Dialysate Bicarbonate Concentration Research Articles

Dialysate bicarbonate concentration: Too much of a good thing?

Acid-base equilibrium is a complex and vital system whose regulation is impaired in chronic kidney disease (CKD). Metabolic acidosis is a common complication of CKD. It is typically due to the accumulation of sulfate, phosphorus, and organic anions. Metabolic acidosis is correlated with several adverse outcomes, such as morbidity, hospitalization and mortality. In patients undergoing hemodialysis, acid-base homeostasis depends on many factors: net acid production, amount of alkali given by the dialysate bath, duration of interdialytic period, as well as residual diuresis, if any. Recent literature data suggest that the development of postdialysis metabolic alkalosis may contribute to adverse clinical outcomes. Unfortunately, no randomized studies exist about the effect of different dialysate bicarbonate concentrations on hard outcomes, such as mortality. Like everything else in dialysis, the quest for the "ideal" dialysate bicarbonate concentration is far from over. The Latin aphorism "ne quid nimis" ie "nothing in excess" (excess of neither acid nor base) probably best summarizes our current state of knowledge in this field. For the present, the clinician should understand that target values for predialysis serum bicarbonate concentrations have been established primarily based on observational studies and expert opinion. On the basis of this information, we should keep predialysis serum bicarbonate concentrations at least at 22mEq/L. Furthermore, a specific focus should be addressed to the clinical and nutritional status of the major outliers on both the acid and alkaline sides of the curve.

Are Target Serum Bicarbonate Levels Achieved in Maintenance Hemodialysis Patients: A Single Centre Experience

Majority of the maintenance hemodialysis patients donot achieve the target predialysisserum bicarbonate levels. Routine monitoring of serum bicarbonate in diaysis patients is not universally done.We aimed to assess whether our dialysis population attained the predialysis serum bicarbonate target of >22 mEq/L as recommended by the NKF-KDOQI. Correlation between predialysis bicarbonate and clinical and biochemical parameters was also assessed. Fifty patients undergoing maintenance hemodialysis in Government Medical College, Thiruvananthapuram were included in the study.All patients received fixed non-individualizeddialysate bicarbonate concentrations. The mean predialysis bicarbonate obtained was 19 ± 4.2 mEq/L. Thirty six patients(72%) had bicarbonate levels less than 22 mEq/L. Nineteen patients (38%) had bicarbonate level less than 17mEq/L and 5 patients (10%) had level greater than 25 mEq/L. Majority of the patients failed to achieve the target serum bicarbonate. A negative correlation was obtained for predialysis bicarbonate levels with BMI, total protein, serum uric acid, serum phosphorus and serum ferritin. Better nutritional status may be associated with reduction in bicarbonate level because of increased acid generation. In conclusion this study emphasizes the importance of regular monitoring of serum bicarbonate levels in our dialysis patients and the need for adjusting the dialysate bicarbonate concentrations accordingly.

A randomized cross-over study comparing the performance of HD integra\u2122 central concentrate system versus pre-produced concentrate in hemodialysis

BackgroundPre-produced bicarbonate concentrates (PPC) are still widely used in developing countries despite its cost and risk but Central Concentrate System (CCS) is lacking in data to support its wider adoption.MethodsWe conducted an 8-week randomized crossover study on 16 Hemodialysis machines to compare CCS versus PPC. Performance is assessed by solute concentrations while safety is assessed by microbial count, endotoxin level and adverse event reporting.ResultsMicrobial counts and endotoxin levels were monitored on 48 occasions during the 8-week study for the CCS arm of the study. The levels were all below the action limit during the study. No patient reported any adverse events. Dialysate Sodium, Chloride and Bicarbonate concentrations were measured on a total of 128 occasions for each arm of the study. The relative deviations of Sodium, Chloride and Bicarbonate concentration were within ±5% of their nominal values for both. The 95% Confidence Intervals for the ratio of the mean solute concentrations on the CCS to PPC lie within the tolerance limit of ±5%.ConclusionModern CCS is bacteriologically safe and its performance statistically equivalent to PPC.

