scholarly journals Synthesis rate of plasma albumin is a good indicator of liver albumin synthesis in sepsis

2000 ◽  
Vol 279 (2) ◽  
pp. E244-E251 ◽  
Author(s):  
Benoît Ruot ◽  
Denis Breuillé ◽  
Fabienne Rambourdin ◽  
Gerard Bayle ◽  
Pierre Capitan ◽  
...  
Keyword(s):  
Synthesis Rate ◽  
Albumin Concentration ◽  
Liver Protein ◽  
Mrna Levels ◽  
Albumin Synthesis ◽  
Plasma Albumin ◽  
Period 2 ◽  
Fractional Synthesis ◽  
Plasma Albumin Concentration

Plasma albumin is well known to decrease in response to inflammation. The rate of albumin synthesis from both liver and plasma was measured in vivo by use of a large dose ofl-[2H3-14C]valine in rats injected intravenously with live Escherichia coli and in pair-fed control rats during the acute-phase period (2 days postinfection). The plasma albumin concentration was reduced by 50% in infected rats compared with pair-fed animals. Infection induced a fall in both liver albumin mRNA levels and albumin synthesis relative to total liver protein synthesis. However, absolute liver albumin synthesis rate (ASR) was not affected by infection. In plasma, albumin fractional synthesis rate was increased by 50% in infected animals compared with pair-fed animals. The albumin ASR estimated in the plasma was similar in the two groups. These results suggest that hypoalbuminemia is not due to reduced albumin synthesis during sepsis. Moreover, liver and plasma albumin ASR were similar. Therefore, albumin synthesis measured in the plasma is a good indicator of liver albumin synthesis.

Albumin Metabolism in Chronic Renal Failure

1970 ◽  
Vol 39 (3) ◽  
pp. 423-435 ◽  
Author(s):  
G. A. Coles ◽  
D. K. Peters ◽  
J. Henry Jones
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Mean Value ◽  
Albumin Concentration ◽  
Albumin Synthesis ◽  
Plasma Albumin ◽  
Maintenance Haemodialysis ◽  
Degradation Rates ◽  
Normal Mean ◽  
Plasma Albumin Concentration

1. Plasma albumin concentration was measured in fifty-eight patients with chronic renal failure. The mean value was 3·27 g/100 ml (SD 0·44 g/100 ml; range 2·4–4·3 g/100 ml) which is significantly lower (P < 0·001) than normal (mean 3·94 g/100 ml; SD 0·23 g/100 ml; range 3·5–4·4 g/100 ml). In thirty-eight of the fifty-eight patients (65%), plasma albumin concentration was below the normal range. Treatment by maintenance haemodialysis or renal transplantation usually corrected the hypoalbuminaemia. 2. Radioactive iodine-labelled albumin turnover was investigated in twelve patients. Although plasma albumin concentration was reduced in eight of the twelve patients, the plasma half-life (T½) of the labelled albumin was normal or increased in all but one of these patients. Fractional and absolute albumin degradation rates (which include urinary albumin loss) were reduced in six of the twelve patients. In two of the four patients with normal plasma albumin concentrations the fractional albumin degradation rate was reduced. 3. Albumin synthesis was estimated by measuring the rate of incorporation into plasma proteins of 14C in two patients on a 20 g protein diet. The values were low in both. 4. Albumin catabolism and albumin synthesis were normal in two patients who had been on regular haemodialysis for 5 and 8 weeks respectively. 5. We conclude that these abnormalities in albumin metabolism were probably due to severe protein depletion, induced either by prolonged anorexia and vomiting or by deliberate restriction of protein in the diet in the course of treatment.

Plasma Albumin and Haemodilution: The Problem of Interpretation in Sequential Studies

1989 ◽  
Vol 26 (2) ◽  
pp. 132-136 ◽  
Author(s):  
D P Taggart ◽  
W D Fraser ◽  
G S Fell ◽  
D J Wheatley ◽  
A Shenkin
Keyword(s):  
Perioperative Period ◽  
Clinical Situation ◽  
Albumin Concentration ◽  
Plasma Albumin ◽  
Short Period ◽  
Stringent Test ◽  
Plasma Albumin Concentration ◽  
Sequential Studies

The ability of four formulae (3 based on packed cell volume and one on alpha-2 macroglobulin) to correct for postoperative dilutional changes in plasma albumin was assessed in 4 patients undergoing coronary artery surgery. Cardiopulmonary bypass is a stringent test of the efficacy of the formulae to correct for haemodilution as a large volume of fluid is added to the circulation in a relatively short period of time. Plasma albumin was measured 8 times in the perioperative period in the 4 patients and the clinical situation was mimicked in vitro by adding various volumes of diluent to whole blood. None of the formulae consistently corrected for predicted changes in plasma albumin concentration in vivo; two of the formulae corrected for in vitro changes in plasma albumin but the same formulae produced considerable over-correction when applied in vivo. The problem of correcting for perioperative dilutional changes in plasma albumin is discussed.

