Retention of Iodine and Expression of Biomarkers for Renal Damage in the Kidney After Application of Iodinated Contrast Media in Rats

Jošt, Gregor; Pietsch, Hubertus; Sommer, Janine; Sandner, Peter; Lengsfeld, Philipp; Seidensticker, Peter; Lehr, Stephan; Hütter, Joachim; Sieber, Martin

doi:10.1097/rli.0b013e318190fbd2

Cited by 61 publications

(33 citation statements)

References 35 publications

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“…This could be related to the higher viscosity of iodixanol as shown in several recent reports. 23,24 Higher viscosity has been associated with damage to cells and generation of oxygen radicals perhaps through the increased contact time of nephrotoxic CM with the tubule epithelial cells and vascular endothelium. 1 …”

Section: Discussionmentioning

confidence: 99%

Evaluation of Intrarenal Oxygenation in Iodinated Contrast-Induced Acute Kidney Injury–Susceptible Rats by Blood Oxygen Level–Dependent Magnetic Resonance Imaging

Lü

Zhou

et al. 2014

Investigative Radiology

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Objectives The objectives of this study were to evaluate differences in intrarenal oxygenation as assessed by blood oxygen level–dependent (BOLD) magnetic resonance imaging in contrast-induced acute kidney injury (CIAKI)–susceptible rats when using 4 contrast media with different physicochemical properties and to demonstrate the feasibility of acquiring urinary neutrophil gelatinase–associated lipocalin (NGAL) levels as a marker of CIAKI in this model. Materials and Methods Our institutional animal care and use committee approved the study. Sixty-six Sprague-Dawley rats were divided into CIAKI-susceptible groups (received nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester [10 mg/kg] and cycloxygenase inhibitor indomethacin [10mg/kg]) and control groups (received saline instead). One of the 4 iodinated contrast agents (iothalamate, iohexol, ioxaglate, or iodixanol) was then administered (1600-mg organic iodine per kilogram of body weight). Multiple blood oxygen level–dependent magnetic resonance images were acquired on a Siemens 3.0-T scanner using a multiple gradient recalled echo sequence at baseline, after N-nitro-L-arginine methyl ester (or saline), indomethacin (or saline), and iodinated contrast agent (or placebo). R2* (R2* = 1/T2*) maps were generated inline on the scanner. A mixed-effects growth curve model with first-order autoregressive variance-covariance was used to analyze the temporal data. Urinary NGAL, a marker of kidney injury (unlike serum creatinine), was measured 4 hours after contrast injection in the 2 subgroups. Results Differences in blood oxygen level–dependent magnetic resonance imaging results between the contrast media were observed in all 4 renal regions. However, the inner stripe of the outer medulla (ISOM) showed the most pronounced changes in the CIAKI-susceptible group and R2* increased significantly (P < 0.01) over time with all 4 contrast media. In the control groups, only iodixanol showed an increase in R2* (P < 0.05) over time. There was an agreement between increases in NGAL and R2* values in ISOM. Conclusions In rats susceptible to CIAKI, those receiving contrast media had significant increases in R2* in renal ISOM compared with those receiving placebo. The agreement between NGAL and R2* values in the ISOM suggests that the observed immediate increase in R2* after contrast injection may be the earliest biomarker of renal injury. Further studies are necessary to establish threshold values of R2* associated with acute kidney injury and address the specificity of R2* to renal oxygenation status.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Intrarenal Oxygenation in Iodinated Contrast-Induced Acute Kidney Injury–Susceptible Rats by Blood Oxygen Level–Dependent Magnetic Resonance Imaging

Lü

Zhou

et al. 2014

Investigative Radiology

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“…A recent study comparing HOCM and IOCM concluded that IOCM was retained longer in the kidneys. The explanation for longer renal handling was the higher viscosity of IOCM due to their dimer structure and the lack of osmotic diuresis [44]. Resistance to flow is linearly proportional with the viscosity of the fluid and the length of the vessel and inversely proportional to the fourth power of the vessel radius (Poiseuille's law).…”

Section: Rcm Classes and Their Osmolality And Viscositymentioning

confidence: 99%

“…Furthermore, viscosity increases exponentially in the tubules during the concentrating procedure leading to slower tubular flow [46]. Thus, hydration may be beneficial by reducing urine concentration and viscosity in tubules [44–46]. Interestingly, the comparison of the highest viscosity iohexol (Omnipaque)® and the lowest viscosity metrizoate (isopaque) did not support the role of high viscosity in CI-AKI, as metrizoate caused more renal damage compared to iohexol [48–50].…”

Section: Rcm Classes and Their Osmolality And Viscositymentioning

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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“…Thus, the low osmolality achieved with the IOCM came at the price of considerably increased viscosity; at comparable iodine concentration and X-ray attenuation nonionic dimer IOCM have about twice the viscosity of nonionic monomer LOCM [95]. The higher viscosity of nonionic dimer IOCM probably relies on a number of the compounds' features including the molecules' shape and the flexibility of the bridge between the two benzene nuclei [96].…”

Section: Risk For Development Of Akimentioning

confidence: 99%

Acute Kidney Injury by Radiographic Contrast Media: Pathogenesis and Prevention

Andreucci

Faga

Pisani

et al. 2014

BioMed Research International

102

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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Retention of Iodine and Expression of Biomarkers for Renal Damage in the Kidney After Application of Iodinated Contrast Media in Rats

Cited by 61 publications

References 35 publications

Evaluation of Intrarenal Oxygenation in Iodinated Contrast-Induced Acute Kidney Injury–Susceptible Rats by Blood Oxygen Level–Dependent Magnetic Resonance Imaging

Evaluation of Intrarenal Oxygenation in Iodinated Contrast-Induced Acute Kidney Injury–Susceptible Rats by Blood Oxygen Level–Dependent Magnetic Resonance Imaging

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Acute Kidney Injury by Radiographic Contrast Media: Pathogenesis and Prevention

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