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      Acute kidney injury induces high-sensitivity troponin measurement changes after cardiac surgery

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          Abstract

          Background

          The value of cardiac troponin as a risk assessment tool for cardiac disease in the setting of end-stage renal diseases (ESRD) is not equivalent to its value in those with normal renal function. This consideration had not been studied in settings of acute kidney injury (AKI). We aim to explore the diagnostic value of high sensitive troponin T (hsTnT) in the settings of cardiac surgery-induced AKI.

          Methods

          Single center observational retrospective study. Based on the AKI Network, patients divided into 2 groups, group I without AKI (259 patients) and group II with AKI (100 patients) where serial testing of hsTnT and creatine kinase (CK)-MB were followed in both groups. Patients with (ESRD) were excluded.

          Results

          The mean age in our study was 55.1 ± 10.2 years. High association of AKI (27.8%) was found in our patients. Both groups were matched regarding the age, gender, body mass index, the association of diabetes or hypertension, and Euro score. AKI group had significantly higher mortality 5% vs group I 1.1% ( p = 0.03). The hsTnt showed a significant sustained rise in the AKI group as compared to the non-AKI group, however CK-MB changes were significant initially but not sustained.

          The AKI group was more associated with heart failure 17.9% vs 4.9% ( p = 0.001); and post-operative atrial fibrillation, 12.4% vs 2.9% ( p = 0.005). Lengths of ventilation, stays in ICU and in hospital were significantly higher in the AKI group.

          Conclusions

          Unlike the CK-MB profile, the hsTnT showed significant changes between both groups all over the course denoting possible delayed clearance in patients with AKI.

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          Most cited references19

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          How to Calculate Sample Size for Different Study Designs in Medical Research?

          Calculation of exact sample size is an important part of research design. It is very important to understand that different study design need different method of sample size calculation and one formula cannot be used in all designs. In this short review we tried to educate researcher regarding various method of sample size calculation available for different study designs. In this review sample size calculation for most frequently used study designs are mentioned. For genetic and microbiological studies readers are requested to read other sources.
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            Elevation of troponin I in sepsis and septic shock.

            To detect myocardial damage in severe systemic inflammation by cTnI measurements in patients without acute coronary syndromes. Prospective case control study. Tertiary referral center. Twenty patients with sepsis, septic shock, and systemic inflammatory response syndrome (SIRS) were examined and compared to controls without coronary artery disease or myocarditis. cTnI levels were assessed in patients with SIRS, sepsis, and septic shock. Eight patients (two female/six male) suffered from septic shock, nine (three female/six male) from sepsis without shock, and three (three male) from SIRS. Seventeen patients (85%) showed elevated cTnI (median 0.57 microg/l; 0.17-15.4), whereas no patient in the control group showed elevated cTnI (P < 0.0001). Six patients (30%),--three with septic shock and three with sepsis--died during hospitalization, five of them with elevated cTnI. Four out of five autopsies showed normal coronary arteries. Coronary angiography, autopsy, and stress echocardiography ruled out significant coronary artery disease in ten cTnI-positive patients (59%). In 41 % of cTnI-positive patients, Streptococcus pneumoniae could be cultured, whereas no cTnI-negative or control patient showed signs of infection due to S. pneumoniae. Cardiac troponin I was elevated in 85% of patients with sepsis, septic shock or SIRS in our study. A high percentage showed infection caused by S. pneumoniae. In what way microorganisms cause cTnI elevations is not yet understood.
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              Cardiac Surgery-Associated Acute Kidney Injury

              Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common and serious postoperative complication of cardiac surgery requiring cardiopulmonary bypass (CPB), and it is the second most common cause of AKI in the intensive care unit. Although the complication has been associated with the use of CPB, the etiology is likely multifactorial and related to intraoperative and early postoperative management including pharmacologic therapy. To date, very little evidence from randomized trials supporting specific interventions to protect from or prevent AKI in broad cardiac surgery populations has been found. The definition of AKI employed by investigators influences not only the incidence of CSA-AKI, but also the identification of risk variables. The advent of novel biomarkers of kidney injury has the potential to facilitate the subclinical diagnosis of CSA-AKI, the assessment of its severity and prognosis, and the early institution of interventions to prevent or reduce kidney damage. Further studies are needed to determine how to optimize cardiac surgical procedures, CPB parameters, and intraoperative and early postoperative blood pressure and renal blood flow to reduce the risk of CSA-AKI. No pharmacologic strategy has demonstrated clear efficacy in the prevention of CSA-AKI; however, some agents, such as the natriuretic peptide nesiritide and the dopamine agonist fenoldopam, have shown promising results in renoprotection. It remains unclear whether CSA-AKI patients can benefit from the early institution of such pharmacologic agents or the early initiation of renal replacement therapy.
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                Author and article information

                Contributors
                a_s_omar@yahoo.com
                khaledmahmoud2000@hotmail.com
                sehanoura73@yahoo.com
                hanyragab73@gmail.com
                drpraveencs@gmail.com
                drsurajsudarsan@gmail.com
                yshouman@hamad.qa
                rsingh@hamad.qa
                abdulalkh@hamad.qa
                Journal
                BMC Anesthesiol
                BMC Anesthesiol
                BMC Anesthesiology
                BioMed Central (London )
                1471-2253
                31 January 2017
                31 January 2017
                2017
                : 17
                : 15
                Affiliations
                [1 ]ISNI 0000 0004 0571 546X, GRID grid.413548.f, Department of Cardiothoracic Surgery/Cardiac Anaesthesia and ICU, Heart Hospital, , Hamad Medical Corporation, ; Doha, PO 3050, Qatar
                [2 ]ISNI 0000 0004 0412 4932, GRID grid.411662.6, Department of Critical Care Medicine, , Beni Suef University, ; Beni Suef, Egypt
                [3 ]ISNI 0000 0004 0582 4340, GRID grid.416973.e, , Weill Cornell Medical College-Qatar, ; Doha, Qatar
                [4 ]ISNI 0000 0004 0571 546X, GRID grid.413548.f, Department of Nephrology, , Hamad Medical Corporation, ; Doha, PO 3050, Qatar
                [5 ]ISNI 0000000103426662, GRID grid.10251.37, Department of Nephrology, Faculty of Medicine, , Mansoura University, ; Mansoura, Egypt
                [6 ]ISNI 0000 0001 2155 6022, GRID grid.411303.4, Department of Anesthesia, , Al-Azhar University, ; Cairo, Egypt
                [7 ]ISNI 0000 0004 0571 546X, GRID grid.413548.f, Department of Cardiology Research Center, , Hamad Medical Corporation, ; Doha, Qatar
                Article
                307
                10.1186/s12871-017-0307-5
                5282923
                28143401
                4f6588fc-8c5e-4b98-a26f-5798ade5e9cc
                © The Author(s). 2017

                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
                : 3 April 2016
                : 19 January 2017
                Funding
                Funded by: Hamad Medical Corporation (QA)
                Award ID: 15068/15
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2017

                Anesthesiology & Pain management
                acute kidney injury,high sensitive troponin,cardiac surgery

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