Intradialytic hypercapnic respiratory failure managed by noninvasive assisted ventilation.

We report a hemodialysis patient with acute hypercapnic respiratory failure managed on noninvasive intermittent positive pressure ventilation and progressive metabolic acidosis. Dialysate bicarbonate concentration of 25 mEq/l was associated with exacerbation of metabolic acidosis, while higher dialysate bicarbonate concentration of 30 mEq/l induced a dangerous increase in PCO(2) level. Excessive bicarbonate buffering and CO(2) production induced by severe metabolic acidosis, malnourishment and tissue hypoxia, could explain inadequate correction of metabolic acidosis and worsening of hypercapnia in this patient. Our findings suggest the need for close monitoring of blood gases and cautious modulation of dialysate bicarbonate concentration in the presence of progressive metabolic acidosis in hypercapnic hemodialysis patients.     

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.     

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.     

Metabolic Acidosis in Hemodialysis Patients: A Study of Prevalence and Factors Affecting Intradialytic Bicarbonate Gain

Abstract The correction of uremic acidosis is one of the goals of hemodialysis; however, despite acceptable hemodialysis protocols, metabolic acidosis remains a common problem. The prevalence of acidosis and significance of factors affecting bicarbonate flux during hemodialysis were studied. A cohort of 70 stable patients receiving high-efficiency hemodialysis for at least 4 months was studied prospectively over a 1-year period. Twenty patients (28%) had a mean predialysis serum bicarbonate of less than 21 mEq/L. The patients with or without metabolic acidosis had similar mean net ultrafiltration and percent ultrafiltration, but acidotic patients had a higher percent increase in bicarbonate during hemodialysis (35 ± 12 versus 27 ± 10 [p = 0.008]). The latter suggests an increased net daily acid gain in patients with metabolic acidosis (1.19 ± 0.32 mEq/kg versus 1.05 ± 0.35 mEq/kg [p = 0.04]). A review of factors affecting intradialytic bicarbonate gain showed that predialysis serum bicarbonate (diffusive gradient) was the most significant with a demonstrated linear relationship between these two variables (R² 0.51). The role of dialysance and blood flow, assessed together using percent urea reduction, was minor as was the effect of ultrafiltration. At our level of dialysis delivery, prevalence of metabolic acidosis is low, and dialysis-related factors do not contribute to the persistence of metabolic acidosis. Net daily acid gain was higher in acidotic patients and accounts for the long-term maintenance of metabolic acidosis. For individual dialysis treatments, the diffusive gradient is the most important determinant of bicarbonate gain, with only a minor role being demonstrated for percent urea reduction and ultrafiltration rate.     

Studies on Circulatory Stability During Bicarbonate Hemodialysis with Constant Dialysate Sodium Versus Acetate Hemodialysis with Sequential Dialysate Sodium

Eight stable patients on maintenance hemodialysis were studied while undergoing (a) acetate hemodialysis with a sequential dialysate sodium concentration from 147 to 137 mEq/L (SNa-HDA) and (b) bicarbonate hemodialysis with a constant dialysate sodium concentration of 140 mEq/L (HDB). Circulatory behavior was observed during both of these methods, and both were found to allow a high volume removal. However, as a consequence of the high sodium load during SNa-HDA, volume was shifted from the extra- to the intravascular space. This stabilizing effect on the circulation disappeared with the sequential decrease of dialysate sodium concentration (despite a constant plasma sodium concentration (despite a constant plasma sodium concentration of approximately 140 mEq/L), which was concomitant with a significant decline of the mean arterial blood pressure and an inadequate compensation of the metabolic acidosis. In contrast, a better circulatory response to comparable volume removal was found during HDB, expressed by a stable mean arterial blood pressure in the presence of well-balanced arterial acid-base values.     

Ventilatory and metabolic changes during high efficiency hemodialysis.

