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      Citrate- vs. acetate-based dialysate in bicarbonate haemodialysis: consequences on haemodynamics, coagulation, acid-base status, and electrolytes

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          Abstract

          Background

          A concentrate for bicarbonate haemodialysis acidified with citrate instead of acetate has been marketed in recent years. The small amount of citrate used (one-fifth of the concentration adopted in regional anticoagulation) protects against intradialyser clotting while minimally affecting the calcium concentration. The aim of this study was to compare the impact of citrate- and acetate-based dialysates on systemic haemodynamics, coagulation, acid-base status, calcium balance and dialysis efficiency.

          Methods

          In 25 patients who underwent a total of 375 dialysis sessions, an acetate dialysate (A) was compared with a citrate dialysate with (C+) or without (C) calcium supplementation (0.25 mmol/L) in a randomised single-blind cross-over study. Systemic haemodynamics were evaluated using pulse-wave analysis. Coagulation, acid-base status, calcium balance and dialysis efficiency were assessed using standard biochemical markers.

          Results

          Patients receiving the citrate dialysate had significantly lower systolic blood pressure (BP) (-4.3 mmHg, p < 0.01) and peripheral resistances (PR) (-51 dyne.sec.cm -5, p < 0.001) while stroke volume was not increased. In hypertensive patients there was a substantial reduction in BP (-7.8 mmHg, p < 0.01). With the C+ dialysate the BP gap was less pronounced but the reduction in PR was even greater (-226 dyne.sec.cm -5, p < 0.001). Analyses of the fluctuations in PR and of subjective tolerance suggested improved haemodynamic stability with the citrate dialysate. Furthermore, an increase in pre-dialysis bicarbonate and a decrease in pre-dialysis BUN, post-dialysis phosphate and ionised calcium were noted. Systemic coagulation activation was not influenced by citrate.

          Conclusion

          The positive impact on dialysis efficiency, acid-base status and haemodynamics, as well as the subjective tolerance, together indicate that citrate dialysate can significantly contribute to improving haemodialysis in selected patients.

          Trial registration

          ClinicalTrials.gov NCT00718289

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          Most cited references 27

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          Low polymorphonuclear cell degranulation during citrate anticoagulation: a comparison between citrate and heparin dialysis.

          Haemodialysis (HD)-induced bio-incompatibility includes alterations in both cellular elements and humoral factors. As far as polymorphonuclear (PMN) cells are concerned, an increase in both adhesion and degranulation has been reported. However, whereas increased PMN adherence and aggregation is highly linked with early transient complement activation, degranulation seems a continuous process, independent from the formation of complement degradation products. In the process of cell activation, including PMN degranulation, divalent cations (Ca2+) appear to play a pivotal role. As regionally administering citrate creates an almost Ca(2+)-free environment within the dialyser, it is tempting to speculate that Ca2+ dependent phenomena of bio-incompatibility, originating within the dialyser, can be attenuated by substituting conventional heparin for citrate. Therefore, both anticoagulation modalities were compared in 10 stable patients, undergoing haemodialysis (HD) treatment with cellulose-triacetate membranes (CTA) only. Apart from the intracellular granule products myeloperoxidase (MPO) and lactoferrin (LF), the classical parameters of bio-incompatibility, peripheral blood neutropenia and complement activation, were measured. Analysis of MPO and LF gradients across the dialyser (concentration in efferent line-concentration in afferent line) suggested that degranulation is an early process, that occurs mainly within the extracorporeal circuit. Citrate abolished the release of MPO almost completely, whereas LF release was partially inhibited. Neither neutropenia, nor complement activation could be correlated with the occurrence of degranulation. HD-induced PMN degranulation seems largely independent from complement activation, but primarily reliant on Ca2+, at least in the case of CTA membranes.
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            Citrate anticoagulation in continuous venovenous hemodiafiltration: a metabolic challenge.

