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      A comparative effectiveness research study of the change in blood pressure during hemodialysis treatment and survival

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          Abstract

          It is not clear to what extent changes in blood pressure (BP) during hemodialysis affect or predict survival. Studying comparative outcomes of BP changes during hemodialysis can have major clinical implications including the impact on management strategies in hemodialysis patients. Here we undertook a retrospective cohort study of 113,255 hemodialysis patients over a 5 year period to evaluate an association between change in BP during hemodialysis and mortality. The change in BP was defined as post- minus pre-hemodialysis BP and mean of BP change values during the hemodialysis session was used as a mortality predictor. The patients averaged 61 years old and consisted of 45% women, 32% African-Americans and 58% diabetics. Over a median follow-up of 2.2 years, a total of 53,461 (47.2%) all-cause and 21,548 (25.7%) cardiovascular deaths occurred. In fully adjusted Cox regression model with restricted cubic splines, there was a U-shaped association between change systolic BP and all-cause mortality. Post-dialytic drops in systolic BP between −30 to 0 mmHg were associated with greater survival, but large decreases of systolic BP (more than −30 mmHg) and any increase in systolic BP (over 0 mmHg) were related to increased mortality. Peak survival was found at a change in systolic BP of −14 mmHg. The U-shaped association was also found for cardiovascular mortality. Thus, modest declines in BP after hemodialysis are associated with the greatest survival, whereas any rise or large decline in BP is associated with worsened survival.

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          Most cited references34

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          Malnutrition-inflammation complex syndrome in dialysis patients: causes and consequences.

          Protein-energy malnutrition (PEM) and inflammation are common and usually concurrent in maintenance dialysis patients. Many factors that appear to lead to these 2 conditions overlap, as do assessment tools and such criteria for detecting them as hypoalbuminemia. Both these conditions are related to poor dialysis outcome. Low appetite and a hypercatabolic state are among common features. PEM in dialysis patients has been suggested to be secondary to inflammation; however, the evidence is not conclusive, and an equicausal status or even opposite causal direction is possible. Hence, malnutrition-inflammation complex syndrome (MICS) is an appropriate term. Possible causes of MICS include comorbid illnesses, oxidative and carbonyl stress, nutrient loss through dialysis, anorexia and low nutrient intake, uremic toxins, decreased clearance of inflammatory cytokines, volume overload, and dialysis-related factors. MICS is believed to be the main cause of erythropoietin hyporesponsiveness, high rate of cardiovascular atherosclerotic disease, decreased quality of life, and increased mortality and hospitalization in dialysis patients. Because MICS leads to a low body mass index, hypocholesterolemia, hypocreatininemia, and hypohomocysteinemia, a "reverse epidemiology" of cardiovascular risks can occur in dialysis patients. Therefore, obesity, hypercholesterolemia, and increased blood levels of creatinine and homocysteine appear to be protective and paradoxically associated with a better outcome. There is no consensus about how to determine the degree of severity of MICS or how to manage it. Several diagnostic tools and treatment modalities are discussed. Successful management of MICS may ameliorate the cardiovascular epidemic and poor outcome in dialysis patients. Clinical trials focusing on MICS and its possible causes and consequences are urgently required to improve poor clinical outcome in dialysis patients.
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            Hemodialysis-induced cardiac injury: determinants and associated outcomes.

            Hemodialysis (HD)-induced myocardial stunning driven by ischemia is a recognized complication of HD, which can be ameliorated by HD techniques that improve hemodynamics. In nondialysis patients, repeated ischemia leads to chronic reduction in left ventricular (LV) function. HD may initiate and drive the same process. In this study, we examined the prevalence and associations of HD-induced repetitive myocardial injury and long-term effects on LV function and patient outcomes. Seventy prevalent HD patients were assessed for evidence of subclinical myocardial injury at baseline using serial echocardiography and followed up after 12 mo. Intradialytic blood pressure, hematologic and biochemical samples, and patient demographics were also collected at both time points. Sixty-four percent of patients had significant myocardial stunning during HD. Age, ultrafiltration volumes, intradialytic hypotension, and cardiac troponin-T (cTnT) levels were independent determinants associated with its presence. Myocardial stunning was associated with increased relative mortality at 12 mo (P = 0.019). Cox regression analysis showed increased hazard of death in patients with myocardial stunning and elevated cTnT than in patients with elevated cTnT alone (P < 0.02). Patients with myocardial stunning who survived 12 mo had significantly lower LV ejection fractions at rest and on HD (P < 0.001). HD-induced myocardial stunning is common, and may contribute to the development of heart failure and increased mortality in HD patients. Enhanced understanding of dialysis-induced cardiac injury may provide novel therapeutic targets to reduce currently excessive rates of cardiovascular morbidity and mortality.
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              Hemodialysis-associated hypotension as an independent risk factor for two-year mortality in hemodialysis patients.