Ventilatory and metabolic changes were measured in seven patients undergoing high efficiency hemodialysis using a cuprophane dialyzer and bicarbonate-containing dialysate. At an HCO3 concentration of 35 mEq/liter and a mean in vivo urea clearance of 3.6 ml/kg/min, hypoxemia was not detected during dialysis (PaO2 was 14.00 and 13.60 kPa before and during dialysis). The new findings, related to high efficiency bicarbonate dialysis, include a sustained rise in minute ventilation (VE, 6.1 to 6.8 liter/min, P less than 0.01), an increase in CO2 excretion (VCO2, 194 to 214 ml/min, P less than 0.05), and O2 consumption (VO2, 215 to 246 ml/min, P less than 0.05). The increment in VE and VCO2 was attributed to the high flux rate of bicarbonate while the rise in VO2 is likely the result of metabolic alkalosis. Arterial pH rose from 7.40 to 7.49 mm Hg and serum HCO3 increased from 23.8 to 29.2 mEq/liter, while pCO2 remained normal at 5.07 kPa throughout the study. The acid-base status of the blood changed from that of a metabolic acidosis to that of a respiratory acidosis across the dialyzer where the pH decreased from 7.47 to 7.41 and pCO2 rose from 5.31 to 7.72 kPa. These data indicate that a healthy ventilatory response is needed to excrete the excess CO2 generated during high efficiency bicarbonate hemodialysis. The significance and etiology of the elevated O2 consumption is undetermined.     

Alkali delivery in chronic hemodialysis: Would more acetate be helpful?

The dialysate alkali used in hemodialysis to replace low body alkali levels in end stage renal disease (ESRD) patients has changed over time from bicarbonate to acetate and finally back to bicarbonate with a small addition of acetate. The ideal way to replace alkali in dialysis patients remains uncertain. Elsewhere in this issue of the journal, Sargent and Gennari, who have contributed greatly to our understanding of dialysis and acid‐base kinetics, suggest that decreasing the currently used concentration of bicarbonate while increasing concentration of acetate in the dialysate may be a much more physiological approach to alkali delivery during hemodialysis. These recommendations are based on results from a series of hemodialysis simulations using mathematical theoretical methods, with the assumption that acetate metabolism will be sufficiently delayed with the higher acetate dialysate and reduce the rate of correction of metabolic acidosis during dialysis. Although valuable in calling attention to the issues surrounding alkali repletion during hemodialysis, these postulations should be tested in clinical trials. We believe, however, that the available evidence suggests that the rate of gain of bicarbonate during dialysis with the higher acetate dialysate would not be slower and that the replacement of some dialysate bicarbonate with acetate will not alter alkali accretion or intradialytic pH.     

Correction of metabolic acidosis and its effect on albumin in chronic hemodialysis patients