            Feasibility and safety evaluation of regional citrate anticoagulation (RCA) versus systemic heparinization for continuous venovenous hemodiafiltration. Combined retrospective and prospective observational study performed in a secondary multidisciplinary intensive care unit of the Ospedale Civico Lugano Switzerland. Twelve hemodynamically unstable patients (median APACHE II score 26, interquartile range 22-29) in whom heparin was judged to be at least temporarily contraindicated. A switch from RCA (predilution setting; same iso-osmotic replacement and dialysis fluid) to heparinization or vice versa was recommended for the final evaluation; 56 dialyzers were used for RCA (1,400 h) and 39 for heparinization (1,271 h). Median dialyzer life span was 24.2 h (interquartile range 17.4-42.3) for RCA and 42.5 h (20.6-69.1) for heparinization. Fluid control and dialysis quality were similar in the two groups and required no additional intervention. The risk of significant hypocalcemia and metabolic alkalosis was higher at the beginning of the RCA program and decreased with the further training of the staff. Seven bleeding episodes occurred with heparinization vs. three in RCA. RCA may be a safe and useful form of anticoagulation which is more expensive than heparinization but helps to minimize bleeding risk. The risk of metabolic complications is higher at the beginning of a new RCA program. For centers lacking experienced staff we suggest reserving this technique for patients with rapid clotting of the extracorporeal circuit if treated without anticoagulation.
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              Unexpected haemodynamic instability associated with standard bicarbonate haemodialysis.

              The bicarbonate concentration in dialysis fluids for intermittent haemodialysis usually is between 32 and 35 mmol/l. The severity of chronic metabolic acidosis secondary to end-stage renal failure is very variable, however, so that in some patients pre-dialysis acidosis is overcorrected. This study aimed to analyse haemodynamic tolerances to metabolic alkalosis during intermittent haemodialysis. In this randomized controlled trial with a single blind, cross-over design, we used dialysis liquids with two different bicarbonate concentrations, 32 (modality A) and 26 (modality B) mmol/l, and in 26 patients, 468 dialysis sessions, compared blood pressure, heart rate, incidence of hypotension and the frequency of corrections required with saline or hypertonic glucose infusions. The results of intradialytic haemodynamic monitoring for modalities A and B, respectively, were: lowest systolic blood pressure 120.8+/-20.8 vs 124.3+/-20.6 mmHg (P < 0.01); mean systolic blood pressure 138.5+/-23.8 vs 144.6+/-24.8 mmHg (P < 0.001); and highest heart rate 73.5+/-12.0 vs 75.8 +/- 12.9 (NS); with modality A, patients had more dialysis sessions with hypotensive episodes (5.55 vs 1.7%, P < 0.05) and required more saline or hypertonic glucose infusions (20.9 vs 13.7% of the dialysis sessions, P < 0.05). Mild metabolic alkalosis resulting from standard bicarbonate haemodialysis (32 mmol/l) may induce symptomatic hypotension. While normalizing chronic metabolic acidosis is desirable, reducing bicarbonate concentrations should be considered in cases of significant alkalaemia or otherwise untreatable haemodynamic instability.
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                Author and article information

                Journal
                BMC Nephrol
                BMC Nephrology
                BioMed Central
                1471-2369
                2009
                5 March 2009
                : 10
                : 7
                Affiliations
                [1 ]Division of Nephrology, Ospedale la Carità, Via Ospedale, 6600 Locarno, Switzerland
                [2 ]Department of Internal Medicine, Ospedale la Carità, Locarno, Switzerland
                [3 ]Department of Internal Medicine, Ospedale San Giovanni, Bellinzona, Switzerland
                [4 ]Department of Hematology, University Hospital of Bern, Bern, Switzerland
                [5 ]Division of Nephrology, University Hospital of Lausanne, Lausanne, Switzerland
                Article
                1471-2369-10-7
                10.1186/1471-2369-10-7
                2657128
                19265544
                Copyright ©2009 Gabutti et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Research Article

                Nephrology

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