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Department of Biomedicine,1 Göteborg University, Göteborg; Gambro AB,2 Lund, Sweden
Correspondence to: M. Braide, Department of Biomedicine, Göteborg University, Box 420, SE 405 30 Göteborg, Sweden. Magnus.Braide{at}gu.se
Background: Exposure to peritoneal dialysis (PD) fluid
induces an inflammatory response in the peritoneal cavity. Blockers of
complement and coagulation have improved ultrafiltration in animal models of
PD. Citrate is a clinically established anticoagulant that also blocks
complement activation.
Objective: The aim of the present study was to evaluate
the effects on ultrafiltration of a gradual substitution of citrate for
lactate in an experimental model of PD.
Methods: Fractions (0, 5, 10, and 15 mmol/L) of the 40
mmol/L lactate buffer of filter-sterilized 2.5% glucose PD fluid were replaced
by citrate. The modified fluids were compared in a rat model of single PD
fluid exposure through an indwelling catheter. The initial kinetics of citrate
and ionized calcium were evaluated in separate, single, short time dwell
experiments.
Results: Replacing 10 and 15 mmol/L of the lactate
buffer by sodium citrate significantly increased osmotic ultrafiltration (by
24.7% ± 7.7% at 10 mmol/L), net ultrafiltration, and glucose retention
at 4 hours of dwell time in the rat model. Osmotic ultrafiltration was
significantly correlated to citrate concentration and glucose concentration.
Citrate was rapidly eliminated from the peritoneal cavity, concentrations
falling to less than half in 1 hour and concentrations of calcium ions
concomitantly normalized.
Conclusions: Substituting citrate for lactate induced a
dose-dependent increase in ultrafiltration. Mechanisms probably involve the
relation between diffusion and ultrafiltration, leading to increased glucose
retention. The increase in ultrafiltration was quantitatively important at a
citrate concentration (10 mmol/L) that is compatible with clinical
applications of citrate.
KEY WORDS: Ultrafiltration; lactate; citrate; rats.
Received 28 June 2007; accepted 12 May 2008.
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