Clinical kidney journal · 2024
Intradialytic cardiovascular injury is lowest in high-volume haemodiafiltration: a randomized cross-over trial in four intermittent dialysis strategies.
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Liu Peiyun, Rootjes Paul A, de Roij van Zuijdewijn Camiel L M, Hau Chi M, Nubé Menso J, Nieuwland Rienk, Wijngaarden Gertrude, Grooteman Muriel P C
Аннотация
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.
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.