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      Is Contrast Medium Osmolality a Causal Factor for Contrast-Induced Nephropathy?

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          Abstract

          The exact pathophysiology of contrast-induced nephropathy (CIN) is not fully clarified, yet the osmotic characteristics of contrast media (CM) have been a significant focus in many investigations of CIN. Osmotic effects of CM specific to the kidney include transient decreases in blood flow, filtration fraction, and glomerular filtration rate. Potentially significant secondary effects include an osmotically induced diuresis with a concomitant dehydrating effect. Clinical experiences that have compared the occurrence of CIN between the various classes of CM based on osmolality have suggested a much less than anticipated advantage, if any, with a lower osmolality. Recent animal experiments actually suggest that induction of a mild osmotic diuresis in association with iso-osmolar agents tends to offset potentially deleterious renal effects of high viscosity-mediated intratubular CM stagnation.

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          Contrast-induced kidney injury: mechanisms, risk factors, and prevention.

          Erdmann Seeliger, Mauricio Sendeski, Charanjit Rihal … (2012)
          In general, iodinated contrast media (CM) are tolerated well, and CM use is steadily increasing. Acute kidney injury is the leading life-threatening side effect of CM. Here, we highlight endpoints used to assess CM-induced acute kidney injury (CIAKI), CM types, risk factors, and CIAKI prevention. Moreover, we put forward a unifying theory as to how CIAKI comes about; the kidney medulla's unique hyperosmolar environment concentrates CM in the tubules and vasculature. Highly concentrated CM in the tubules and vessels increases fluid viscosity. Thus, flow through medullary tubules and vessels decreases. Reducing the flow rate will increase the contact time of cytotoxic CM with the tubular epithelial cells and vascular endothelium, and thereby damage cells and generate oxygen radicals. As a result, medullary vasoconstriction takes place, causing hypoxia. Moreover, the glomerular filtration rate declines due to congestion of highly viscous tubular fluid. Effective prevention aims at reducing the medullary concentration of CM, thereby diminishing fluid viscosity. This is achieved by generous hydration using isotonic electrolyte solutions. Even forced diuresis may prove efficient if accompanied by adequate volume supplementation. Limiting the CM dose is the most effective measure to diminish fluid viscosity and to reduce cytotoxic effects.
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            Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media.

            Anna Carlisle, Adam Barrett (1993)
            To determine whether low-osmolality contrast media (LOCM) are less nephrotoxic than high-osmolality contrast media (HOCM), the authors searched MEDLINE and EMBASE databases and other sources to find randomized trials with data collected on changes in glomerular filtration rate or serum creatinine (SCr) level with LOCM and HOCM. Forty-five trials were found. Data were unavailable from 14 trials. When the P values from the other 31 trials were pooled, an overall P value of .02 was found. Among 24 trials with available data, the mean change in SCr was 0.2-6.2 mumol/L less with LOCM than HOCM. Among 25 trials with available data, the pooled odds of a rise in SCr level of more than 44 mumol/L with LOCM was 0.61 (95% confidence interval [CI], 0.48-0.77) times that after HOCM. For patients with existing renal failure, this odds ratio was 0.5 (CI, 0.36-0.68), while it was 0.75 (CI, 0.52-1.1) in patients without prior renal failure. Greater changes in SCr level occurred only in those with existing renal failure and were less common with LOCM (odds ratio, 0.44; CI, 0.26-0.73). Use of LOCM may be beneficial in patients with existing renal failure.
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              Osmotic nephrosis: acute kidney injury with accumulation of proximal tubular lysosomes due to administration of exogenous solutes.

              Michael Dickenmann, Michael Mihatsch, Tobias Oettl (2008)
              Osmotic nephrosis describes a morphological pattern with vacuolization and swelling of the renal proximal tubular cells. The term refers to a nonspecific histopathologic finding rather than defining a specific entity. Osmotic nephrosis can be induced by many different compounds, such as sucrose, hydroxyethyl starch, dextrans, and contrast media. It has a broad clinical spectrum that includes acute kidney injury and chronic kidney failure in rare cases. This article discusses the pathological characteristics, pathogenesis, and various clinical entities of osmotic nephrosis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date (Print): 2014
                Publication date (Electronic): 31 March 2014
                Volume: 2014
                Electronic Location Identifier: 931413
                Affiliations
                1Department of Radiology and Radiological Science, Medical University of South Carolina, 25 Courtenay Drive MSC 226, Charleston, SC 29425, USA
                2Department of Diagnostic and Interventional Radiology, Johann Wolfgang Goethe University Hospital, 60590 Frankfurt am Main, Germany
                3Department of Radiological Sciences, Oncology and Pathology, University of Rome “Sapienza”-Polo Pontino, Latina, Italy
                4Institute for Clinical Radiology, Ludwig-Maximilians-University Hospital, Marchioninistr. 15, 81377 Munich, Germany
                5Department of Radiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China
                6Heidelberg Kidney Center, Department of Nephrology, University Hospital Heidelberg, INF 162, 69120 Heidelberg, Germany
                Author notes
                *U. Joseph Schoepf: schoepf@ 123456musc.edu

                Academic Editor: Michele Andreucci

                Article
                DOI: 10.1155/2014/931413
                PMC ID: 3988854
                PubMed ID: 24800254
                SO-VID: e793ffcf-2008-43da-b080-05aabaf18427
                Copyright © Copyright © 2014 Andreas M. Bucher et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 October 2013
                Date revision received : 27 January 2014
                Date accepted : 15 February 2014
                Funding
                Funded by: Bayer, Bracco, GE, and Siemens
                Funded by: Guerbet and Siemens
                Categories
                Subject: Review Article

                Data availability:

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