TY - JOUR
T1 - Reduction in platelet activation by citrate anticoagulation does not prevent intradialytic hemodynamic instability
AU - Gritters, Mareille
AU - Borgdorff, Piet
AU - Grooteman, Muriel P C
AU - Schoorl, Marianne
AU - Schoorl, Margreet
AU - Bartels, Piet C M
AU - Tangelder, Geert Jan
AU - Nubé, Menso J
N1 - Copyright 2007 S. Karger AG, Basel.
PY - 2007
Y1 - 2007
N2 - BACKGROUND: The etiology of intradialytic hemodynamic instability is multifactorial. Of the various factors involved, a rise in core temperature seems to be crucial. In this respect, the bioincompatibility of hemodialysis (HD) treatment might play an important role. The application of cool dialysate reduces the number of periods of intradialytic hypotension (IDH) considerably. In rats, roller pump perfusion caused hypotension by shear stress induced platelet aggregation and subsequent serotonin release. During clinical HD, citrate anticoagulation abolished platelet activation almost completely. Hence, citrate anticoagulation might reduce IDH, whereas the beneficial effect of cool dialysate might be partly explained by reduced platelet activation.METHODS: In the present study, blood pressure, IDH episodes, platelet activation, platelet aggregation, and serotonin release were studied crossover in 10 patients during HD with dalteparin anticoagulation at normal and low dialysate temperatures and during HD with citrate.RESULTS: Citrate strongly reduced platelet activation, but did not improve IDH. The blood pressure was best preserved during cool-temperature HD, despite manifest platelet activation. Platelet activation was not accompanied by a rise in the plasma serotonin concentration.CONCLUSIONS: Three major conclusions can be drawn: (1) it is unlikely that platelet activation and subsequent serotonin release underlie IDH in the clinical situation; (2) the protective effects of cool dialysate on IDH appear to be independent of HD-induced platelet activation, and (3) extrapolating results from rat experiments to the human situation requires uppermost prudence.
AB - BACKGROUND: The etiology of intradialytic hemodynamic instability is multifactorial. Of the various factors involved, a rise in core temperature seems to be crucial. In this respect, the bioincompatibility of hemodialysis (HD) treatment might play an important role. The application of cool dialysate reduces the number of periods of intradialytic hypotension (IDH) considerably. In rats, roller pump perfusion caused hypotension by shear stress induced platelet aggregation and subsequent serotonin release. During clinical HD, citrate anticoagulation abolished platelet activation almost completely. Hence, citrate anticoagulation might reduce IDH, whereas the beneficial effect of cool dialysate might be partly explained by reduced platelet activation.METHODS: In the present study, blood pressure, IDH episodes, platelet activation, platelet aggregation, and serotonin release were studied crossover in 10 patients during HD with dalteparin anticoagulation at normal and low dialysate temperatures and during HD with citrate.RESULTS: Citrate strongly reduced platelet activation, but did not improve IDH. The blood pressure was best preserved during cool-temperature HD, despite manifest platelet activation. Platelet activation was not accompanied by a rise in the plasma serotonin concentration.CONCLUSIONS: Three major conclusions can be drawn: (1) it is unlikely that platelet activation and subsequent serotonin release underlie IDH in the clinical situation; (2) the protective effects of cool dialysate on IDH appear to be independent of HD-induced platelet activation, and (3) extrapolating results from rat experiments to the human situation requires uppermost prudence.
KW - Adult
KW - Aged
KW - Aged, 80 and over
KW - Anticoagulants/administration & dosage
KW - Blood Pressure/drug effects
KW - Citric Acid/administration & dosage
KW - Female
KW - Humans
KW - Hypertension/etiology
KW - Male
KW - Middle Aged
KW - Platelet Activation/drug effects
KW - Renal Dialysis/adverse effects
KW - Renal Insufficiency/complications
U2 - 10.1159/000100496
DO - 10.1159/000100496
M3 - Article
C2 - 17347579
VL - 106
SP - c9-16
JO - Nephron. Clinical practice
JF - Nephron. Clinical practice
SN - 1660-2110
IS - 1
ER -