Correcting Acidosis during Hemodialysis: Current Limitations and a Potential Solution.

The deleterious catabolic and pro-inflammatory effects of acidosis in hemodialysis (HD) patients and the importance of its correction for limiting mineral bone disease (MBD) are well known. Although oral base therapy could be a solution for correcting acidosis in HD patients, it increases their already enormous medication load and sodium intake; this approach is not used commonly. Therefore, we need to rely more on correcting acidosis during the HD procedure, which is difficult to achieve, in part, because HD is an intermittent therapy. The currently used fixed dialysate bicarbonate concentrations are associated with pre-HD acidosis and intra-dialytic alkalosis. We suggest that a decreasing dialysate bicarbonate concentration from an initially high concentration be considered as a means of correcting acidosis with limited intra-dialytic alkalosis. Some evidence, as well as theoretical considerations, supports such an approach.

Acid-base disorders associated with serum electrolyte patterns in patients on hemodiafiltration

BackgroundMetabolic acidosis (MAC) is a common aspect of dialysis-dependent patients. It is definitely caused by acid retention; however, the influence of other plasma ions is unclear. Understanding the mechanism of MAC and its correction is important when choosing the dialysis solution. Therefore, we assessed the relationship between intradialytic change of acid-base status and serum electrolytes. MethodsWe studied 68 patients on post-dilution hemodiafiltration, using dialysate bicarbonate concentration 32mmol/L. The acid-base disorders were evaluated by the traditional Siggaard-Anderson and modern Stewart approaches. ResultsThe mean pre-dialysis pH was 7.38, standard base excess (SBE) −1.5, undetermined anions (UA−) 7.5, sodium-chloride difference (Diff(NaCl)) 36.2mmol/L. MAC was present in 34% of patients, of which 83% had an increased UA− as a major cause of MAC. The mean nPCR was 0.99g/kg/day and correlated negatively with SBE. After dialysis, metabolic alkalosis predominated in 81%. The mean post-dialysis pH was 7.45, SBE 4, UA− 2.6, Diff(NaCl) 36.9mmol/L. ΔSBE significantly correlated with ΔUA−, but not with ΔDiff(NaCl) or ΔCl−. ConclusionsMAC in patients on hemodiafiltration is mainly caused by acid retention and is associated with higher protein intake. We did not prove the effect of sodium or chloride on acid-base balance. Even though we used a relatively low concentration of dialysate bicarbonate, we recorded a high proportion of post-dialysis alkalosis caused by the excessive decrease of undetermined anions, which had been completely replaced by bicarbonate and indicated the elimination of undesirable anions, as well as of normal endogenous anions.

Approach to the Hemodialysis Patient With an Abnormal Serum Bicarbonate Concentration

We present a patient receiving hemodialysis with a persistently high serum bicarbonate concentration to illustrate the evaluation and management issues for patients with both high (>25 mEq/L) and low (<20 mEq/L) pretreatment values. Patients with high serum bicarbonate concentrations typically are malnourished and have low rates of endogenous acid production. Evaluation should begin with assessment of whether an acute and potentially reversible cause of metabolic alkalosis is present. If not, management should be directed at treating malnutrition. By contrast, patients with low predialysis serum bicarbonate concentrations, in the absence of an acute and reversible cause, may benefit from increasing the level by an adjustment in dialysate bicarbonate concentration. However, the level at which one should intervene and to what extent serum bicarbonate concentration should be increased are unresolved issues. Whether such an intervention will reduce mortality risk has not been determined.

