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      Influence of acute kidney injury on high sensitive troponin after cardiac surgery. a single center retrospective observational study

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      , , , , , , , ,
      Intensive Care Medicine Experimental
      Springer International Publishing
      ESICM LIVES 2015
      3-7 October 2015

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          Abstract

          Introduction The risk assessment of cardiac troponin and other cardiac biomarkers in end-stage renal disease is not equivalent where clinical decision making in patients with renal diseases based on cardiac biomarkers needs justification in relation to patient management or outcomes [1]. Long-term outcome could be influenced by acute kidney injury (AKI) in cardiac surgery [2], but cardiac troponins need exploration in theses settings. Objectives Assess the diagnostic performance of high sensitive troponin T (hsTnT) in the settings of cardiac surgery-induced AKI. Link it with mortality as well as the lengths of ventilation, ICU stay and hospital stay. Methods Single center observational retrospective study. A database was available for all patients (sex, age, body mass index, duration of the operation, duration of ICU and hospital length of stay, levels of cardiac enzymes, evidence of perioperative myocardial infarction, early mortality. The lengths of ventilation, stay in ICU, and hospitalization. Based on the Acute Kidney Injury Network, AKI was defined as an abrupt (within 48 h) reduction in kidney function, defined as an absolute increase in serum creatinine concentration of 0.3 mg/dL (26.4 µmol/L) or greater or a percentage increase of 50% or greater (1.5-fold from baseline). Patients divided into 2 groups, group I without AKI (259 patients) and group II with AKI (100 patients) where serial of hsTnT and creatine kinase (CK)-MB followed. Both groups compared and statistically analyzed. We enrolled 359 patients, patients with ESRD were excluded. Results The mean age in our study population 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 6% vs group I 1.7% (p = 0.026). The hsTnT significant changes between both groups remain all over the course, which unparalleled to those of CK-MB (Figures 1&2). The AKI group with more associated with heart failure 17.9% vs 4.9% (p=.000); 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 (Table 1). Figure 1 Changes in hsTnT in both groups Figure 2 Changes in CK-MB in both groups Table 1 Comparison between both groups. Variable Group I (No AKI) 259 (%) Group II (AKI) 100 (%) P- Value Age 54.43 ± 10.8 56.09 ± 10.7 0.13 Diabetes 138 (53.2) 56 (56) 0.38 Euro score 3.8 ± 2.4 5.1 ± 3.6 0.06 POAF 7 (2.7) 12 (12) 0.005 Mortality 5 (1.9) 7 (7) 0.026 LOV(minutes) 364.1 ± 112 575.5 ± 199 0.001 LOSICU (hours) 52.9 ± 41.1 109.4 ± 89 0.000 LOH (days) 10.8 ± 6.4 15.8 ± 7.3 0.007 POAF: post operative atrial fibrillation, LOSICU length of stay in ICU, LOV length of ventilation, LOH hospital length of stay 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 that needs to put in consideration in interpreting post-operative myocardial injury and infarction in this population. Grant Acknowledgment All members of CT department and medical research center, HMC, Doha, Qatar

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          Natriuretic peptides and acute renal failure.

          Atrial natriuretic peptides (ANPs) are a family of peptide hormones, e.g., ANP, long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide synthesized by the ANP gene. Brain natriuretic peptide (BNP) and C-type natriuretic peptide are also members of this family but are synthesized by separate genes. Within the kidney, the ANP prohormone's posttranslational processing is different from that of other tissues, resulting in an additional four amino acids added to the NH2 terminus of ANP (e.g., urodilatin). Each of these natriuretic and diuretic peptides increases within the circulation with acute renal failure (ARF). Renal transplantation but not hemodialysis returns their circulating concentrations to those of healthy individuals. BNP and adrenomedullin, a 52-amino acid natriuretic peptide, have beneficial effects on glomerular hypertrophy and glomerular injury but do not improve tubular injury (i.e., acute tubular necrosis). Vessel dilator ameliorates acute tubular necrosis with regeneration of the brush borders of proximal tubules. Vessel dilator decreases mortality in ARF from 88 to 14% at day 6 of ARF, even when given 2 days after renal failure has been established.
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            Acute kidney injury after cardiac surgery: the injury that keeps on hurting?*.

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              Author and article information

              Conference
              Intensive Care Med Exp
              Intensive Care Med Exp
              Intensive Care Medicine Experimental
              Springer International Publishing (Cham )
              2197-425X
              1 October 2015
              1 October 2015
              December 2015
              : 3
              Issue : Suppl 1 Issue sponsor : The publication charges for this supplement were funded by Intensive Care Medicine Experimental.
              : A633
              Affiliations
              [ ]Hamad Medical Corporation, Cardiothoracic Surgery-Heart Hospital, Doha, Qatar
              [ ]Faculty of Medicine, Critical Care Medicine, Beni Suef University, Beni Suef, Egypt
              [ ]Faculty of Medicine, Anaesthesiology, Alazhar University, Cairo, Egypt
              [ ]Hamad Medical Corporation, Biomedical Statistics, Medical Research Center, Doha, Qatar
              Article
              774
              10.1186/2197-425X-3-S1-A633
              4796159
              502f1efd-c83b-4d3e-8aa6-558146939970
              © Omar et al.; 2015

              This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

              ESICM LIVES 2015
              Berlin, Germany
              3-7 October 2015
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