Intradialytic cardiovascular injury is lowest in high-volume haemodiafiltration: a randomized cross-over trial in four intermittent dialysis strategies

Author:

Liu Peiyun12,Rootjes Paul A134ORCID,de Roij van Zuijdewijn Camiel L M145ORCID,Hau Chi M6,Nubé Menso J14,Nieuwland Rienk6ORCID,Wijngaarden Gertrude14,Grooteman Muriel P C14

Affiliation:

1. Department of Nephrology, Amsterdam UMC, location Vrije Universiteit Amsterdam , Amsterdam , the Netherlands

2. Department of Renal Medicine, Singapore General Hospital, Singapore , Singapore

3. Department of Internal Medicine, Gelre Hospitals , Apeldoorn , the Netherlands

4. Amsterdam Cardiovascular Sciences (ACS), Diabetes & Metabolism , Amsterdam , the Netherlands

5. Department of Internal Medicine , Spaarne Gasthuis, Haarlem , the Netherlands

6. Laboratory of Experimental Clinical Chemistry, Amsterdam University Medical Center, University of Amsterdam , Amsterdam , the Netherlands

Abstract

ABSTRACT Background Intradialytic hypotension (IDH) and subsequent tissue damage may contribute to the poor outcome of chronic haemodialysis (HD) patients. While the IDH-incidence is lower in high-volume haemodiafiltration (HV-HDF) than in standard HD (S-HD), survival is better in HV-HDF. Tissue injury, as measured by extracellular vesicle (EV)-release, was compared between four modalities. Methods Forty chronic patients were cross-over randomized to S-HD, cool-HD (C-HD), low-volume HDF (LV-HDF), and HV-HDF. Blood pressure was recorded every 15 minutes. EVs from circulating blood-cell-elements (bio-incompatibility-related) and cardiovascular (CV) tissues (CV-related), were measured before and after dialysis. The influence of modalities and IDH on the rate of change of EVs was assessed. Both crude and haemoconcentration-adjusted analyses were performed. Results Leukocyte and erythrocyte-derived EVs increased in all modalities. Platelet-derived EVs increased more in LV-HDF and HV-HDF (68.4 respectively 56.1 × 106/ml) than in S-HD (27.5 × 106/ml), P values for interaction were <.01 respectively .06. Endothelial-derived CD144+ (2.3 × 106/ml in HV-HDF and 9.8 × 106/ml in S-HD) and cardiomyocyte-derived Connexin-43+ (12.0 respectively 31.9 × 106/ml) EVs increased less in HV-HDF than in S-HD (P for interaction .03 respectively .06). Correction for haemoconcentration attenuated all changes, although the increase in platelet-derived EVs remained significant in LV-HDF and HV-HDF, and CD144+ and Connexin-43+ EVs increased most in S-HD. EV release was similar in patients with varying IDH susceptibility and in sessions with and without IDH. Conclusions Most EVs increase during HD and HDF. Regarding platelet-derived EVs, HDF appears less biocompatible than HD. Considering CV-related EVs, tissue injury seems less pronounced in HV-HDF. The finding that EV release is IDH-independent needs confirmation.

Funder

Niercentrum aan de Amstel, Amstelveen, The Netherlands

B. Braun Avitum AG, Melsungen

Publisher

Oxford University Press (OUP)

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