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      High sensitivity Troponin-I levels in asymptomatic hemodialysis patients

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          Abstract

          Reduction in renal clearance and removal by hemodialysis adversely affect the level and utility of high-sensitivity troponin I (hsTnI) for diagnosis of acute myocardial infarction (AMI) in hemodialysis (HD) patients. Furthermore, HD process itself might cause undesirable myocardial injury and enhance post HD hsTnI levels. This comparative cross-sectional study was conducted to compare the hsTnI levels between 100 asymptomatic HD patients and their 107 matched non-chronic kidney disease (CKD) population. The hsTnI levels in HD group were higher than non-CKD group [median (IQR): 54.3 (20.6–152.7) vs. 18 (6.2–66.1) ng/L, p < .001)]. The hsTnI levels reduced after HD process from 54.3 (20.6–152.7) ng/L in pre-HD to 27.1 (12.3–91.4) ng/L in post-HD ( p = .015). Of interest, 25% of HD patients had increment of hsTnI after HD and might represent HD-induced myocardial injury. The significant risk factors were high hemoglobin level and high blood flow rate. In conclusion, the baseline hsTnI levels in asymptomatic HD patients were higher than non-CKD population. The dynamic change of hsTnI over time would be essential for the diagnosis of AMI. Certain numbers of asymptomatic HD patients had HD-induced silent myocardial injury and should be aggressively investigated to prevent further cardiovascular mortality.

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          Correction of anemia with epoetin alfa in chronic kidney disease.

          Anemia, a common complication of chronic kidney disease, usually develops as a consequence of erythropoietin deficiency. Recombinant human erythropoietin (epoetin alfa) is indicated for the correction of anemia associated with this condition. However, the optimal level of hemoglobin correction is not defined. In this open-label trial, we studied 1432 patients with chronic kidney disease, 715 of whom were randomly assigned to receive a dose of epoetin alfa targeted to achieve a hemoglobin level of 13.5 g per deciliter and 717 of whom were assigned to receive a dose targeted to achieve a level of 11.3 g per deciliter. The median study duration was 16 months. The primary end point was a composite of death, myocardial infarction, hospitalization for congestive heart failure (without renal replacement therapy), and stroke. A total of 222 composite events occurred: 125 events in the high-hemoglobin group, as compared with 97 events in the low-hemoglobin group (hazard ratio, 1.34; 95% confidence interval, 1.03 to 1.74; P=0.03). There were 65 deaths (29.3%), 101 hospitalizations for congestive heart failure (45.5%), 25 myocardial infarctions (11.3%), and 23 strokes (10.4%). Seven patients (3.2%) were hospitalized for congestive heart failure and myocardial infarction combined, and one patient (0.5%) died after having a stroke. Improvements in the quality of life were similar in the two groups. More patients in the high-hemoglobin group had at least one serious adverse event. The use of a target hemoglobin level of 13.5 g per deciliter (as compared with 11.3 g per deciliter) was associated with increased risk and no incremental improvement in the quality of life. (ClinicalTrials.gov number, NCT00211120 [ClinicalTrials.gov].). Copyright 2006 Massachusetts Medical Society.
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            A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease.

            Anemia is associated with an increased risk of cardiovascular and renal events among patients with type 2 diabetes and chronic kidney disease. Although darbepoetin alfa can effectively increase hemoglobin levels, its effect on clinical outcomes in these patients has not been adequately tested. In this study involving 4038 patients with diabetes, chronic kidney disease, and anemia, we randomly assigned 2012 patients to darbepoetin alfa to achieve a hemoglobin level of approximately 13 g per deciliter and 2026 patients to placebo, with rescue darbepoetin alfa when the hemoglobin level was less than 9.0 g per deciliter. The primary end points were the composite outcomes of death or a cardiovascular event (nonfatal myocardial infarction, congestive heart failure, stroke, or hospitalization for myocardial ischemia) and of death or end-stage renal disease. Death or a cardiovascular event occurred in 632 patients assigned to darbepoetin alfa and 602 patients assigned to placebo (hazard ratio for darbepoetin alfa vs. placebo, 1.05; 95% confidence interval [CI], 0.94 to 1.17; P=0.41). Death or end-stage renal disease occurred in 652 patients assigned to darbepoetin alfa and 618 patients assigned to placebo (hazard ratio, 1.06; 95% CI, 0.95 to 1.19; P=0.29). Fatal or nonfatal stroke occurred in 101 patients assigned to darbepoetin alfa and 53 patients assigned to placebo (hazard ratio, 1.92; 95% CI, 1.38 to 2.68; P<0.001). Red-cell transfusions were administered to 297 patients assigned to darbepoetin alfa and 496 patients assigned to placebo (P<0.001). There was only a modest improvement in patient-reported fatigue in the darbepoetin alfa group as compared with the placebo group. The use of darbepoetin alfa in patients with diabetes, chronic kidney disease, and moderate anemia who were not undergoing dialysis did not reduce the risk of either of the two primary composite outcomes (either death or a cardiovascular event or death or a renal event) and was associated with an increased risk of stroke. For many persons involved in clinical decision making, this risk will outweigh the potential benefits. (ClinicalTrials.gov number, NCT00093015.) 2009 Massachusetts Medical Society
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              Cardiac diseases in maintenance hemodialysis patients: results of the HEMO Study.