Serum albumin concentration has been strongly associated with risk of death in hemodialysis patients, with mortality increasing as albumin decreases. Metabolic acidosis stimulates protein catabolism and decreases protein synthesis. A study was undertaken to investigate the effect of increasing predialysis serum bicarbonate (HCO3) concentrations on the nutrition of hemodialysis patients as measured by albumin and total lymphocyte count (TLC). Metabolic acidosis was defined as a predialysis serum bicarbonate concentration of < or = 18 mEq/L. Thirty-six hemodialysis patients were enrolled in the study. Each had been stable on hemodialysis for > or = 3 months and each had a mean serum bicarbonate concentration of < or = 18 mEq/L on predialysis monthly laboratory values during the preceding 3 months. The subjects were randomized into 2 groups. The first group consisted of 18 control subjects who were dialyzed on a standard bicarbonate bath of 35 mEq/L. The second group consisted of 18 experimental patients who were dialyzed on a bicarbonate bath of 40 mEq/L. Subjects in the experimental group who had predialysis serum bicarbonate concentrations less than 22 mEq/L after 2 weeks on the higher bicarbonate bath were additionally supplemented with oral sodium bicarbonate at a dosage of 1 mEq/kg dry weight/d. Monthly predialysis laboratory values were checked for all subjects and included serum electrolytes, blood urea nitrogen, calcium, and albumin. TLCs were obtained at the initiation and at the conclusion of the study. Intact parathyroid hormone, blood pressures, and interdialytic weight gains were also followed. The study lasted 16 weeks; 32 subjects completed the study (16 in each group). There were no statistically significant differences between the two groups at the initiation of the study. The serum bicarbonate concentrations were significantly different between the two groups at the end of the study (control HCO3 17.3 +/- 3.2 mEq/L v experimental HCO3 20.2 +/- 2.9 mEq/L; P = 0.01). Serum albumin concentrations and TLCs were not statistically different (P > 0.05) between the two groups at the end of the study (control albumin 3.88 +/- 0.28 g/dL v experimental albumin 3.76 +/- 0.26 g/dL and control TLC 1,780.0 +/- 779.4/mm3 v experimental TLC 2,020.1 +/- 888.0/mm3). Potassium, intact parathyroid hormone, interdialytic weight gain, blood pressures, Kt/Vs, and protein catabolic rates did not differ. We found that the change in serum bicarbonate concentration was well-tolerated and was without any demonstrable side effects. We conclude that increasing the serum bicarbonate concentration by 3 mEq/L for 16 weeks has no effect on the indicators of nutrition that we measured (serum albumin and TLC).     

Predictive factors of low HCO3- levels in peritoneal dialysis patients

BACKGROUND: Metabolic acidosis is a major metabolic abnormality in end-stage renal disease (ESRD) and alkali is provided with dialysis treatment to patients on chronic peritoneal dialysis (CPD) to keep their acid-base balance within normal serum HCO3- levels. METHODS AND RESULTS: We examined the levels of venous serum HCO3- in 163 patients on CPD and the predictive factors for HCO3- levels low enough to indicate metabolic acidosis. The mean value for HCO3- was 26+/-2.4 mmol/l and for anion gap was 13.1+/-3.1 mEq/l. A serum bicarbonate concentration of less than 24 mmol/l, compatible with metabolic acidosis, was observed in 13.5% of the patients. In a multivariate analysis HCO3- levels were directly correlated with older age and use of CaCO3- as phosphate binders, and inversely associated with serum potassium, the use of sevelamer and low lactate dialysis solutions. Higher serum urea levels, the use of low lactate solutions and sevelamer instead of CaCO3 were significantly predictive factors for HCO3- levels < 24 mmol/l. CONCLUSIONS: Venous HCO3- and anion gap values were within the normal ranges in stable CPD patients. In 13.5% of them, however, chronic metabolic acidosis was observed based on venous HCO3- levels < 24 mmol/l. Dietary protein intake, the use of sevelamer and low (35 mmol/l) concentration of lactate in dialysis solutions are important predictive factors for chronic metabolic acidosis in these patients.     

Effects of acetate and bicarbonate dialysate in stable chronic dialysis patients

The effects of acetate and bicarbonate dialysate on the biochemical and clinical parameters of 16 stable chronic hemodialysis patients were investigated in a double-blind crossover study. A central delivery system was used for both types of dialysates with identical sodium concentrations (138 mEq/liter) and osmolality in a single-pass dialysate flow. The results indicate that dialysis with bicarbonate leads to significantly less hypoxemia (P less than or equal to 0.001) and hypotensive episodes (P less than or equal to 0.002) than with acetate. Pre- to post-dialysis blood pressure changes were also more marked during acetate dialysis. Older patients with recurrent hypotension on acetate benefit most from bicarbonate dialysate. This group of patients appears to metabolize acetate more slowly and has a significantly lower post-dialysis bicarbonate concentration (P less than or equal to 0.005) than asymptomatic patients during dialysis with acetate dialysate.     