Hemodialysis: Core Curriculum 2014

From the Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, TN. Received May 1, 2013. Accepted in revised form July 1, 2013. Originally published online November 21, 2013. Address correspondence to Thomas A. Golper, MD, S3303 Medical Center North, Vanderbilt University Medical Center, 21st Ave S, Nashville, TN 37232. E-mail: thomas.golper@vanderbilt. edu 2013 by the National Kidney Foundation, Inc. 0272-6386/$36.00 http://dx.doi.org/10.1053/j.ajkd.2013.07.028 PRINCIPLES OF DIALYSIS AND HOW MODALITIES DIFFER

A step towards optimal dialysate bicarbonate concentration

The optimal dialysate bicarbonate concentration is one that prevents acidosis at the beginning of the next dialysis session while avoiding postdialysis alkalosis. Few studies have assessed the effect of different dialysate bicarbonate levels on patient outcomes, but Tentori et al. now report that high dialysate bicarbonate concentrations may contribute to adverse outcomes.

Association of Dialysate Bicarbonate Concentration With Mortality in the Dialysis Outcomes and Practice Patterns Study (DOPPS)

Most hemodialysis patients worldwide are treated with bicarbonate dialysis using sodium bicarbonate as the base. Few studies have assessed outcomes of patients treated with different dialysate bicarbonate levels, and the optimal concentration remains uncertain. The Dialysis Outcomes and Practice Patterns Study (DOPPS) is an international prospective cohort study. This study included 17,031 patients receiving thrice-weekly in-center hemodialysis from 11 DOPPS countries (2002-2011). Dialysate bicarbonate concentration. All-cause and cause-specific mortality and first hospitalization, using Cox regression to estimate the effects of dialysate bicarbonate concentration, adjusting for potential confounders. Demographics, comorbid conditions, laboratory values, and prescriptions were abstracted from medical records. Mean dialysate bicarbonate concentration was 35.5 ± 2.7 (SD) mEq/L, ranging from 32.2 ± 2.3 mEq/L in Germany to 37.0 ± 2.6 mEq/L in the United States. Prescription of high dialysate bicarbonate concentration (≥38 mEq/L) was most common in the United States (45% of patients). Approximately 50% of DOPPS facilities used a single dialysate bicarbonate concentration. 3,913 patients (23%) died during follow-up. Dialysate bicarbonate concentration was associated positively with mortality (adjusted HR, 1.08 per 4 mEq/L higher [95% CI, 1.01-1.15]; HR for dialysate bicarbonate ≥38 vs 33-37 mEq/L, 1.07 [95% CI, 0.97-1.19]). Results were consistent across levels of pre-dialysis session serum bicarbonate and between facilities that used a single dialysate bicarbonate concentration and those that prescribed different concentrations to individual patients. The association of dialysis bicarbonate concentration with mortality was stronger in patients with longer dialysis vintage. Due to the observational nature of the present study, we cannot rule out that the reported associations may be biased by unmeasured confounders. High dialysate bicarbonate concentrations, especially prolonged exposure, may contribute to adverse outcomes, likely through the development of postdialysis metabolic alkalosis. Additional studies are warranted to identify the optimal dialysate bicarbonate concentration.

Management of hypophosphatemia in nocturnal hemodialysis with phosphate-containing enema: A technical study

Hypophosphatemia is observed in patients undergoing nocturnal hemodialysis. Phosphate is commonly added to the dialysate acid bath, but systematic evaluation of the safety and reliability of this strategy is lacking. The objectives of this study were 4-fold. First, we determined whether predictable final dialysate phosphate concentrations could be achieved by adding varying amounts of Fleet® enema. Second, we assessed the stability of calcium (Ca) and phosphate dialysate levels under simulated nocturnal hemodialysis conditions. Third, we assessed for Ca-phosphate precipitate. Finally, we evaluated whether dialysate containing Fleet® enema met the current sterility standards. We added serial aliquots of enema to 4.5 L of dialysate acid concentrate and proportioned the solution on Gambro and Althin/Baxter dialysis machines for up to 8 hours. We measured dialysate phosphate, Ca, pH, and bicarbonate concentrations at baseline, and after simulated dialysis at 4 and 8 hours. We evaluated for precipitation visually and by assessing optical density at 620 nm. We used inoculation of agar to detect bacteria and Pyrotell reaction for endotoxin. For every 30 mL of Fleet® (1.38 mmol/mL of phosphate) enema added, the dialysate phosphate concentration increased by 0.2 mmol/L. There were no significant changes in dialysate phosphate, Ca, pH, and bicarbonate concentrations over 8 hours. No precipitate was observed in the dialysate by optical density measures at 620 nm for additions of up to 90 mL of enema. Bacterial and endotoxin testing met sterility standards. The addition of Fleet® enema to dialysate increases phosphate concentration in a predictable manner, and no safety problems were observed in our in vitro studies.

