scholarly journals Peritoneal Dialysis for Chronic Congestive Heart Failure

2015 ◽  
Vol 40 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Karlien François ◽  
Claudio Ronco ◽  
Joanne M. Bargman

Maladaptive responses between a failing heart and the kidneys ultimately lead to permanent chronic kidney disease, referred to as cardiorenal syndrome type 2. In this narrative review, we discuss the pathophysiological pathways in the progression of cardiorenal failure and review the current evidence on peritoneal dialysis as a treatment strategy in cardiorenal syndrome type 2. A patient with heart failure can present with clinical symptoms related to venous congestion even in the absence of end-stage renal disease. Diuretics remain the cornerstone for the treatment of fluid overload related to heart failure. However, with chronic use, diuretic resistance can supervene. When medical therapy is no longer able to relieve congestive symptoms, ultrafiltration might be needed. Patients with heart failure tolerate well the gentle rate of fluid removal through peritoneal dialysis. Recent publications suggest a positive impact of starting peritoneal dialysis in patients with cardiorenal syndrome type 2 on the hospitalisation rate, functional status and quality of life.

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Qiuyuan Shao ◽  
Yangyang Xia ◽  
Min Zhao ◽  
Jing Liu ◽  
Qingyan Zhang ◽  
...  

Aims. To evaluate the effectiveness and safety of peritoneal dialysis (PD) in treating refractory congestive heart failure (RCHF) with cardiorenal syndrome (CRS).Methods. A total of 36 patients with RCHF were divided into type 2 CRS group (group A) and non-type 2 CRS group (group B) according to the patients’ clinical presentations and the ratio of serum urea to creatinine and urinary analyses in this prospective study. All patients were followed up till death or discontinuation of PD. Data were collected for analysis, including patient survival time on PD, technique failure, changes of heart function, and complications associated with PD treatment and hospitalization.Results. There were 27 deaths and 9 patients quitting PD program after a follow-up for 73 months with an average PD time of22.8±18.2months. A significant longer PD time was found in group B as compared with that in group A (29.0±19.4versus13.1±10.6months,p=0.003). Kaplan–Meier curves showed a higher survival probability in group B than that in group A (p<0.001). Multivariate regression demonstrated that type 2 CRS was an independent risk factor for short survival time on PD. The benefit of PD on the improvement of survival and LVEF was limited to group B patients, but absent from group A patients. The impairment of exercise tolerance indicated by NYHA classification was markedly improved by PD for both groups. The technique survival was high, and the hospital readmission was evidently decreased for both group A and group B patients.Conclusions. Our data suggest that PD is a safe and feasible palliative treatment for RCHF with type 2 CRS, though the long-term survival could not be expected for patients with the type 2 CRS. Registration ID Number isChiCTR1800015910.


2013 ◽  
Vol 33 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Masaaki Nakayama

Cardiorenal syndrome (CRS) type II is a serious condition in which chronic cardiac abnormalities cause worsening kidney function, leading to permanent chronic kidney damage. Management of CRS type II coupled with diuretic-resistant congestive heart failure (CHF) has been an issue of dispute. However, since the early 1990s, reports indicating the clinical usefulness of peritoneal dialysis (PD) as maintenance therapy for intractable CHF in this population have been accumulating. The present manuscript reviews the mechanisms by which kidney dysfunction develops within CHF, and then examines recent experiences of PD as chronic supportive therapy for intractable CRS type II, reviews the contributing mechanisms, and discusses the rationale for using PD as a new therapeutic approach in the nonuremic setting of CHF.


2015 ◽  
Vol 6 (1) ◽  
pp. 61-72 ◽  
Author(s):  
Annalisa Angelini ◽  
Chiara Castellani ◽  
Grazia Maria Virzì ◽  
Marny Fedrigo ◽  
Gaetano Thiene ◽  
...  

Background: In cardiorenal syndrome type 2 (CRS2), the role of systemic congestion in heart failure (HF) is still obscure. We studied a model of CRS2 [monocrotaline (MCT)-treated rats] secondary to pulmonary hypertension and right ventricular (RV) failure in order to evaluate the contribution of prevalent congestion to the development of kidney injury. Methods: Ten animals were treated with MCT for 4 weeks until they developed HF. Eleven animals were taken as controls. Signs of hypertrophy and dilatation of the right ventricle demonstrated the occurrence of HF. Brain natriuretic peptide (BNP), serum creatinine (sCreatinine), both kidney and heart neutrophil gelatinase-associated lipocalin (NGAL), matrix metallopeptidase 9 (MMP9), serum cytokines as well as kidney and heart cell death, as assessed by TUNEL, were studied. Results: Rats with HF showed higher BNP levels [chronic HF (CHF) 4.8 ± 0.5 ng/ml; controls 1.5 ± 0.2 ng/ml; p < 0.0001], marked RV hypertrophy and dilatation (RV mass/RV volume: CHF 1.46 ± 0.31, controls 2.41 ± 0.81; p < 0.01) as well as pleural and peritoneal effusions. A significant increase in proinflammatory cytokines and sCreatinine was observed (CHF 3.06 ± 1.3 pg/ml vs. controls 0.54 ± 0.23 pg/ml; p = 0.04). Serum (CHF 562.7 ± 93.34 ng/ml vs. controls 245.3 ± 58.19 ng/ml; p = 0.02) as well as renal and heart tissue NGAL levels [CHF 70,680 ± 4,337 arbitrary units (AU) vs. controls 32,120 ± 4,961 AU; p = 0.001] rose significantly, and they were found to be complexed with MMP9 in CHF rats. A higher number of kidney TUNEL-positive tubular cells was also detected (CHF 114.01 ± 45.93 vs. controls 16.36 ± 11.60 cells/mm2; p = 0.0004). Conclusion: In this model of CHF with prevalent congestion, kidney injury is characterized by tubular damage and systemic inflammation. The upregulated NGAL complexed with MMP9 perpetuates the vicious circle of kidney/heart damage by enhancing the enzymatic activity of MMP9 with extracellular matrix degradation, worsening heart remodeling.


