Differences in Renal Tubular Toxicity of High- and Low-Osmolality Contrast Media

Kaneko, Kazunari; Ikebe, Akiko; Shimazaki, Shinjiro; Yabuta, Keijiro

doi:10.1159/000185409

Cited by 6 publications

(3 citation statements)

References 3 publications

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“…The mechanisms behind the development of CIN are complex. They include potential interplay of vasoconstriction, oxidative stress, and direct tubular toxicity leading to hypoxia of the outer medulla [ 15 - 21 ]. Studies have shown that the contrast administration not only results in vasoconstriction, but toxicity results in proximal tubularvacuolar transformation, interstitial edema and tubular degeneration [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Urine metabolomic analysis to detect metabolites associated with the development of contrast induced nephropathy

et al. 2016

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ObjectiveContrast induced nephropathy (CIN) is a result of injury to the proximal tubules. The incidence of CIN is around 11% for imaging done in the acute care setting. We aim to analyze the metabolic patterns in the urine, before and after dosing with intravenous contrast for computed tomography (CT) imaging of the chest, to determine if metabolomic changes exist in patients who develop CIN.MethodsA convenience sample of high risk patients undergoing a chest CT with intravenous contrast were eligible for enrollment. Urine samples were collected prior to imaging and 4 to 6 hours post imaging. Samples underwent gas chromatography/mass spectrometry profiling. Peak metabolite values were measured and data was log transformed. Significance analysis of microarrays and partial least squares was used to determine the most significant metabolites prior to CT imaging and within subject. Analysis of variance was used to rank metabolites associated with temporal change and CIN. CIN was defined as an increase in serum creatinine level of ≥ 0.5 mg/dL or ≥ 25% above baseline within 48 hours after contrast administration.ResultsWe sampled paired urine samples from 63 subjects. The incidence of CIN was 6/63 (9.5%). Patients without CIN had elevated urinary citric acid and taurine concentrations in the pre-CT urine. Xylulose increased in the post CT sample in patients who developed CIN.ConclusionDifferences in metabolomics patterns in patients who do and do not develop CIN exist. Metabolites may be potential early identifiers of CIN and identify patients at high-risk for developing this condition prior to imaging.

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Section: Discussionmentioning

confidence: 99%

Urine metabolomic analysis to detect metabolites associated with the development of contrast induced nephropathy

et al. 2016

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“…It has been suggested that the development of CIN is a result of the interplay of vasoconstriction, oxidative stress, and direct tubular toxicity leading to hypoxia of the outer medulla 13,14–15. Numerous studies have reported on the effects of contrast media on various urinary enzymes and markers of glomerular and tubular function 16–20. The complex pathophysiology behind the renal effects of intravenous contrast provides the opportunity to identify multiple markers of potential renal injury 21…”

Section: Discussionmentioning

confidence: 99%

Urinary Metabolomic Analysis to Detect Changes After Intravenous, Non-ionic, Low Osmolar Iodinated Radiocontrast for Computerized Tomographic Imaging

Diercks¹,

Owen²,

Tolstikov³

et al. 2014

WestJEM

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IntroductionContrast-induced nephropathy is a result of injury to the proximal tubules caused by oxidative stress and ischemia. Metabolomics is a novel technique that has been used to identify renal damage from drug toxicities. The objective of this study is to analyze the metabolic changes in the urine after dosing with intravenous (IV) contrast for computed tomograph (CT) of the chestMethodsA convenience sample of patients undergoing a chest CT with IV contrast who had at least one of the following: age ≥50 years, diabetes, heart failure, chronic kidney disease, coronary artery disease, or diastolic blood pressure >90 mmHg -- were eligible for enrollment. Urine samples were collected prior to imaging and 4–6 hours post imaging. Samples underwent gas chromography/mass spectrometry profiling. We measured peak metabolite values and log transformed data. Paired T tests were calculated. We used significance analysis of microarrays (SAM) to determine the most significant metabolites.ResultsThe cohort comprised 14 patients with matched samples; 9/14 (64.3) were males, and the median age was 61 years (IQR 50–68). A total of 158 metabolites were identified. Using SAM we identified 9 metabolites that were identified as significant using a delta of 1.6.ConclusionChanges in urinary metabolites are present soon after contrast administration. This change in urinary metabolites may be potential early identifiers of contrast-induced nephropathy and could identify patients at high-risk for developing this condition.

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“…The clinical studies on nephrotoxicity due to CM are sometimes conflicting (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25) and it is often difficult to compare their results. Furthermore, many of the studies addressed to compare the nephrotoxicity of cardiac angiography with high-osmolar versus low-osmolar CM have some methodological limitations (2).…”

Section: Discussionmentioning

confidence: 99%

Renal Effects of Cardiac Angiography With Different Low-Osmolar Contrast Media

et al. 2001

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The aim of this study was to evaluate the renal effects of cardiac angiography performed with three low-osmolar contrast media (CM): iopromide (IPR), ioversol (IVR) and ioxaglate (IOX). IPR and IVR are non-ionic CM, IOX is an ionic CM. Different parameters of renal function were determined before and 6, 24, 48, 72 hrs after angiography in 45 patients: 15 patients were examined with IPR, 15 with IVR and 15 with IOX. Glomerular effects--Plasma creatinine increased slightly at the 24th hour after IVR and IOX and at 48 hours after IOP. A significant increase in plasma beta2-microglobulin was observed, at the same time, only after IOX. A significant decrease in creatinine clearance was found at 6 hours after IOX. No significant variations in glomerular filtration rate (GFR) and in effective renal plasma flow were found at 48 hours after cardiac angiography; while filtration fraction was significantly reduced after IOP and IOX. Tubular effects--A marked decrease in sodium clearance and a relevant increase of urinary activities of different tubular enzymes were found after cardiac angiography with all CM, but were more evident after the ionic CM IOX, than after the two non-ionic agents. These tubular effects reached the maximum between 6 and 24 hours and returned to baseline within 72 hrs after cardiac angiography. In conclusion, slight glomerular effects were observed mainly after IOX. A reversible tubular malfunction was found with the three low-osmolar CM and was more evident after ionic CM IOX. thus suggesting that other mechanisms, besides osmolarity, play a role in tubular toxicity due to CM. In no patient did the glomerular and tubular effects of CM have a clinical relevance.

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Differences in Renal Tubular Toxicity of High- and Low-Osmolality Contrast Media

Cited by 6 publications

References 3 publications

Urine metabolomic analysis to detect metabolites associated with the development of contrast induced nephropathy

Urine metabolomic analysis to detect metabolites associated with the development of contrast induced nephropathy

Urinary Metabolomic Analysis to Detect Changes After Intravenous, Non-ionic, Low Osmolar Iodinated Radiocontrast for Computerized Tomographic Imaging

Renal Effects of Cardiac Angiography With Different Low-Osmolar Contrast Media

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