Acute hypercapnic respiratory failure associated with hemodialysis

AbstractPatients undergoing hemodialysis are subject to recurrent acid‐base perturbations. Prior to each dialysis treatment, they are relatively acidemic, which is corrected rapidly during dialysis. We report a patient with obesity, obstructive lung disease, and pneumonia who developed acute respiratory failure triggered by an influx of high bicarbonate during dialysis. This case emphasizes that in patients with severely compromised respiratory reserve, a large amount of bicarbonate influx during hemodialysis may cause acute CO2 accumulation and ventilatory distress. An individualized approach with judicious adjustment of the dialysate bicarbonate concentration may be necessary. Dial. Transplant. © 2011 Wiley Periodicals, Inc.

Lanthanum Carbonate Versus Sevelamer Hydrochloride: Improvement of Metabolic Acidosis and Hyperkalemia in Hemodialysis Patients

Sevelamer hydrochloride (SH) has been reported to aggravate metabolic acidosis and hyperkalemia. This study was performed to evaluate acid-base status and serum potassium changes after replacing SH with lanthanum carbonate (LC) in hemodialysis patients. SH was prescribed for 24 weeks in 14 stable hemodialysis patients and replaced by LC in a similar treatment schedule. Laboratory tests, including indices of acid-base status, nutrition, bone/mineral metabolism, and dialysis adequacy, were performed monthly during the study. Dialysate bicarbonate, potassium and calcium concentrations remained constant. Serum bicarbonate and pH rose, and serum potassium dropped significantly under LC. Alkaline phosphatase also decreased significantly under LC. No significant differences were observed in the other studied parameters between the two treatment periods. Control of serum phosphate was similar under both phosphate-binders and no differences were observed in calcium, Ca × P product, CRP, or lipid levels. Dialysis adequacy was constantly kept within K/DOQI target-range. Although full compliance to treatment was reported, three patients on LC complained of gastrointestinal upset and/or a metallic taste, and four had difficulty chewing the LC tablet. LC improves metabolic acidosis and hyperkalemia in hemodialysis patients previously under SH. Although both medications are well-tolerated, the gastrointestinal side-effects appear to occur more frequently with LC; a fact that, together with difficulties in chewing the tablet, may result in decreased compliance.

Lanthanum Carbonate Is an Effective Hypophosphatemic Agent for Hemodialysis Patients Intolerant of Other Phosphate Binders

