The influence of bicarbonate supplementation on plasma levels of branched-chain amino acids in haemodialysis patients with metabolic acidosis (original) (raw)
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Seminars in …, 2000
In a cross-sectional study of more than 30% of French dialysis patients (N = 7,123), we evaluated the relationships between predialysis plasma bicarbonate concentration and nutritional markers. Data including age, gender, cause of end-stage renal disease (ESRD), time on dialysis, body mass index (BMI), blood levels of midweek predialysis albumin, prealbumin, and bicarbonate were collected. Normalized protein catabolic rate (nPCR), dialysis adequacy parameters, and estimation of lean body mass (LBM) were computed from pre-and postbicarbonate-dialysis urea and creatinine levels according to the classical formulas of Garred. Average values (±1 SD) were age 61 ± 16 years, BMI 23.3 ± 4.6 kg/m 2 , dialysis time 12.4 ± 2.7 h/week, HCO 3 22.8 ± 3.5 mmol/L, albumin 38.7 ± 5.3 g/L, prealbumin 340 ± 90 mg/L, Kt/V 1.36 ± 0.36, nPCR 1.13 ± 0.32 g/kg BW/day, and LBM 0.86 ± 0.21% of ideal LBM. A highly significant negative correlation was observed between predialysis bicarbonate levels (within a range of 16-30 mmol/L, 95% of this population) and nPCR confirmed by analysis of variance using bicarbonate classes (p < 0.0001). Bicarbonate was also negatively correlated with albumin, prealbumin, BMI, and LBM. No relationship was noted between bicarbonate and Kt/V despite a positive correlation between Kt/V and nPCR. It is likely that a persistent acidosis observed despite standard bicarbonate dialysis was caused by a high dietary protein intake which results in an increased acid load, but also overcomes the usual catabolic effects of acidosis.
The relationship between metabolic acidosis and nutritional parameters in patients on hemodialysis
Indian Journal of Nephrology
The progressive loss of kidney function is accompanied by metabolic acidosis. The relationship between metabolic acidosis, nutritional status, and oral bicarbonate supplementation has not been assessed in the Indian chronic kidney disease (CKD) population who are on maintenance hemodialysis (MHD). This is a single-center prospective study conducted in the Western part of India. Thirty-five patients, who were receiving MHD were assessed for metabolic acidosis along with various nutritional parameters at the baseline and at the follow-up after 3 months, postcorrection of acidosis with oral sodium bicarbonate supplements. The relationship between the correction of metabolic acidosis with oral bicarbonate supplements and changes in dietary and various nutritional parameters were evaluated. Metabolic acidosis at the baseline evaluation was found in 62.86% cases of the cohort with a mean serum bicarbonate value of 20.18 ± 4.93 mmol/L. The correction of acidosis with increment in the mean dosage of oral sodium bicarbonate supplements from 0.69 ± 0.410 mmol/kg/day at baseline to 1.04 ± 0.612 mmol/kg/day, significantly reduced the prevalence of metabolic acidosis to 23.33% cases at the follow-up. Improvement in serum bicarbonate level showed significant dietary, anthropometric, and nutritional improvements in these patients. Hence, we conclude that correction of metabolic acidosis with optimal oral bicarbonate supplementation plays a pivotal role in the treatment of malnourished CKD patients on MHD.
ACID-BASE IN RENAL FAILURE: Acidosis and Nutritional Status in Hemodialyzed Patients
Seminars in Dialysis, 2001
In a cross-sectional study of more than 30% of French dialysis patients (N = 7,123), we evaluated the relationships between predialysis plasma bicarbonate concentration and nutritional markers. Data including age, gender, cause of end-stage renal disease (ESRD), time on dialysis, body mass index (BMI), blood levels of midweek predialysis albumin, prealbumin, and bicarbonate were collected. Normalized protein catabolic rate (nPCR), dialysis adequacy parameters, and estimation of lean body mass (LBM) were computed from pre-and postbicarbonate-dialysis urea and creatinine levels according to the classical formulas of Garred. Average values (±1 SD) were age 61 ± 16 years, BMI 23.3 ± 4.6 kg/m 2 , dialysis time 12.4 ± 2.7 h/week, HCO 3 22.8 ± 3.5 mmol/L, albumin 38.7 ± 5.3 g/L, prealbumin 340 ± 90 mg/L, Kt/V 1.36 ± 0.36, nPCR 1.13 ± 0.32 g/kg BW/day, and LBM 0.86 ± 0.21% of ideal LBM. A highly significant negative correlation was observed between predialysis bicarbonate levels (within a range of 16-30 mmol/L, 95% of this population) and nPCR confirmed by analysis of variance using bicarbonate classes (p < 0.0001). Bicarbonate was also negatively correlated with albumin, prealbumin, BMI, and LBM. No relationship was noted between bicarbonate and Kt/V despite a positive correlation between Kt/V and nPCR. It is likely that a persistent acidosis observed despite standard bicarbonate dialysis was caused by a high dietary protein intake which results in an increased acid load, but also overcomes the usual catabolic effects of acidosis.
