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      Metabolic Acidosis of Chronically Hemodialyzed Patients

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          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 ≧22 mmol/l should be a goal of the management of patients undergoing chronic hemodialysis.

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          Most cited references 11

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          Management of life-threatening acid-base disorders. First of two parts.

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            Nutrition in CAPD: serum bicarbonate and the ubiquitin-proteasome system in muscle.

            Metabolic acidosis in chronic renal failure (CRF) induces loss of lean body mass while elimination of acidosis during a one year trial improved anthropometric indices in continuous ambulatory peritoneal dialysis (CAPD) patients. In rats with CRF, the mechanisms causing loss of lean body mass have been linked to acidosis-induced destruction of the essential, branched-chain amino acids (BCAA) and activation of the ubiquitin-proteasome system that degrades muscle protein; the latter response includes increased transcription of the ubiquitin gene. Our aim was to determine if increasing the serum bicarbonate (HCO3) concentration of CAPD patients would improve their nutritional status, increase plasma BCAA levels, and reduce ubiquitin mRNA in their muscle as an index of suppressed activity of the ubiquitin-proteasome system. Eight, stable, long-term CAPD patients underwent vastus lateralis muscle biopsy before being randomized to continue 35 mmol/L lactate dialysate or convert to a 40 mmol/L lactate dialysate. After four weeks, measurements were repeated. Serum HCO3 increased in all patients and final values did not differ statistically between the two groups so results for all patients were combined. Weight and body mass index increased significantly as did plasma BCAA. Muscle levels of ubiquitin mRNA decreased significantly; serum tumor necrosis factor-alpha (TNF-alpha) also decreased. Our results indicate that even a small correction of serum HCO3 improves nutritional status, and provide evidence for down-regulation of BCAA degradation and muscle proteolysis via the ubiquitin-proteasome system. Whether acidosis and inflammatory cytokines (such as, TNF-alpha) interact to impair nutrition is unknown.
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              Relationship between interdialytic weight gain and acid-base status in hemodialysis by bicarbonate.

              The aim of this study was to determine the relationship between interdialytic weight gain and acid-base balance pre- and posthemodialysis in uremic patients undergoing hemodialysis with a high bicarbonate dialysate (39 mmol/L). To this end we studied 8 stable uremic patients on regular hemodialysis thrice weekly who had stable hematocrit values for at least 3 months, similar clinical characteristics including dry weight but widely varying interdialytic weight gain. Arterial line blood samples were collected anaerobically in heparinized syringes pre- and posthemodialysis in 4 consecutive hemodialysis sessions for the determination of pH, Paco2, and HCO3. Prehemodialysis values (mean +/- SD) were pH = 7.34 +/- 0.03, Paco2 = 36.43 +/- 1.4, and Hco3 = 20.1 +/- 1.55. Posthemodialysis values were pH= 7.47 +/- 0.02, Paco2 = 38.72 +/- 2.0, and HCO3 = 27.73 +/- 1.72. In other words, patients were moderately acidemic prior to and moderately alkalemic after the hemodialysis session. Of note, a significant negative correlation was revealed between the interdialytic weight gain and the values of prehemodialysis blood pH (r = -0.721, p < 0.001) and HCO3 (r = -0.836, p < 0.001) and posthemodialysis pH (r = -0.533, p < 0.001), Paco2 (r = -0.623, p < 0.001) and HCO3 (r = -0.815, p < 0.001), suggesting an important role of the interdialytic weight gain on acid-base equilibrium of uremic patients undergoing hemodialysis. Thus, patients with high interdialytic weight gains may require higher bicarbonate concentrations to achieve normal acid-base status whereas patients with low interdialyic weight gains may require lower bicarbonate concentrations to prevent alkalemia at the end of dialysis.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                June 2003
                16 May 2003
                : 23
                : 3
                : 158-164
                aHemodialysis Department, Health Center Trogir, Croatia; bUrgent Medicine Department, Health Center Ploce, Croatia and cMedizinische Klinik und Poliklinik 2, Klinische Forschergruppe ‘Respiratorische Insuffizienz’, Giessen, Germany
                70205 Am J Nephrol 2003;23:158–164
                © 2003 S. Karger AG, Basel

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                Page count
                References: 90, Pages: 7
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                Original Article: Basic Sciences

                Cardiovascular Medicine, Nephrology

                Metabolic acidosis, Hemodialysis, Bicarbonate


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