Late Hypoalbuminaemia and Albumin Metabolism in Paraplegic and Tetraplegic Patients

1972 ◽  
Vol 43 (5) ◽  
pp. 639-644 ◽  
Author(s):  
P. Ranløv ◽  
N. Rossing ◽  
M. Schwartz ◽  
B. Eskesen ◽  
G. Rasmussen
Keyword(s):  
Average Rate ◽  
Colloid Osmotic Pressure ◽  
Albumin Concentration ◽  
Fractional Catabolic Rate ◽  
Albumin Synthesis ◽  
Compensatory Mechanisms ◽  
Plasma Albumin ◽  
Cross Sectional ◽  
Catabolic Rate ◽  
Plasma Albumin Concentration

1. Plasma albumin concentration was decreased in thirty-five of eighty-six mobilized para- or tetra-plegic patients studied months or years after injury to the spinal cord causing a medullary cross-sectional syndrome. The colloid osmotic pressure was low in thirty-one of eighty-one patients in whom it was measured. Plasma volume was normal in thirty and slightly elevated in three of thirty-three patients in whom it was determined. None had oedema at the time of the investigation. 2. Albumin metabolism was studied in ten patients by means of 131I-labelled albumin. Six of these had a decreased plasma albumin concentration. This was probably caused by an increased fractional catabolic rate, although a statistically significant causal relationship could not be demonstrated. 3. in spite of the low plasma albumin concentration normal compensatory mechanisms such as an increase in rate of albumin synthesis and shift of albumin from the extravascular to the intravascular compartment were not found. On the contrary, for unexplained reasons, the average rate of synthesis and the ratio intravascular/total albumin mass were both decreased.

The response of liver albumin synthesis to infection in rats varies with the phase of the inflammatory process

2001 ◽  
Vol 102 (1) ◽  
pp. 107-114 ◽  
Author(s):  
Benoît RUOT ◽  
Fabienne BÉCHEREAU ◽  
Gérard BAYLE ◽  
Denis BREUILLÉ ◽  
Christiane OBLED
Keyword(s):  
Food Intake ◽  
Food Restriction ◽  
Specific Effect ◽  
Synthesis Rate ◽  
Albumin Concentration ◽  
Mrna Levels ◽  
Albumin Synthesis ◽  
Acute Response ◽  
Absolute Synthesis ◽  
Albumin Mrna

To discriminate between the effects of infection and of anorexia associated with infection, liver albumin synthesis was measured in well-fed rats, in rats injected with live Escherichia coli and in pair-fed rats at different stages of the inflammatory response (1, 6 and 10 days after infection) using a large dose of l-[1-14C]valine. Albuminaemia and albumin mRNA levels were unchanged following food restriction. However, absolute albumin synthesis was decreased in pair-fed rats compared with control animals after 1 day of food restriction, and had returned to normal values by day 10 when food intake was restored. Infection was characterized by a decrease in the plasma albumin concentration (35%, 45% and 28% as compared with pair-fed rats at 1, 6 and 10 days after infection respectively). Albumin mRNA levels and relative albumin synthesis were reduced in infected rats as compared with both control and pair-fed animals at all stages of infection. However, during the early acute response, the albumin absolute synthesis rate was similar in infected rats and pair-fed rats, indicating no specific effect of infection at this stage. Later in the course of infection, the amount of albumin synthesized by the liver was lower in infected than in pair-fed rats, and hypoalbuminaemia was probably maintained due to a lack of stimulation of synthesis despite increased food intake.

Acute Stimulation of Albumin Synthesis Rate with Oral Meal Feeding in Healthy Subjects Measured with [Ring-2H5]Phenylalanine

1995 ◽  
Vol 88 (2) ◽  
pp. 235-242 ◽  
Author(s):  
K. A. Hunter ◽  
P. E. Ballmer ◽  
S. E. Anderson ◽  
J. Broom ◽  
P. J. Garlick ◽  
...  
Keyword(s):  
Oral Feeding ◽  
Synthesis Rate ◽  
Liver Protein ◽  
Albumin Synthesis ◽  
Adult Rats ◽  
Fed State ◽  
Total Liver ◽  
Fractional Rate ◽  
Fractional Synthesis ◽  
Stimulation Of