              The relationship between blood pressure (BP) and mortality in hemodialysis patients has remained controversial. Some studies suggested that a lower pre- or postdialysis BP was associated with excess mortality, while others showed poorer outcome in patients with uncontrolled hypertension. We conducted a multicenter prospective cohort study to evaluate the impact of hemodialysis-associated hypotension on mortality. We recruited 1244 patients (685 males; mean age, 60 +/- 13 years) who underwent hemodialysis in 28 units during the two-year study period beginning in December 1999. Pre-, intra-, and postdialysis BP, and BP upon standing soon after hemodialysis, were measured in all patients at entry. Logistic regression analysis was used to assess the effect on mortality of pre-, intra-, and postdialysis BP, a fall in BP during hemodialysis, and a fall in BP upon standing soon after hemodialysis. During the study period, 149 patients died. Logistic models identified the lowest intradialysis systolic blood pressure (SBP) and degree of fall in SBP upon standing soon after hemodialysis as significant factors affecting mortality, but not pre- or postdialysis SBP and diastolic BP. The adjusted odds ratio for death was 0.79 (95% CI 0.64-0.98) when the lowest intradialysis SBP was analyzed in increments of 20 mm Hg, and was 0.82 (95% CI 0.67-0.98) when the fall in SBP upon standing soon after hemodialysis was analyzed in increments of 10 mm Hg. These results suggest that intradialysis hypotension and orthostatic hypotension after hemodialysis are significant and independent factors affecting mortality in hemodialysis patients.
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                Author and article information

                Journal
                0323470
                5428
                Kidney Int
                Kidney Int.
                Kidney international
                0085-2538
                1523-1755
                7 June 2013
                19 June 2013
                October 2013
                01 April 2014
                : 84
                : 4
                : 795-802
                Affiliations
                [1 ]Harold Simmons Center for Kidney Disease Research and Epidemiology, University of California, Irvine, School of Medicine, Orange, CA, USA
                [2 ]Division of Nephrology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea
                [3 ]Division of Nephrology, Brigham and Women’s Hospital, Boston, MA, USA
                [4 ]Division of Nephrology and Hypertension, Kaiser Permanente Medical Center, Los Angeles, CA, USA
                [5 ]Division of Nephrology, Kyungpook National University School of Medicine, Daegu, Republic of Korea
                [6 ]Division of Nephrology and Hypertension, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA
                [7 ]Division of Nephrology, Memphis Veterans Affairs Medical Center, Memphis, TN, USA
                [8 ]Division of Nephrology, University of Tennessee Health Science Center, Memphis, TN, USA
                [9 ]Department of Epidemiology, UCLA Fielding School of Public Health, Los Angeles, CA, USA
                Author notes
                Correspondence: Kamyar Kalantar-Zadeh, MD, MPH, PhD, Harold Simmons Center for Kidney Disease Research & Epidemiology, Division of Nephrology & Hypertension, University of California Irvine, School of Medicine, 101 The City Drive South, City Tower, Suite 400 - ZOT: 4088, Orange, California 92868-3217, Tel: (714) 456-5142, Fax: (714) 456-6034, kkz@ 123456uci.edu
                Article
                NIHMS481065
                10.1038/ki.2013.237
                3788841
                23783241
                02ed9b65-86be-436b-a9ff-e913bf1d1cef
                History
                Funding
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R13 DK094686 || DK
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: R01 DK078106 || DK
                Funded by: National Institute of Diabetes and Digestive and Kidney Diseases : NIDDK
                Award ID: K24 DK091419 || DK
                Categories
                Article

                Nephrology
                Nephrology

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