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      Haemodynamic consequences of changing bicarbonate and calcium concentrations in haemodialysis fluids

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          Abstract

          Background. In a previous study we demonstrated that mild metabolic alkalosis resulting from standard bicarbonate haemodialysis induces hypotension. In this study, we have further investigated the changes in systemic haemodynamics induced by bicarbonate and calcium, using non-invasive procedures.

          Methods. In a randomized controlled trial with a single-blind, crossover design, we sequentially changed the dialysate bicarbonate and calcium concentrations (between 26 and 35 mmol/l for bicarbonate and either 1.25 or 1.50 mmol/l for calcium). Twenty-one patients were enrolled for a total of 756 dialysis sessions. Systemic haemodynamics was evaluated using pulse wave analysers. Bioimpedance and BNP were used to compare the fluid status pattern.

          Results. The haemodynamic parameters and the pre-dialysis BNP using either a high calcium or bicarbonate concentration were as follows: systolic blood pressure (+5.6 and −4.7 mmHg; P < 0.05 for both), stroke volume (+12.3 and +5.2 ml; P < 0.05 and ns), peripheral resistances (−190 and −171 dyne s cm −5; P < 0.05 for both), central augmentation index (+1.1% and −2.9%; ns and P < 0.05) and BNP (−5 and −170 ng/l; ns and P < 0.05). The need of staff intervention was similar in all modalities.

          Conclusions. Both high bicarbonate and calcium concentrations in the dialysate improve the haemodynamic pattern during dialysis. Bicarbonate reduces arterial stiffness and ameliorates the heart tolerance for volume overload in the interdialytic phase, whereas calcium directly increases stroke volume. The slight hypotensive effect of alkalaemia should motivate a probative reduction of bicarbonate concentration in dialysis fluid for haemodynamic reasons, only in the event of failure of classical tools to prevent intradialytic hypotension.

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          Most cited references26

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          Mechanisms for defects in muscle protein metabolism in rats with chronic uremia. Influence of metabolic acidosis.

          Chronic renal failure (CRF) is associated with metabolic acidosis and abnormal muscle protein metabolism. As we have shown that acidosis by itself stimulates muscle protein degradation by a glucocorticoid-dependent mechanism, we assessed the contribution of acidosis to changes in muscle protein turnover in CRF. A stable model of uremia was achieved in partially nephrectomized rats (plasma urea nitrogen, 100-120 mg/dl, blood bicarbonate less than 21 meq/liter). CRF rats excreted 22% more nitrogen than pair-fed controls (P less than 0.005), so muscle protein synthesis and degradation were measured in perfused hindquarters. CRF rats had a 90% increase in net protein degradation (P less than 0.001); this was corrected by dietary bicarbonate. Correction of acidosis did not reduce the elevated corticosterone excretion rate of CRF rats, nor did it improve a second defect in muscle protein turnover, a 34% lower rate of insulin-stimulated protein synthesis. Thus, abnormal nitrogen production in CRF is due to accelerated muscle proteolysis caused by acidosis and an acidosis-independent inhibition of insulin-stimulated muscle protein synthesis.
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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
                Nephrol Dial Transplant
                ndt
                ndt
                Nephrology Dialysis Transplantation
                Oxford University Press
                0931-0509
                1460-2385
                March 2009
                8 October 2008
                8 October 2008
                : 24
                : 3
                : 973-981
                Affiliations
                [1 ]Division of Nephrology, Ospedale la Carità, Locarno
                [2 ]Department of Internal Medicine, Ospedale la Carità, Locarno
                [3 ]Department of Internal Medicine, Ospedale San Giovanni, Bellinzona
                [4 ]Division of Nephrology, University Hospital of Lausanne , Lausanne, Switzerland
                Author notes
                Correspondence and offprint requests to: Luca Gabutti, Division of Nephrology, Ospedale la Carità, via Ospedale 1, 6600 Locarno, Switzerland. Tel: +41918114693; Fax: +41918114533; E-mail: luca.gabutti@ 123456eoc.ch
                Article
                gfn541
                10.1093/ndt/gfn541
                2644633
                18842671
                57e98780-83ce-4592-8f14-634cfe0a50d9
                © The Author [2008].

                The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

                History
                : 25 May 2008
                : 3 September 2008
                Categories
                Dialysis

                Nephrology
                haemodynamics,alkalosis,bicarbonate,calcium,haemodialysis
                Nephrology
                haemodynamics, alkalosis, bicarbonate, calcium, haemodialysis

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