Nephrology Dialysis Transplantation, 1998
considered with caution as an estimate of the dietary protein intake in HD patients in the presence of Background. Malnutrition in haemodialysis (HD) patients has been referred to underdialysis with low metabolic acidosis. protein intake, and to acidosis. However, the separate Key words: acidosis; haemodialysis; nutrition; PCRn; effects of underdialysis and acidosis on nutrition have Kt/V; serum albumin not been clearly demonstrated. To evaluate the role of the dialysis dose and of metabolic acidosis on nutrition, we measured the predialysis serum HCO 3 , pH, serum albumin, PCRn, Kt/V, and BMI in 81 uraemic patients Introduction on maintenance bicarbonate HD for 93±80 months. Patients with chronic liver diseases, malignancies, and Protein-energy malnutrition is present in a large procachexia were excluded. portion of maintenance haemodialysis (HD) patients Results. Mean age was 59±17 years, Kt/V was [1]. Low levels of serum albumin concentrations have 1.29±0.21, PCRn 1.06±0.22 g/kg/day, serum albubeen associated with increased morbidity and mortality min 4.07±0.28 g/dl, BMI 23±4 kg/m2, HCO 3 [2,3]. Many causes predispose to malnutrition in HD 21.1±1.9 mmol/l, pH 7.36±0.04. Serum albumin patients but recently the role of reduced values of showed a significant direct correlation with: PCRn protein catabolic rate (PCRn) and Kt/V, as expression (P=0.001), HCO 3 (P=0.00l ), pH (P=0.002), but no of low nutritional intake and anorexia associated with correlation with Kt/V and BMI. Serum HCO 3 correlsuboptimal dialysis prescription [4,5], and metabolic ated inversely with PCRn (P=0.027). Multiple regresacidosis [6 ] have been stressed. Studies aimed to meassion analysis confirmed the significant role of serum ure protein degradation in humans have shown that bicarbonate and age, but not of Kt/V, on serum the induction of acidosis increases the whole-body albumin concentrations. The role of PCRn appeared protein degradation [7]. The correction of acidosis in to be marginal compared to serum bicarbonate in chronic renal failure patients [8,9] and in haemodialysis determining serum albumin levels. Dividing patients patients [10], has been shown to reduce protein into two groups, serum albumin was 3.96±0.22 g/dl degradation and amino-acid oxidation. However, the with HCO 3 ∏20 mmol/l and 4.18±0.31 g/dl in those respective effects of both underdialysis and acidosis on with serum HCO 3 Á23 mmol/l (P=0.002). PCRn in nutritional status have not yet been clearly demonthe same groups was respectively 1.14±0.24 g/kg/day strated in the clinical setting. Aim of this study was to and 1.01±0.23 g/kg/day (P=0.03). Most importantly, elucidate the respective roles of the dialysis dose and serum albumin levels did not appear to be affected by metabolic acidosis on serum albumin concentrations the dialysis dose, with Kt/V ranging from 0.90 to 1.88. and PCRn in a large in-centre HD population. Conclusions. In HD patients with adequate Kt/V, metabolic acidosis exerts a detrimental effect on serum albumin concentrations partially independently of the Subjects and methods protein intake, as evaluated by PCRn. In the presence of moderate to severe metabolic acidosis, PCRn does Eighty-one uraemic patients (52 men, 29 women) on regular not reflect the real dietary protein intake of the patients, chronic haemodialysis for 6-315 months (median 67 months) probably as a result of increased catabolism of were studied. Patients with neoplasia, systemic diseases, endogenous proteins. For this reason PCRn should be chronic liver diseases, and cachexia were excluded. All of them were treated by bicarbonate HD thrice weekly, with 1.3-1.8 m2 cellulosic membranes (Gambro Lun-Dia A700; ranged from 180 to 270 min (median 228 min). Blood flow
Acidosis and Nutritional Status in Hemodialyzed Patients
Seminars in Dialysis, 2000
In a cross-sectional study of more than 30% of French dialysis patients (N = 7,123), we evaluated the relationships between predialysis plasma bicarbonate concentration and nutritional markers. Data including age, gender, cause of end-stage renal disease (ESRD), time on dialysis, body mass index (BMI), blood levels of midweek predialysis albumin, prealbumin, and bicarbonate were collected. Normalized protein catabolic rate (nPCR), dialysis adequacy parameters, and estimation of lean body mass (LBM) were computed from pre- and postbicarbonate-dialysis urea and creatinine levels according to the classical formulas of Garred. Average values (±1 SD) were age 61 ± 16 years, BMI 23.3 ± 4.6 kg/m2, dialysis time 12.4 ± 2.7 h/week, HCO3 22.8 ± 3.5 mmol/L, albumin 38.7 ± 5.3 g/L, prealbumin 340 ± 90 mg/L, Kt/V 1.36 ± 0.36, nPCR 1.13 ± 0.32 g/kg BW/day, and LBM 0.86 ± 0.21% of ideal LBM. A highly significant negative correlation was observed between predialysis bicarbonate levels (within a range of 16–30 mmol/L, 95% of this population) and nPCR confirmed by analysis of variance using bicarbonate classes (p < 0.0001). Bicarbonate was also negatively correlated with albumin, prealbumin, BMI, and LBM. No relationship was noted between bicarbonate and Kt/V despite a positive correlation between Kt/V and nPCR. It is likely that a persistent acidosis observed despite standard bicarbonate dialysis was caused by a high dietary protein intake which results in an increased acid load, but also overcomes the usual catabolic effects of acidosis.
