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acidosis/알부민

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Chronic metabolic acidosis decreases albumin synthesis and induces negative nitrogen balance in humans.

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Chronic metabolic acidosis has been previously shown to stimulate protein degradation. To evaluate the effects of chronic metabolic acidosis on nitrogen balance and protein synthesis we measured albumin synthesis rates and urinary nitrogen excretion in eight male subjects on a constant metabolic

Acute metabolic acidosis decreases muscle protein synthesis but not albumin synthesis in humans.

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Chronic metabolic acidosis induces negative nitrogen balance by either increased protein breakdown or decreased protein synthesis. Few data exist regarding effects of acute metabolic acidosis on protein synthesis. We investigated fractional synthesis rates (FSRs) of muscle protein and albumin,

Increase in bilirubin binding to albumin with correction of neonatal acidosis.

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Twenty-six serial measurements of free bilirubin concentration and apparent association constant of bilirubin for albumin (Ka) at a bilirubin: albumin molar ratio of 0.8 were performed and compared with baseline values in 11 newborn infants with acidosis before treatment and during recovery from

Albumin versus normal saline for dehydrated term infants with metabolic acidosis due to acute diarrhea.

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To compare the efficacy of albumin to normal saline (NS) for initial hydration therapy for dehydrated term infants with severe metabolic acidosis due to acute diarrhea. METHODS We randomized 33 infants presenting with moderate-to-severe dehydration and metabolic acidosis (pH <7.25 or base excess

Comparison of albumin versus bicarbonate treatment for neonatal metabolic acidosis.

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In this study the effectiveness of 4.5% human albumin was compared with 4.2% sodium bicarbonate for neonatal metabolic acidosis, using a randomised controlled trial. The change in median pH following bicarbonate was more than twice that in the albumin group. This was statistically
The aim of this study was to assess if albumin infusion in hypotensive, preterm infants improved blood pressure (BP), metabolic acidosis and core peripheral temperature difference, indicating that such infants had been hypovolemic. Thirty-seven infants, median gestational age 27 weeks (range 23-34)

Metabolic acidosis components in advanced chronic kidney disease: association with serum albumin and parathyroid hormone.

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OBJECTIVE To investigate the associations between the 2 main components of metabolic acidosis (unmeasured anions [UA] and hyperchloremia) with serum albumin and intact parathormone (iPTH) in patients with advanced chronic kidney disease. METHODS Cross-sectional study with advanced chronic kidney

Quantitative relationships among plasma lactate, inorganic phosphorus, albumin, unmeasured anions and the anion gap in lactic acidosis.

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BACKGROUND Quantitative relationships among plasma [Lactate], [Pi], [Albumin], unmeasured anions ([UA]) and the anion gap (AGK) in lactic acidosis (LA) are not well defined. METHODS A mathematical model featuring compensatory potassium and chloride shifts and respiratory changes in LA demonstrated:

Dilutional acidosis following hetastarch or albumin in healthy volunteers.

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BACKGROUND The intent of this study was to evaluate the impact of the commonly used colloids-hetastarch and albumin-on in vivo acid-base balance. From this evaluation, a better understanding of the mechanism of dilutional acidosis was expected. METHODS In a prospective, randomized fashion, 11

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

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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

Impact of metabolic acidosis on serum albumin and other nutritional parameters in long-term CAPD patients.

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To evaluate the effects of metabolic acidosis on serum albumin and other nutritional parameters in long-term continuous ambulatory peritoneal dialysis (CAPD) patients, we undertook a retrospective study involving 106 CAPD patients who had monthly biochemical measurements and urea kinetic studies
Insufficient oxygenation (hypoxia), acidic pH (acidosis), and elevated levels of reactive oxygen species (ROS), such as H2O2, are characteristic abnormalities of the tumor microenvironment (TME). These abnormalities promote tumor aggressiveness, metastasis, and resistance to therapies. To date,
BACKGROUND Metabolic acidosis in haemodialysis (HD) patients increases whole body protein degradation while the correction of acidosis reduces it. However, the effects of the correction of acidosis on nutrition have not been clearly demonstrated. METHODS In this study we have evaluated the effects

Correction of metabolic acidosis on serum albumin and protein catabolism in hemodialysis patients.

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BACKGROUND The effect of the correction of metabolic acidosis (MA) on serum albumin concentrations (sAlbs) in hemodialysis (HD) patients is controversial. This study evaluated the role of the correction of MA on sAlb concentrations, normalized protein catabolic rate (nPCR), and the effect of the
BACKGROUND Base deficit (BD), anion gap (AG), and albumin corrected anion gap (ACAG) are used by clinicians to assess the presence or absence of hyperlactatemia (HL). We set out to determine if these tools can diagnose the presence of HL using cotemporaneous samples. METHODS We conducted a chart
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