Improved effect of hemodialysis on acidemic patients from an acetate concentration of 38 mmol/l

A high frequency of metabolic acidosis in a group of 30 patients on regular dialysis treatment initiated a study of the effect (and possible side effects) of a higher concentration of acetate in the dialysate. The concentration of acetate in the dialysate was increased from 32.6 ('low ac') to 38.2 mmol/l ('high ac'). The 'low ac' dialysis treatment changes the metabolic acidoses (mean pH = 7.34; base excess, BEb = - 8.3 mmol/l) to chronic hypocapnia (pH = 7.40; BEb = - 5.4 mmol/l). 'High ac' normalized the acid base status (pH = 7.44; BEb = -0.6 mmol/l). No side effects occurred. Since PaCO2 does not change much during hemodialysis it is convenient to look at the linearly related changes of the pH and the logarithmic standard bicarbonate concentration along iso-PCO2 lines in a log standard bicarbonate-pH-nomogram.     

Acetate-Free Biofiltration: A Viable Alternative to Bicarbonate Dialysis

Eight patients were studied during four sessions of acetate-free biofiltration (AFBF). AFBF is a new dialysis technique with no base replacement agents in the dialysate and with the addition in postdilution mode of bicarbonate (HCO3) solution directly into the extracorporeal blood circuit. In this study the effects on acid-base balance of different infusions of sodium bicarbonate (NaHCO3) ranging from 751 to 1,002 mEq per session was evaluated. There were significant positive correlations between the HCO3 infused and net HCO3 gained (r = 0.776, p less than 0.0001) and between HCO3 infused and plasma intratreatment HCO3 changes (n = 0.562, p less than 0.001). Stepwise multiple linear regression analysis demonstrated that HCO3 infused and plasma predialysis HCO3 values played the major role in HCO3 balance in AFBF. The best correction of metabolic acidosis was obtained with the infusion of 900-1,000 mEq of HCO3. The use of substitution fluid with 145 mEq/L of Na concentration avoids the risk of a positive intratreatment Na balance.     

Safety and efficacy of low-potassium dialysate

To evaluate the safety and efficacy of low-potassium dialysate, 11 patients with stable end-stage renal disease and with no history of arrhythmia or digitalis use were studied. All were treated with hemodialysis three times per week. Dialysates with potassium concentrations of 2 mEq/L, 1 mEq/L, or 0 mEq/L were compared. Each patient (exceptions noted in text) was studied once at each bath potassium concentration. Cardiac rhythm was recorded by Holter monitor during and for six hours following dialysis. Single PVCs and APCs were common with all potassium concentrations. Only one patient had high-grade ventricular ectopy. It was seen with each of the three potassium concentrations, but was most severe with the potassium-free dialysate. The potassium-free dialysate removed significantly more potassium (78.5 +/- 2.6 mEq) than the 1-K dialysate (62.9 +/- 5.1 mEq) or the 2-K dialysate (50.6 +/- 6 mEq), and the 1-K dialysate removed significantly more potassium than the 2-K dialysate. There were small but significant differences in serum potassium concentrations with the three different dialysates. It was concluded that (1) in all but one of our patients potassium-free dialysate did not produce new ectopy; (2) potassium-free dialysate was 24% more effective than 1-K dialysate and 50% more effective than 2-K dialysate in removing body potassium; and (3) 1-K dialysate was 20% more effective than 2-K dialysate in removing body potassium.     