Association of acidosis and nutritional parameters in hemodialysis patients
American Journal of Kidney Diseases, 1999
There is extensive literature supporting an important role for acidosis in inducing net protein breakdown, both in experimental animals and humans. However, the clinical importance of the moderate intermittent metabolic acidosis frequently observed in hemodialysis patients has not been determined. We performed a cross-sectional analysis of the baseline laboratory data in the first 1,000 patients recruited to the Hemodialysis Study, looking for correlations between predialysis serum total carbon dioxide levels and parameters related to dietary intake and nutritional status. We found the mean predialysis serum total carbon dioxide level was moderately low (21.6 ؎ 3.4 mmol/L; mean ؎ SD) despite the use of bicarbonate dialysate and an average single-pool Kt/V of 1.54. Predialysis serum total carbon dioxide level correlated negatively with normalized protein catabolic rate (P F 0.001), suggesting patients with lower serum total carbon dioxide levels have a greater protein intake. The degree of acidosis observed in our patients does not seem to have a deleterious effect on the nutritional status of these patients because correlation of serum total carbon dioxide level with nutritional parameters, such as serum creatinine and serum albumin levels, was either negative or not statistically significant. Further investigation of the effect of modifying serum bicarbonate concentration on nutritional markers is needed to test these hypotheses.
Metabolic acidosis and its association with nutritional status in hemodialysis
Jornal Brasileiro de Nefrologia, 2015
Metabolic acidosis is a common problem in dialysis patients and plays an important role in the pathogenesis of protein-energy malnutrition in these patients. Objectives: To assess the prevalence of metabolic acidosis in hemodialysis and search their association with nutritional status. Methods: A cross-sectional study was performed in hemodialysis patients at a single center. Nutritional status was assessed by anthropometric, biochemical and multifrequency bioelectrical impedance analysis. Metabolic acidosis was defined as serum bicarbonate (BIC) < 22 mEq/L and patients were divided into 3 groups according to BIC (< 15.15 to 21.9 and ≥ 22). The association between BIC and continuous variables was investigated using the Kruskal Wallis test. The linear correlation between BIC and the variables of the study was also tested. Results: We studied 95 patients, 59% male, mean age 52.3 years. The prevalence of metabolic acidosis was 94.7%. BMI, interdialytic weight gain and PTH were significantly different among the 3 groups of BIC. The BIC was negatively correlated with urea, phosphorus and interdialytic weight gain. There was no significant correlation with albumin, phase angle and lean body mass index. Conclusion: The prevalence of metabolic acidosis was high in this population, and a lower BIC correlated with higher levels of urea, PTH, phosphorus, interdialytic weight gain and lower BMI. The evaluation of acid-basic status should be routinely implemented in dialysis patients by considering the negative effects of acidosis on the nutritional status, inflammation and bone disease.
Nutrition in Hemodialysis: Its Measurement and Meaning
Seminars in Dialysis, 1994
Nutrition is one of the essential elements of the dialysis prescription (1). In contrast to the dialysis itself, nutrition can only be guided by the physician and dietician; it is ultimately controlled by the patient either voluntarily or involuntarily by disease. It mirrors the success of dialysis but can be an independent risk factor for morbidity and mortality when controlled by another disease (e.g., tuberculosis). Hemodialysis, because of its intermittent nature, offers an opportunity for measuring an important aspect of nutrition, the patient's protein intake, from simple measurements of blood urea nitrogen (BUN). Protein intake is estimated from the patient's protein catabolic rate (PCR), calculated from the change in BUN between dialyses. The other elements of the prescription that are easily measured in hemodialyzed patients are the midweek predialysis BUN and Kt/V (where K is the urea clearance of the dialyzer, t is time on dialysis, and V is the volume of urea distribution). KzIV reflects the amount of dialysis prescribed or delivered during each treatment. BUN only expresses the ratio of dietary protein intake/amount of dialysis treatment.
Metabolic Acidosis of Chronically Hemodialyzed Patients
American Journal of Nephrology, 2003
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 endstage renal patients could be successfully corrected with bicarbonate hemodialysis and with peroral bicarbonatecontaining 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 622 mmol/l should be a goal of the management of patients undergoing chronic hemodialysis.