverse effects of intravenous contrast media in computed tomography

Leow¹,

Wu²,

Tan³

2015

smedj

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Renal-related adverse effects of intravascular contrast media (CM) include contrast-induced nephropathy in computed tomography and angiography. While large retrospective studies have been published, the exact pathogenesis of this condition is still unknown. We review the main international guidelines, including the American College of Radiology white paper and the guidelines of European Society of Urogenital Radiology, Royal College of Radiologists and Canadian Association of Radiologists, as well as their references, regarding this subject. We present a simplified, concise approach to renal-related adverse effects of CM, taking into consideration the basis for each recommendation in these published guidelines. This will allow the reader to better understand the rationale behind appropriate patient preparation for crosssectional imaging.

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Contrast Medium–induced Nephrotoxicity: Which Pathway?

Cited by 73 publications

References 37 publications

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

Urinary kidney injury molecule-1 as an early indicator to predict contrast-induced acute kidney injury in patients with diabetes mellitus undergoing percutaneous coronary intervention

Renal-related adverse effects of intravenous contrast media in computed tomography

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