Risks of chronic metabolic acidosis in patients with chronic kidney disease

Risks of chronic metabolic acidosis in patients with chronic kidney disease. Metabolic acidosis is associated with chronic renal failure (CRF). Often, maintenance dialysis therapies are not able to reverse this condition. The major systemic consequences of chronic metabolic acidosis are increased protein catabolism, decreased protein synthesis, and a negative protein balance that improves after bicarbonate supplementation. Metabolic acidosis also induces insulin resistance and a decrease in the elevated serum leptin levels associated with CRF. These three factors may promote protein catabolism in maintenance dialysis patients. Available data suggest that metabolic acidosis is both catabolic and anti-anabolic. Several clinical studies have shown that correction of metabolic acidosis in maintenance dialysis patients is associated with modest improvements in nutritional status. Preliminary evidence indicates that metabolic acidosis may play a role in beta2-microglobulin accumulation, as well as the hypertriglyceridemia seen in renal failure. Interventional studies for metabolic acidosis have yielded inconsistent results in CRF and maintenance hemodialysis patients. In chronic peritoneal dialysis patients, the mitigation of acidemia appears more consistently to improve nutritional status and reduce hospitalizations. Large-scale, prospective, randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in maintenance hemodialysis patients. To avoid adverse events, an aggressive management approach is necessary to correct metabolic acidosis. Clinicians should attempt to adhere to the National Kidney Foundation Kidney Disease Outcome Quality Initiative (K/DOQI) guidelines for maintenance dialysis patients. The guidelines recommend maintenance of serum bicarbonate levels at 22 mEq/L or greater.     

Dialysate Sodium Control During Modeling in Hemodialysis

Dialysate sodium (Na+) modeling in hemodialysis requires precise individual adjustment and control of Na+ dialysate concentration. In practice, variations of Na+ concentration can be important and can affect the accuracy of Na+ modeling. Variations relate mainly to the low accuracy of dialysate concentrate (+/- 2.5% for Na+ is tolerated by the European Pharmacopeias), purity of hemodialysis water (2.17 mEq/L is the limit fixed by the French Pharmacopeia), and precision of the proportioning delivery systems for hemodialysis bath preparation. To minimize these difficulties, this study focused on the following points: (a) Na+ concentration is maintained constant (133 mEq/L) in the dialysate manufacturing unit. In 1982, 268 dialysate preparations (177,000 L) were made, and the mean value for Na+ concentration was 133.1 +/- 0.3 mEq/L with a probability of 99.9%. (b) The purity of the water, especially for Na+, Ca2+, and K+, is controlled for two times a day. (c) The accuracy of the proportioning delivery system is controlled by two conductivity monitors, and the variation of Na+ concentration around 133 mEq/L is smaller than +/- 0.5%. As the composition of the basic dialyzing fluid remains constant before adaptation, conductivity values reflect exactly Na+ variation, and are not affected by variations of other elements (K+, Ca2+, Mg2+) that may occur when modification of the dialysate is used for Na+ modeling. (d) Na+ dialysate concentration is adapted for each patient's need by a bedside monitor with sterile Na+ solutions (5 mol/L).(ABSTRACT TRUNCATED AT 250 WORDS)     

A double-blind evaluation of sodium gradient hemodialysis

In a double-blind, crossover trial, 7 chronic hemodialysis patients underwent three 4-week treatment periods. During one period, dialysate contained 135 mEq/l sodium. During another period, dialysate contained 143 mEq/l sodium. During the remaining period, we used "sodium gradient' dialysate, the sodium concentration of which was decreased from 160 to 133 mEq/l during each 4-hour dialysis session. Ultrafiltration was performed at a constant rate to achieve a predetermined post-dialysis weight. Interdialytic weight gain, thirst, blood pressure control, and incidence of side effects were monitored. There was a significant difference in interdialytic weight gain for the 3 treatments (p = 0.005). Interdialytic weight gain using 135 mEq/l sodium dialysate (2.2 +/- 0.9 kg, mean +/- SD) was significantly less than that using either 143 mEq/l sodium dialysate (2.6 +/- 0.8 kg) or sodium gradient dialysate (2.8 +/- 0.7 kg). Self-reported thirst tended to be less severe with 135 mEq/l sodium dialysate than with 143 mEq/l sodium dialysate or with sodium gradient dialysate, but changes in thirst were not statistically significant (p = 0.13). The incidence of intradialytic hypotensive episodes was comparable with the 3 levels of dialysate sodium. The results suggest that the described sodium gradient method does not prevent the increased interdialytic weight gain and thirst seen with other forms of high-sodium dialysis, and probably does not reduce the incidence of side effects.     

