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      Antithrombin III Protects Against Contrast-Induced Nephropathy

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          Abstract

          We previously reported that insufficiency of antithrombin III (ATIII), the major anti-coagulation molecule in vivo, exacerbated renal ischemia-reperfusion injury in animal models and possibly humans. In the present study, we investigated the relationship between ATIII level and contrast induced nephropathy (CIN) in patients and examined therapeutic effect of ATIII on CIN in Sprague-Dawley rats. Patients with low ATIII activity presented a higher incidence of acute kidney injury (AKI) following coronary angiography. ATIII (500 μg/kg) was intravenously injected before or after the induction of AKI in rats. Our data demonstrated ATIII significantly attenuated the elevation of serum creatinine, blood urea nitrogen, and renal histological injury. The beneficial effects of ATIII were accompanied by diminished renal inflammatory response, oxidative stress, cell apoptosis and improved renal blood flow in rats. In conclusion, ATIII appears to attenuate CIN through inhibiting inflammation, oxidative stress, apoptosis and improving renal blood flow. ATIII administration may represent a promising strategy for the prevention and treatment of contrast-induced AKI.

          Highlights

          • •

            Patients with low ATIII activity presented a higher incidence of acute kidney injury following coronary angiography.

          • •

            ATIII supplementation attenuated renal injury in animal models of contrast induced nephropathy.

          • •

            ATIII exerted renoprotective effect by inhibiting inflammation, oxidative stress, apoptosis and improving renal blood flow.

          Antithrombin III (ATIII), a potent anti-coagulation molecule in vivo, has been reported that it can exert reno-protective effects in ischemia-reperfusion model. Nevertheless, whether exogenous ATIII administration can protect against contrast induced nephropathy (CIN) in animal models remains unclear. This study revealed that ATIII administration has therapeutic effects against CIN in Sprague-Dawley Rats. Furthermore, the reno-protection conferred by ATIII might be mediated by inhibition of inflammation, oxidative stress, apoptosis and improving renal blood flow. ATIII supplementation represents a promising prophylactic and treatment strategies for contrast induced AKI.

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          Acute Kidney Injury and Mortality in Hospitalized Patients

          Henry Wang, Paul Muntner, Glenn Chertow … (2012)
          Background: The objective of this study was to determine the incidence of acute kidney injury (AKI) and its relation with mortality among hospitalized patients. Methods: Analysis of hospital discharge and laboratory data from an urban academic medical center over a 1-year period. We included hospitalized adult patients receiving two or more serum creatinine (sCr) measurements. We excluded prisoners, psychiatry, labor and delivery, and transferred patients, ‘bedded outpatients’ as well as individuals with a history of kidney transplant or chronic dialysis. We defined AKI as (a) an increase in sCr of ≥0.3 mg/dl; (b) an increase in sCr to ≥150% of baseline, or (c) the initiation of dialysis in a patient with no known history of prior dialysis. We identified factors associated with AKI as well as the relationships between AKI and in-hospital mortality. Results: Among the 19,249 hospitalizations included in the analysis, the incidence of AKI was 22.7%. Older persons, Blacks, and patients with reduced baseline kidney function were more likely to develop AKI (all p < 0.001). Among AKI cases, the most common primary admitting diagnosis groups were circulatory diseases (25.4%) and infection (16.4%). After adjustment for age, sex, race, admitting sCr concentration, and the severity of illness index, AKI was independently associated with in-hospital mortality (adjusted odds ratio 4.43, 95% confidence interval 3.68–5.35). Conclusions: AKI occurred in over 1 of 5 hospitalizations and was associated with a more than fourfold increased likelihood of death. These observations highlight the importance of AKI recognition as well as the association of AKI with mortality in hospitalized patients.
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            Contrast-induced acute kidney injury.

            Richard Solomon, Harold Dauerman (2010)
            Article 0 comments Cited 60 times – based on 0 reviews     Review now
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              Neutrophil-independent mechanisms of caspase-1- and IL-18-mediated ischemic acute tubular necrosis in mice.

              Vyacheslav Y. Melnikov, Sarah Faubel, Britta Siegmund … (2002)
              Having recently described the injurious role of caspase-1-mediated production of the proinflammatory cytokine IL-18 in ischemic acute renal failure (ARF), we report here on the effect of the newly developed caspase inhibitor Quinoline-Val-Asp(Ome)-CH(2)-OPH (OPH-001) on caspase-1, IL-18, neutrophil infiltration, and renal function in ischemic ARF. C57BL/6 mice with ischemic ARF treated with OPH-001 had a marked (100%) reduction in blood urea nitrogen (BUN) and serum creatinine and a highly significant reduction in morphological acute tubular necrosis (ATN) score compared with vehicle-treated mice. OPH-001 significantly reduced the increase in caspase-1 activity and IL-18 and prevented neutrophil infiltration in the kidney during ischemic ARF. To evaluate whether this lack of neutrophil infiltration was contributing to the protection against ischemic ARF, a model of neutrophil depletion was developed. Neutrophil-depleted mice had a small (18%) reduction in serum creatinine during ischemic ARF but no reduction in ATN score despite a lack of neutrophil infiltration in the kidney. Remarkably, caspase-1 activity and IL-18 were significantly increased in the kidney in neutrophil-depleted mice with ARF. In addition, IL-18 antiserum-treated neutrophil-depleted mice with ischemic ARF had a significant (75%) reduction in serum creatinine and a significant reduction in ATN score compared with vehicle-treated neutrophil-depleted mice. These results suggest a novel neutrophil-independent mechanism of IL-18-mediated ischemic ARF.
              Article 0 comments Cited 50 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Zeyuan Lu
                Dongsheng Cheng
                Jianyong Yin
                Rui Wu
                Guangyuan Zhang
                Qing Zhao
                Niansong Wang
                Feng Wang
                Mingyu Liang
                Journal
                Journal ID (nlm-ta): EBioMedicine
                Journal ID (iso-abbrev): EBioMedicine
                Title: EBioMedicine
                Publisher: Elsevier
                ISSN (Electronic): 2352-3964
                Publication date PMC-release: 12 February 2017
                Publication date Collection: March 2017
                Publication date (Electronic): 12 February 2017
                Volume: 17
                Pages: 101-107
                Affiliations
                [a ]Department of Nephrology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China
                [b ]Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
                [c ]Center of Systems Molecular Medicine, Medical College of Wisconsin, Milwaukee, WI, USA
                [d ]Department of Urology, Zhongda Hospital, Southeast University, Nanjing, China
                [e ]Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China
                Author notes
                [* ]Corresponding author at: 600 Yishan Road, Shanghai 200233, China.600 Yishan RoadShanghai200233China zyzwq1030@ 123456hotmail.com
                [1]

                Drs. Zeyuan Lu, Dongsheng Cheng and Jianyong Yin contributed to this work equally.

                Article
                Publisher ID: S2352-3964(17)30068-3
                DOI: 10.1016/j.ebiom.2017.02.009
                PMC ID: 5360582
                PubMed ID: 28219627
                SO-VID: b5db9fe3-7f7e-446d-84e4-2a50b33ca4c5
                Copyright © © 2017 Published by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 17 April 2016
                Date revision received : 8 February 2017
                Date accepted : 10 February 2017
                Categories
                Subject: Research Paper

                Keywords: antithrombin iii,acute kidney injury,contrast induced nephropathy,inflammation
                Data availability:
                Keywords: antithrombin iii, acute kidney injury, contrast induced nephropathy, inflammation

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