Author(s):  
Paula Sienes Bailo ◽  
José Luis Bancalero Flores ◽  
Raquel Lahoz Alonso ◽  
María Santamaría González ◽  
Alex Gutiérrez Dalmau ◽  
...  

ABSTRACT Objectives Patients with Alport syndrome develop progressive kidney function deterioration, sensorineural hearing loss, and ocular abnormalities. This condition is caused by mutations in COL4A5 (X-linked inheritance), COL4A3 and COL4A4 (autosomal dominant or recessive inheritance), and encoding type IV collagen α3, α4, and α5, respectively. If left untreated, clinical symptoms progress from microscopic hematuria to proteinuria, progressive kidney failure, and end-stage kidney disease. At present, kidney transplantation is the only effective approach. Next-generation sequencing is the method of choice for the diagnosis of this condition. Case presentation We report the case of a young man with chronic kidney disease who eventually underwent transplantation. Molecular testing made it possible to determine the etiology of his clinical symptoms and autosomal recessive Alport syndrome type 2. The patient was found to be a compound heterozygote for two missense variants (trans configuration) in the COL4A3 gene: A likely pathogenic variant c.4981C>T (p.Arg1661Cys) in exon 52 inherited from the mother (described elsewhere), and another variant of uncertain significance, c.943G>A (p.Gly315Ser), in exon 17 inherited from the father that has not been previously reported in the literature or found in relevant databases. Conclusions Following genetic confirmation, genetic counseling was provided to the patient and his direct relatives.


2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Agnieszka Gala-Błądzińska ◽  
Janusz Romanek ◽  
Danuta Mazur ◽  
Tomasz Stepek ◽  
Marcin Braun ◽  
...  

Background. Patients with chronic cardiorenal syndrome type 2 (T2-CRS) who qualify for resynchronization therapy (CRT) are exposed perioperatively to potentially nephrotoxic factors including contrast agents and blood loss. Methods. The objective of this prospective interventional study was to assess the effects of CRT on renal function in patients with T2-CRS within the first 48 hours following implantation. Initially, 76 patients (15% female; aged 69 ± 9.56 years) with heart failure (New York Heart Association classes II–IV), ejection fraction ≤ 35%, and QRS > 130 ms were included in the study. During CRT implantation, a nonionic contrast agent (72.2 ± 44.9 mL) was administered. Prior to and 48 hours following implantation, renal function was evaluated using the following serum biomarkers: creatinine (sCr), estimated glomerular filtration rate (using the Chronic Kidney Disease Epidemiology Collaboration equation [eGFRCKD-EPI]), and the electrolyte and urine biomarkers albumin (uAlb), albumin/creatinine ratio (UACR), and neutrophil gelatinase-associated lipocalin (uNGAL). Results. Before CRT, patients classified as NYHA class III or IV had higher uNGAL levels in comparison to uNGAL levels after CRT (43.63 ± 60.02 versus 16.63 ± 18.19; p=0.041). After CRT implantation, uAlb, UACR, and potassium levels were reduced (p<0.05), and uNGAL, sCr, and eGFRCKD-EPI were unchanged. The contrast medium volume did not correlate with the test biomarkers (p>0.05). Conclusions. In patients with T2-CRS, uNGAL is a biomarker of kidney injury that correlates with the NYHA classes. A stable uNGAL value before and after CRT implantation confirms the lack of risk of contrast-induced nephropathy. Reduced albuminuria and blood potassium are biomarkers of improving T2-CRS in the early post-CRT period.


2016 ◽  
Vol 12 (3) ◽  
pp. 186-194 ◽  
Author(s):  
Jois Preeti ◽  
Mebazaa Alexandre ◽  
Pupalan Iyngkaran ◽  
Thomas C. Merlin ◽  
Ronco Claudio

2019 ◽  
Vol 9 (2) ◽  
pp. 117-124 ◽  
Author(s):  
Amir Kazory ◽  
Abhilash Koratala ◽  
Claudio Ronco

Background: Peritoneal dialysis (PD) has emerged as a mechanistically relevant therapeutic option for patients with heart failure (HF), volume overload, and varying degrees of renal dysfunction (i.e., chronic cardiorenal syndrome). Congestion has been identified as a potent ominous prognostic factor in this patient population, outperforming a number of established risk factors. As such, excess fluid removal is recognized as a relevant therapeutic target in this setting. Methods: Accumulating evidence points to the importance of sodium removal as part of any decongestive strategy because extraction of sodium-free water has little or no impact on the outcomes of these patients. Hence, optimization of sodium removal by PD should be the primary focus in the setting of HF and cardiorenal syndrome, especially if PD is started when the patient still has adequate residual renal function for clearance of waste products. Results: Herein, we provide an overview of approaches that can tailor PD treatment to the patients’ characteristics and clinical needs (e.g., choice of PD modality) to fully exploit its decongestive properties. Other methods that could prove helpful in the future will also be briefly discussed. Conclusion: While these strategies could help with efficient sodium extraction and volume optimization, future studies are needed to evaluate their impact on the outcomes of this specific patient population.


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