Lanthanum carbonate (LC) is a noncalcium-containing phosphate binder of proven utility in treating hyperphosphatemia in dialysis patients, and displays a good tolerability profile. This study addressed whether this tolerability profile could result in improved phosphate control in patients intolerant of other phosphate binders, and who remain hyperphosphatemic despite intensive dietary advice and adequate dialysis provision. This 18-month study, from a large urban hemodialysis unit, studied 55 patients identified by the multidisciplinary team as fulfilling the following criteria: persistent hyperphosphatemia; intolerance of, or admitted nonadherence to, prescribed phosphate binders (either calcium-based or sevelamer); and provision of adequate dialysis (urea reduction ratio, >65%). LC was substituted for existing phosphate binders, and results were compared between baseline and 3 months after the initiation of LC. A significant fall in phosphate level from 2.28+/-0.55mmol/L to 1.89+/-0.45mmol/L (7.06+/-1.70mg/dL to 5.85+/-1.39mg/dL) was evident 3 months after the medication switch (P < .001). This fall was associated with a significant increase in the number of patients achieving United Kingdom Renal Association guidelines for serum phosphate level (17% to 48%; P=.001). Mean phosphate-binder pill burden fell significantly by 3 months after the initiation of LC, from 7.8+/-3.4 tablets daily to 3.6+/-2.3 tablets daily. A small but significant increase also occurred in serum bicarbonate levels, from 23.3+/-2.2mmol/L (23.3+/-2.2 mEq/L) at baseline to 23.9+/-2.5mmol/L (23.9+/-2.5 mEq/L) at 3 months (P=.03). This was observed despite a prescribed reduction in dialysate bicarbonate concentration across the population (P=.03). This study demonstrated the utility of LC in hemodialysis patients intolerant of alternative phosphate binders, and suggests an advantage of this agent in this patient group.

Haemodynamic consequences of changing bicarbonate and calcium concentrations in haemodialysis fluids

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.

Varying Dialysate Bicarbonate Concentrations in Maintenance Hemodialysis Patients Affect Post-dialysis Alkalosis but not Pre-dialysis Acidosis

This study aimed to assess the effects of different dialysate bicarbonate concentrations in correcting acid-base imbalance in 53 stable hemodialysis patients in a university-hemodialysis unit. Three different bicarbonate concentrations were assigned, i.e. 25 mEq/L in 10, 30 mEq/L in 30, and 35 mEq/L in 13 patients. Blood gas analyses from arterial line blood samples before and after dialysis in the mid-week were performed for the determination of pH and serum bicarbonate (HCO3-) concentration. The mean values of predialysis arterial HCO3- were mildly acidotic in all 3 groups, but not significantly different among them, whereas those of post-dialysis arterial HCO3- were alkalotic, especially in the group of 35 mEq/L as compared with the other two groups. The mean blood pH was not significantly different among the 3 groups. As expected, there was a positive correlation between pre-dialysis pH and post-dialysis pH (r=0.45, p=0.001), and pre-dialysis HCO3- and post-dialysis HCO3- (r=0.58, p=0.000), but with a negative correlation between pre-dialysis HCO3- and the increment of intradialytic HCO3- following hemodialysis (r=-0.46, p=0.001). In conclusion, this study shows that the impact of conventional dialysate bicarbonate concentrations ranging from 25 to 35 mEq/L is not quite different on the mild degree of predialysis acidemia, but the degree of postdialysis alkalemia is more prominent in higher bicarbonate concentrations. Base supply by hemodialysis alone does not seem to be the main factor to determine the predialysis acidosis in end-stage renal disease patients on chronic maintenance hemodialysis.

Determinants of metabolic acidosis among hemodialysis patients

Metabolic acidosis is frequently present, poorly controlled, and associated with adverse effects among hemodialysis patients. Potential determinants of metabolic acidosis include endogenous acid production, administration of alkali, neutralization of acid by buffers, dilution of serum bicarbonate by interdialytic fluid gain, and loss of bicarbonate in stool. Understanding the relative importance of these determinants may help guide efforts to manage metabolic acidosis. We used chart abstraction, patient interviews, and laboratory testing to assess variables related to acid production (protein breakdown), alkali administration (dialysis dose, missed treatments, dialysate bicarbonate concentration, oral bicarbonate supplements), acid buffering (phosphorus binders), dilution of bicarbonate (interdialytic weight gain), and loss of bicarbonate in stool (diarrhea) for 190 randomly selected patients from 44 hemodialysis facilities. We used multivariate analyses to determine which potential determinants were independently associated with predialysis serum bicarbonate levels. Of all patients, 30% had metabolic acidosis (serum bicarbonate level <22 mEq/L). On multivariate analysis, metabolic acidosis was more likely with increased protein nitrogen appearance (odds ratio [OR] 1.60 per 0.2 g/kg/day, p=0.001) and less likely with increased Kt/V (OR 0.61 per 0.20 increase in Kt/V, p<0.001) and with increased calcium carbonate use (OR 0.38 per 2 g/day, p=0.003). Key determinants of metabolic acidosis among hemodialysis patients are protein breakdown, dialysis dose, and specific phosphorus binders. Further work is needed to develop interventions to address these determinants.