Optimal correction of acidosis changes progression of dialysis osteodystrophy

To investigate an eventual role of acidosis on hemodialysis osteodystrophy we prospectively studied 21 patients who were dialyzed with different amounts of bicarbonate in the dialysate for 18 months. According to the level of bone formation rate (BFR) on a prestudy bone biopsy, patients were split in two subgroups. Inside these two subgroups patients were randomly allocated to two therapeutics groups: 10 patients (group A) were dialyzed with the conventional amount of bicarbonate (33 +/- 2 mmol/liter) in the dialysate; the rest of the patients (group B, N = 11) had 7 to 15 mmol/liter sodium bicarbonate added to the dialysate to obtain 24 mEq predialysis bicarbonate plasma levels. An effective correction of acidosis was shown in group B by a higher predialysis plasma bicarbonate level (15.6 +/- 1 group A vs. 24.0 +/- 0.6 mEq/liter group B, P less than 0.005), which was reached three months after start of the study. Compared to the prestudy bone biopsy, osteoid and osteoblastic surfaces increased in group A but not in group B on the bone biopsies performed at the end of the study. Parathormone plasma level (iPTH), measured with an antiserum which cross reacts with the 44-68 region of PTH molecule, increased during the study in group A but not in group B. This finding suggested progression of secondary hyperparathyroidism (HPT) only in group A patients. Osteocalcin plasma values increased in both groups during the 18 months of the study. Consequently the two subgroups of patients formed on the basis of BFR level were evaluated separately.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-Term use of a “Stable” Bicarbonate Containing Dialysate

We present an original method for the preparation of “stable” dialysate containing 35 mEq/1 of bicarbonate. The dialysate was utilized with 4 patients for periods ranging from 4 months to 1 year according to a short-term recirculated dialysis schedule in closed circuit (20-40L) (2-2 1/2 hrs) on alternate days. Preliminary results are reported here with respect to the tollerance of the dialytic run and correction of the acid-base balance equilibrium. The clinical tollerance is excellent despite high dehydration rates even in patients particularly sensitive to ultrafiltration. The acidosis correction would seem to be much better with bicarbonate than with traditional dialysis. The difference is even higher if we consider the brevity of the dialysis. During the bicarbonate dialysis we do not observe any fall of the PC0₂ or significant difference in PO₂ in the patient's blood. The correction of acidosis probably causes the normalization of pre-dialytic potassiemia in spite the “net” removal of K with short dialysis is considerably less.     

Metabolic acidosis of chronically hemodialyzed patients

Metabolic acidosis is a condition that is commonly encountered in both chronic renal failure and in end-stage renal disease. Metabolic acidosis is associated with many adverse effects: negative nitrogen balance, increased protein decomposition, anorexia, fatigue, bone lesions, impaired function of the cardiovascular system, impaired function of the gastrointestinal system, hormonal disturbances, insulin resistance, hyperkalemia, altered gluconeogenesis and triglyceride metabolism, increased progression of chronic renal failure, and growth retardation in children. Even 'minor' degrees of metabolic acidosis are deleterious. Metabolic acidosis of end-stage renal patients could be successfully corrected with bicarbonate hemodialysis and with peroral bicarbonate-containing phosphate binders, i.e. calcium carbonate. Bicarbonate powder compared with bicarbonate solutions has some advantages and enables a stabile composition of electrolytes. 'High' dialysate bicarbonate (40- 42 mmol/l) is a safe, well-tolerated and useful tool for better correction of the metabolic acidosis and must become a standard of hemodialysis treatment. Measured postdialysis blood bicarbonate concentration should be obtained at least every month and correction of metabolic acidosis by maintaining serum bicarbonate >or=22 mmol/l should be a goal of the management of patients undergoing chronic hemodialysis.