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      Metabolic Acidosis of Chronically Hemodialyzed Patients

      , ,
      American Journal of Nephrology
      S. Karger AG

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          Abstract

          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 references11

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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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              Effect of metabolic acidosis on hyperlipidemia in uremia.

              R Mak (1999)
              Nine patients (aged 18+/-1 years) on maintenance hemodialysis with metabolic acidosis and hyperlipidemia were studied before and after 2 weeks of oral sodium bicarbonate (NaHCO(3)) treatment to correct the acidosis. To control for the effect of additional sodium, they were also studied after 2 weeks of an equivalent amount of oral sodium chloride (NaCl). Oral NaHCO(3 )treatment led to significant increases in venous pH, serum bicarbonate, and serum 1, 25-dihydroxyvitamin D(3) concentrations, but no significant change in total and ionized calcium, phosphate, sodium, potassium, creatinine, blood urea nitrogen, and intact parathyroid hormone concentrations. Oral NaCl did not change any of the biochemical parameters. Before treatment of acidosis, these uremic patients had high serum triglycerides, low serum high-density lipoprotein (HDL) cholesterol, but normal total cholesterol compared with controls. Following 2 weeks of NaHCO(3) treatment, there was a significant decrease in the serum concentrations of triglycerides (P<0.01). HDL and total cholesterol did not change. There were no changes in triglycerides, HDL or total cholesterol from baseline values following 2 weeks of NaCl. Thus treatment of metabolic acidosis ameliorated hypertriglyceridemia but had no effect on HDL and total cholesterol in patients with uremia on hemodialysis. The underlying mechanism may involve 1,25-dihydroxyvitamin D3.
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                Author and article information

                Journal
                American Journal of Nephrology
                Am J Nephrol
                S. Karger AG
                0250-8095
                1421-9670
                June 1 2003
                2003
                May 16 2003
                : 23
                : 3
                : 158-164
                Article
                10.1159/000070205
                6e1481e4-527d-49a1-b6a3-5fc69083de60
                © 2003

                https://www.karger.com/Services/SiteLicenses

                https://www.karger.com/Services/SiteLicenses

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