Long-Term Management of Sevelamer Hydrochloride-Induced Metabolic Acidosis Aggravation and Hyperkalemia in Hemodialysis Patients

Sevelamer hydrochloride use in hemodialysis patients is complicated by metabolic acidosis aggravation and hyperkalemia. Rare reports about a short-term correction of this complication have been published. The current authors investigated the long-term correction of metabolic acidosis and hyperkalemia in sevelamer hydrochloride-treated patients at doses adequate to achieve serum phosphate levels within K/DOQI™ recommendations. The authors followed 20 hemodialysis patients for 24 months in an open-label prospective study. The dialysate bicarbonate concentration was increased stepwise to a maximum 40 mEq/L and adjusted to reach patient serum bicarbonate levels of 22 mEq/L, according to K/DOQI™ recommendations. Laboratory results for serum bicarbonate, potassium, calcium, phosphate, albumin, alkaline phosphatase, iPTH, cholesterol (HDL-LDL), triglycerides, Kt/V, systolic-diastolic arterial pressure were recorded. Sevelamer hydrochloride-induced metabolic acidosis aggravation and hyperkalemia in hemodialysis patients were corrected, on the long-term, by an increase in dialysate bicarbonate concentration. Further improvement in bone biochemistry was noted with this adequate acidosis correction and parallel sevelamer hydrochloride administration, in sufficiently large doses to achieve K/DOQI™ phosphate recommendations.

The faster potassium-lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients

Hyperkalaemia is common in patients with advanced renal disease. In this double-blind, randomized, three-sequence, crossover study, we compared the effect of three dialysate bicarbonate concentrations ([HCO3-]) on the kinetics of serum potassium (K+) reduction during a conventional haemodialysis (HD) session in chronic HD patients. We studied eight stable HD patients. The choice of dialysate [HCO3-] followed a previously assigned treatment protocol and the [HCO3-] used were low bicarbonate (LB; 27 mmol/l), standard bicarbonate (SB; 35 mmol/l) and high bicarbonate (HB; 39 mmol/l). Polysulphone dialysers and automated machines provided blood flow rates of 300 ml/min and dialysis flow rates of 500 ml/min for each HD session. Blood samples were drawn at 0 (baseline), 15, 30, 60 and 240 min from the arterial extracorporeal line to assess blood gases and serum electrolytes. In three of the eight patients, we measured serum K+ 1 h post-dialysis as well as K+ removal by the dialysis. The same procedures were followed until the completion of the three arms of the study, with a 1 week interval between each experimental arm. Serum K+ decreased from 5.4+/-0.26 (baseline) to 4.96+/-0.20, 4.90+/-0.19, 4.68+/-0.13 and 4.24+/-0.15 mmol/l at 15, 30, 60 and 240 min, respectively, with LB; from 5.38+/-0.21 to 5.01+/-0.23, 4.70+/-0.25, 4.3+/-0.15 and 3.8+/-0.19 mmol/l, respectively, with SB; and from 5.45+/-0.25 to 4.79+/-0.17, 4.48+/-0.17, 3.86+/-0.16 and 3.34+/-0.11 mmol/l, respectively, with HB (P<0.05 for high vs standard and low [HCO3-] at 60 and 240 min). The decrease in serum K+ correlated with the rise in serum [HCO3-] in all but LB (P<0.05). Potassium rebound was 3.9+/-10.2%, 5.2+/-6.6% and 8.9+/-4.9% for LB, SB and HB dialysates, respectively (P=NS), while total K+ removal (mmol/dialysis) was 116.4+/-21.6 for LB, 73.2+/-12.8 for SB and 80.9+/-15.4 for HB (P=NS). High dialysate [HCO3-] was associated with a faster decrease in serum K+. Our results strongly suggest that this reduction was due to the enhanced shifting of K+ from the extracellular to the intracellular fluid compartment rather than its removal by dialysis. This finding could have an impact for those patients with life-threatening pre-HD hyperkalaemia.

