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      Predicting acute kidney injury using urinary liver-type fatty-acid binding protein and serum N-terminal pro-B-type natriuretic peptide levels in patients treated at medical cardiac intensive care units

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          Abstract

          Background

          The early prediction of acute kidney injury (AKI) can facilitate timely intervention and prevent complications. We aimed to understand the predictive value of urinary liver-type fatty-acid binding protein (L-FABP) levels on admission to medical (non-surgical) cardiac intensive care units (CICUs) for AKI, both independently and in combination with serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels.

          Methods

          We prospectively investigated the predictive value of L-FABP and NT-proBNP for AKI in a large, heterogeneous cohort of patients treated in medical CICUs. Baseline urinary L-FABP and serum NT-proBNP were measured on admission. AKI was diagnosed according to the Kidney Disease: Improving Global Outcomes criteria. We studied 1273 patients (mean age, 68 years), among whom 46% had acute coronary syndromes, 38% had acute decompensated heart failure, 5% had arrhythmia, 3% had pulmonary hypertension, 2% had acute aortic syndrome, 2% had infective endocarditis, and 1% had Takotsubo cardiomyopathy.

          Results

          Urinary L-FABP levels correlated with serum NT-proBNP levels ( r = 0.17, p < 0.0001). AKI occurred in 224 patients (17.6%), including 48 patients with stage 2 or 3 disease. Patients who developed AKI had higher one-week and 6-month mortality than those who did not develop AKI ( p = 0.0002 and p = 0.003, respectively). In the multivariate logistic analysis, both L-FABP ( p < 0.0001) and NT-proBNP ( p = 0.006) were independently associated with the development of AKI. Adding L-FABP and NT-proBNP to a baseline model that included established risk factors further improved reclassification ( p < 0.001) and discrimination ( p < 0.01) beyond that of the baseline model or any single biomarker individually.

          Conclusions

          Urinary L-FABP and serum NT-proBNP levels on admission are independent predictors of AKI, and when used in combination, improve early prediction of AKI in patients hospitalized at medical CICUs.

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          Most cited references29

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          Acute kidney injury, mortality, length of stay, and costs in hospitalized patients.

          The marginal effects of acute kidney injury on in-hospital mortality, length of stay (LOS), and costs have not been well described. A consecutive sample of 19,982 adults who were admitted to an urban academic medical center, including 9210 who had two or more serum creatinine (SCr) determinations, was evaluated. The presence and degree of acute kidney injury were assessed using absolute and relative increases from baseline to peak SCr concentration during hospitalization. Large increases in SCr concentration were relatively rare (e.g., >or=2.0 mg/dl in 105 [1%] patients), whereas more modest increases in SCr were common (e.g., >or=0.5 mg/dl in 1237 [13%] patients). Modest changes in SCr were significantly associated with mortality, LOS, and costs, even after adjustment for age, gender, admission International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis, severity of illness (diagnosis-related group weight), and chronic kidney disease. For example, an increase in SCr >or=0.5 mg/dl was associated with a 6.5-fold (95% confidence interval 5.0 to 8.5) increase in the odds of death, a 3.5-d increase in LOS, and nearly 7500 dollars in excess hospital costs. Acute kidney injury is associated with significantly increased mortality, LOS, and costs across a broad spectrum of conditions. Moreover, outcomes are related directly to the severity of acute kidney injury, whether characterized by nominal or percentage changes in serum creatinine.
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            Cardiorenal syndrome.

            The term cardiorenal syndrome (CRS) increasingly has been used without a consistent or well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of heart-kidney interactions, we present a new classification of the CRS with 5 subtypes that reflect the pathophysiology, the time-frame, and the nature of concomitant cardiac and renal dysfunction. CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other. Type 1 CRS reflects an abrupt worsening of cardiac function (e.g., acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type 2 CRS comprises chronic abnormalities in cardiac function (e.g., chronic congestive heart failure) causing progressive chronic kidney disease. Type 3 CRS consists of an abrupt worsening of renal function (e.g., acute kidney ischemia or glomerulonephritis) causing acute cardiac dysfunction (e.g., heart failure, arrhythmia, ischemia). Type 4 CRS describes a state of chronic kidney disease (e.g., chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g., sepsis) causing both cardiac and renal dysfunction. Biomarkers can contribute to an early diagnosis of CRS and to a timely therapeutic intervention. The use of this classification can help physicians characterize groups of patients, provides the rationale for specific management strategies, and allows the design of future clinical trials with more accurate selection and stratification of the population under investigation.
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              Acute Kidney Injury Recovery Pattern and Subsequent Risk of CKD: An Analysis of Veterans Health Administration Data.

              Studies suggest an association between acute kidney injury (AKI) and long-term risk for chronic kidney disease (CKD), even following apparent renal recovery. Whether the pattern of renal recovery predicts kidney risk following AKI is unknown.
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                Author and article information

                Contributors
                hnaruse@fujita-hu.ac.jp
                +81 562 93 2312 , jishii@fujita-hu.ac.jp
                hirotaka@fujita-hu.ac.jp
                fkitaga@fujita-hu.ac.jp
                hidetonishimura0621@gmail.com
                hidekikawai@xc4.so-net.ne.jp
                takam@fujita-hu.ac.jp
                mharada@fujita-hu.ac.jp
                a-yamada@fujita-hu.ac.jp
                sadakom@fujita-hu.ac.jp
                matsui44@fujita-hu.ac.jp
                muhayasi@med.nagoya-u.ac.jp
                msarai@fujita-hu.ac.jp
                enwatan@mtj.biglobe.ne.jp
                izawa@fujita-hu.ac.jp
                ozakiyuk@fujita-hu.ac.jp
                Journal
                Crit Care
                Critical Care
                BioMed Central (London )
                1364-8535
                1466-609X
                18 August 2018
                18 August 2018
                2018
                : 22
                : 197
                Affiliations
                [1 ]ISNI 0000 0004 1761 798X, GRID grid.256115.4, Department of Joint Research Laboratory of Clinical Medicine, , Fujita Health University School of Medicine, ; 1-98 Kutsukake-cho, Dengakugakubo, Toyoake, 470-1192 Japan
                [2 ]ISNI 0000 0004 1761 798X, GRID grid.256115.4, Division of Statistics, , Fujita Health University School of Medicine, ; 1-98 Kutsukake-cho, Dengakugakubo, Toyoake, 470-1192 Japan
                [3 ]ISNI 0000 0004 1761 798X, GRID grid.256115.4, Department of Cardiology, , Fujita Health University School of Medicine, ; 1-98 Kutsukake-cho, Dengakugakubo, Toyoake, 470-1192 Japan
                [4 ]Department of Cardiology, Banbuntane Houtokukai Hospital, 3-10 Otoubashi 3-cyome, Nakagawa-ku, Nagoya, 454-8509 Japan
                Article
                2120
                10.1186/s13054-018-2120-z
                6098639
                30119691
                46853d64-0a88-45f2-89a0-a3af58627f71
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 29 March 2018
                : 3 July 2018
                Funding
                Funded by: JSPS KAKENHI
                Award ID: 17K08995
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2018

                Emergency medicine & Trauma
                liver-type fatty-acid binding protein,n-terminal pro-b-type natriuretic peptide,acute kidney injury,medical cardiac intensive care units

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