              Cardiac disease is a common cause of death in chronic hemodialysis patients. A subanalysis of the data on cardiac diseases in the Hemodialysis (HEMO) Study was performed. The specific objectives were: (1) to analyze the prevalence of cardiac disease at baseline; (2) to characterize the incidence of various types of cardiac events during follow-up; (3) to examine the association of cardiac events during follow-up with baseline cardiac diseases; and (4) to examine the effect of dose and flux interventions on various types of cardiac events. The HEMO Study is a randomized multi-center trial on 1846 chronic hemodialysis patients at 15 clinical centers comprising 72 dialysis units. The scheduled maximum follow-up duration was 0.9 to 6.6 years, with the mean actual follow-up of 2.84 years. The interventions were standard-dose versus high-dose and low-flux versus high-flux hemodialysis in a 2 x 2 factorial design. At baseline, 80% of patients had cardiac diseases, including ischemic heart disease (IHD) (39%), congestive heart failure (40%), arrhythmia (31%), and other heart diseases (63%). There were a total of 1685 cardiac hospitalizations, with angina and acute myocardial infarction accounting for 42.7% of these hospitalizations. There were 343 cardiac deaths during follow-up, accounting for 39.4% of all deaths. IHD was implicated in 61.5% of the cardiac deaths. Any cardiac disease at baseline was highly predictive of cardiac death during follow-up [relative risk (RR) 2.57; 95% CI 1.73-3.83]. There were no significant effects of dose or flux assignments on the primary outcome of all-cause mortality or the main secondary cardiac composite outcome of first cardiac hospitalization or all-cause mortality. Assignment to high-flux dialysis was, however, associated with decreased cardiac mortality and the composite outcome of first cardiac hospitalization or death from cardiac causes. The HEMO Study identified IHD to be a major cause of cardiac hospitalizations and cardiac deaths. Future strategies for the prevention of cardiac diseases in the maintenance hemodialysis population should focus on this entity. Although high-flux dialysis did not reduce all-cause mortality, it might improve cardiac outcomes. This hypothesis needs to be further examined.
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                Author and article information

                Journal
                Ren Fail
                Ren Fail
                IRNF
                irnf20
                Renal Failure
                Taylor & Francis
                0886-022X
                1525-6049
                2019
                28 May 2019
                : 41
                : 1
                : 393-400
                Affiliations
                [a ]Emergency Medicine Unit, Outpatient Department, King Chulalongkorn Memorial Hospital, The Thai Red Cross Society , Bangkok, Thailand;
                [b ]Emergency Medicine Unit, Department of Medicine, Faculty of Medicine, Chulalongkorn University , Bangkok, Thailand;
                [c ]Bhumirajanakarindra Kidney Institute Hospital , Bangkok, Thailand;
                [d ]Division of Nephrology, Department of Medicine, King Chulalongkorn Memorial Hospital, Thai Red Cross Society and Faculty of Medicine, Chulalongkorn University , Bangkok, Thailand
                Author notes
                [*]

                Tanawat Tarapan and Khrongwong Musikatavorn equally share as the first author.

                CONTACT Khajohn Tiranathanagul Khajohn.T@ 123456chula.ac.th Division of Nephrology, Department of Medicine, King Chulalongkorn Memorial Hospital and Faculty of Medicine, Chulalongkorn University , Bangkok10330, Thailand
                Author information
                https://orcid.org/0000-0002-5746-0724
                http://orcid.org/0000-0002-6236-8893
                https://orcid.org/0000-0001-9813-9219
                https://orcid.org/0000-0002-6214-7855
                https://orcid.org/0000-0003-0136-8942
                Article
                1603110
                10.1080/0886022X.2019.1603110
                6542185
                31132904
                d23ca00c-2e7a-4f82-a75b-5b3cda3a9a95
                © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

                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.

                History
                : 04 July 2018
                : 26 March 2019
                : 26 March 2019
                Page count
                Figures: 1, Tables: 3, Pages: 8, Words: 4736
                Funding
                This work was funded by Ratchadapiseksompotch MD.CU. Grant number 520/2014, Faculty of Medicine, Chulalongkorn University.
                Categories
                Clinical Study

                Nephrology
                hemodialysis,troponin i,myocardial injury
                Nephrology
                hemodialysis, troponin i, myocardial injury

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