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      Peritoneal dialysis as therapeutic option in heart failure patients

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          Abstract

          Aims

          Each episode of acute decompensated heart failure (HF) incrementally adds to mortality. Peritoneal dialysis (PD) offers an alternative therapeutic option in refractory HF and reduces the incidence of decompensation episodes. The objective of this study was to determine the efficacy of PD, in terms of functional status, surrogate endpoints, rate of hospitalizations, and mortality.

          Methods and results

          This study is based on the registry of the German Society of Nephrology, involving 159 patients receiving PD treatment due to refractory HF between January 2010 and December 2014. Body weight was reduced by PD (82.2 ± 14.9 to 78.4 ± 14.8 kg, P < 0.001), and significant improvements in New York Heart Association functional class (3.38 ± 0.55 to 2.85 ± 0.49, P < 0.001) were found already after 3 months. Left ventricular ejection fraction did not change (31.5 ± 13.8 to 34.0 ± 15.7%, P = 0.175). C‐reactive protein improved with PD treatment (33.7 ± 52.6 to 17.1 ± 26.3 mg/L, P = 0.004). Blood urea nitrogen/creatinine ratio decreased significantly (148.7 ± 68.3 to 106.7 ± 44.8 mg/dL, P < 0.001). Hospitalization rates decreased significantly (total number 2.86 ± 1.88 to 1.90 ± 1.78, P = 0.001, and 39.2 ± 30.7 to 27.1 ± 25.2 days, P = 0.004). One year mortality was 39.6% in end‐stage HF patients treated with PD.

          Conclusions

          Peritoneal dialysis offers an additional therapeutic option in end‐stage HF and is associated with improved New York Heart Association classification and reduced hospitalization. Although PD treatment was associated with various benefits, further studies are necessary to identify which patients benefit the most from PD.

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          Most cited references38

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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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            Importance of venous congestion for worsening of renal function in advanced decompensated heart failure.

            To determine whether venous congestion, rather than impairment of cardiac output, is primarily associated with the development of worsening renal function (WRF) in patients with advanced decompensated heart failure (ADHF). Reduced cardiac output is traditionally believed to be the main determinant of WRF in patients with ADHF. A total of 145 consecutive patients admitted with ADHF treated with intensive medical therapy guided by pulmonary artery catheter were studied. We defined WRF as an increase of serum creatinine >/=0.3 mg/dl during hospitalization. In the study cohort (age 57 +/- 14 years, cardiac index 1.9 +/- 0.6 l/min/m(2), left ventricular ejection fraction 20 +/- 8%, serum creatinine 1.7 +/- 0.9 mg/dl), 58 patients (40%) developed WRF. Patients who developed WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm Hg vs. 12 +/- 6 mm Hg, p < 0.001) and after intensive medical therapy (11 +/- 8 mm Hg vs. 8 +/- 5 mm Hg, p = 0.04). The development of WRF occurred less frequently in patients who achieved a CVP <8 mm Hg (p = 0.01). Furthermore, the ability of CVP to stratify risk for development of WRF was apparent across the spectrum of systemic blood pressure, pulmonary capillary wedge pressure, cardiac index, and estimated glomerular filtration rates. Venous congestion is the most important hemodynamic factor driving WRF in decompensated patients with advanced heart failure.
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              Heart failure.

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                Author and article information

                Contributors
                leonie.grossekettler@med.uni-heidelberg.de
                Journal
                ESC Heart Fail
                ESC Heart Fail
                10.1002/(ISSN)2055-5822
                EHF2
                ESC Heart Failure
                John Wiley and Sons Inc. (Hoboken )
                2055-5822
                27 February 2019
                April 2019
                : 6
                : 2 ( doiID: 10.1002/ehf2.v6.2 )
                : 271-279
                Affiliations
                [ 1 ] Department of Internal Medicine III, Cardiology, Angiology and Pulmonology University Hospital of Heidelberg Im Neuenheimer Feld 410 69120 Heidelberg Germany
                [ 2 ] Clinic for Cardiac Surgery University Hospital of Heidelberg Heidelberg Germany
                [ 3 ] Clinic for Cardiology Heart and Vascular Center Bad Bevensen Germany
                [ 4 ] Department of Nephrology Medical Center Bad Bevensen Germany
                [ 5 ] Department of Nephrology Clinic Braunschweig Braunschweig Germany
                [ 6 ] Department of Internal Medicine I, Endocrinology and Nephrology University Hospital of Heidelberg Heidelberg Germany
                [ 7 ] Department of Kidney, Blood Pressure and Autoimmune Diseases Katharinenhospital, Klinikum Stuttgart Stuttgart Germany
                Author notes
                [*] [* ] Correspondence to: Leonie Grossekettler, Department of Internal Medicine III, Cardiology, Angiology and Pulmonology, University Hospital of Heidelberg, Im Neuenheimer Feld 410, Heidelberg 69120, Germany. Tel: +49 6221 56 8611; Fax: +49 6221 56 8612. Email: leonie.grossekettler@ 123456med.uni-heidelberg.de

                [†]

                These authors contributed equally to this work.

                Article
                EHF212411 ESCHF-18-00084
                10.1002/ehf2.12411
                6437425
                30815994
                ae47aeaf-58b8-495c-ab16-77d2ddbc973c
                © 2019 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 12 April 2018
                : 06 January 2019
                Page count
                Figures: 5, Tables: 3, Pages: 9, Words: 2854
                Funding
                Funded by: Deutsche Gesellschaft für Nephrologie e.V. (DGfN)
                Categories
                Original Research Article
                Original Research Articles
                Custom metadata
                2.0
                ehf212411
                April 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.1 mode:remove_FC converted:28.03.2019

                heart failure,cardiorenal syndrome,peritoneal dialysis,ultrafiltration

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