Citrate Dialysis - Adverse Effects

Trisodium citrate 33% as anticoagulant is routinely used in several indications for acute dialysis patients, with very good clinical tolerance and results. But in chronic dialysis patients two problems arose after some weeks : 1/ In all of them hypernatremia and alcalosis developed : the pre dialysis sodium and bicarbonate level raised progressively. This could be tempered by lowering the sodium and dialysate bicarbonate concentration respectively from 140 mEq/l to 132 mEq/l and from 37 mEq/l to 25 mEq/l. 2/ The second problem was a progressive rise in serum Aluminum (Al) level in some patients: from a mean 3 μg/l to 38 μg/l; after excluding water, concentrate, dialysate, medication, etc. as possible cause, we finally controlled the Al level in the glass bottles, containing the trisodium citrate solution, and we noted very high values:35,300 μg/l. After replacement of the glass bottles by polyvinyl bags (with a neglectable Al content), the serum Al levels returned to normal. It is known that citrate chelates also the Al present in the glass of the bottles or vials themselves; our warning is not to use glass containers for citrate solutions. A short overview of different glass types is given.

A new system for regional citrate anticoagulation in continuous venovenous hemodialysis (CVVHD).

CVVHD is an established renal replacement therapy in hemodynamically unstable ICU patients. Various methods for regional citrate anticoagulation have been developed to minimize bleeding complications. Metabolic alkalosis, the risk of severe hypocalcemia and need for continuous calcium substitution as well as treatment-associated hypernatremia have limited the success of systems employed so far. We have developed a new technique for regional citrate anticoagulation in CVVHD to overcome these deficiencies and have performed a validation study. One hundred and thirty-three filters with an overall treatment duration of 3,324 hours were used in 19 critically ill patients with bleeding complications. We used a calcium-containing dialysate (1.81 mmol/l Ca) to avoid mandatory systemic calcium supplementation. Sodium bicarbonate was added to the dialysate in variable concentrations (13 - 34 mmol/l) to control acid-base status and prevent hypernatremia. The resulting dialysate sodium concentrations were between 121 and 140 mmol/l. Blood flow was set at 75 ml /min. Infusion of a solution containing trisodium citrate and citric acid with an overall citrate concentration of 113 mmol/l was started at 250 ml/h. Primary endpoints were pre- and post-filter ionized calcium (Ca(i)) concentrations, base excess and serum sodium. Filter life was assessed as a secondary end-point. Control of electrolyte balance and azotemia was excellent (prefilter serum Ca(i) 1.06 +/- 0.012 mmol/l (+/- SEM), post-filter Ca(i) 0.23 +/- 0.01 mmol/l, base excess -0.39 +/- 0.4 mmol/l, serum sodium 137 +/- 4 mmol/l, mean serum creatinine 1.8 +/- 0.07 mg/dl). Normal base excess was achieved with a mean dialysate bicarbonate concentration of 26 mmol/l at a mean citrate infusion rate of 266 +/- 4 ml/h. After 48 hours, 25% of filters were still patent, mean filter life was 26 +/- 1.6 hours. No patient developed serious CVVHD-related adverse events. The new regional citrate anticoagulation system for CVVHD is safe, feasible and can avoid major complications of previously described methods, especially hypocalcemia, alkalosis and hypernatremia.