1. The short-term effect of oral feeding on albumin synthesis rate was investigated in 12 healthy volunteers using two meal regimens. Albumin synthesis was measured over 90 min after injection of a ‘flooding’ amount (43 mg/kg body weight) of phenylalanine enriched to 7.5, 10 or 15 atoms% with the stable isotope [ring-2H5]phenylalanine. 2. In one set of subjects, consumption of five small hourly meals resulted in a consistent and significant increase (P < 0.05) in albumin fractional synthesis rate from a mean (± SEM) fasting value of 5.8 (± 0.4)%/day to 7.1 (± 0.4)%/day in the fed state. 3. A second study in which albumin synthesis was measured 30 min after consumption of a single larger meal was carried out in another set of volunteers. The fractional rate of albumin synthesis was again significantly elevated after feeding (P < 0.05), rising from 7.1 (± 0.4)%/day in the fasted state to 9.1 (± 0.6)%/day in the fed state. In both studies, similar responses were observed in the absolute rate of albumin synthesis (mg day−1 kg−1). 4. Albumin secretion time was significantly shorter (P < 0.05) after feeding in both studies, suggesting that the acute stimulation in albumin synthesis observed after feeding may in part be mediated via a post-transcriptional mechanism. 5. The response of total liver protein synthesis to oral feeding was investigated in an animal model employing adult rats studied with a flooding amount of [2,6-3H]phenylalanine. 6. The results indicated a stimulation of 20% with no difference in the proportion of albumin synthesis relative to total liver synthesis, determined from the immunoprecipitation of albumin from the liver.

Evidence for increased synthesis of lipoprotein(a) in the nephrotic syndrome.

1998 ◽  
Vol 9 (8) ◽  
pp. 1474-1481
Author(s):  
M G De Sain-Van Der Velden ◽  
D J Reijngoud ◽  
G A Kaysen ◽  
M M Gadellaa ◽  
H Voorbij ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Synthesis Rate ◽  
Fractional Synthesis Rate ◽  
Lipoprotein A ◽  
Control Subjects ◽  
Apolipoprotein A ◽  
Catabolic Rate ◽  
Fractional Synthesis ◽  
The Mean

In patients with the nephrotic syndrome, markedly increased levels of lipoprotein(a) (Lp(a)) concentration have been frequently reported, and it has been suggested that this may contribute to the increased cardiovascular risk in these patients. The mechanism, however, is not clear. In the present study, in vivo fractional synthesis rate of Lp(a) was measured using incorporation of the stable isotope 13C valine. Under steady-state conditions, fractional synthesis rate equals fractional catabolic rate (FCR). FCR of Lp(a) was estimated in five patients with the nephrotic syndrome and compared with five control subjects. The mean plasma Lp(a) concentration in the patients (1749+/-612 mg/L) was higher than in control subjects (553+/-96 mg/L). Two patients were heterozygous for apolipoprotein(a) (range, 19 to 30 kringle IV domains), whereas all control subjects were each homozygous with regard to apolipoprotein(a) phenotype (range, 18 to 28 kringle IV domains). The FCR of Lp(a) was comparable between control subjects (0.072+/-0.032 pools/d) and patients (0.064+/-0.029 pools/d) despite the wide variance in plasma concentration. This suggests that differences in Lp(a) levels are caused by differences in synthesis rate. Indeed, the absolute synthetic rate of Lp(a) correlated directly with plasma Lp(a) concentration (P < 0.0001) in all subjects. The present results demonstrate that increased synthesis, rather than decreased catabolism, causes elevated plasma Lp(a) concentrations in the nephrotic syndrome.

scholarly journals Biological basis of hypoalbuminemia in ESRD.

1998 ◽  
Vol 9 (12) ◽  
pp. 2368-2376 ◽  
Author(s):  
G A Kaysen
Keyword(s):  
Peritoneal Dialysis ◽  
Acute Phase ◽  
Synthesis Rate ◽  
Albumin Concentration ◽  
Albumin Synthesis ◽  
Dialysis Patients ◽  
Extravascular Space ◽  
Amyloid A ◽  
Stage Renal Disease ◽  
End Stage

Hypoalbuminemia is associated with mortality in patients with end-stage renal disease (ESRD) maintained either on peritoneal dialysis (PD) or hemodialysis (HD). Serum albumin concentration is determined by its rate of synthesis, by the catabolic rate constant (the fraction of the vascular pool catabolized per unit time), by external losses, and by redistribution from the vascular to the extravascular space. Hypoalbuminemia in dialysis patients is primarily a consequence of reduced albumin synthesis rate in both HD and PD patients, and in the case of PD patents, of transperitoneal albumin losses as well. Continuous ambulatory peritoneal dialysis patients are able to increase albumin synthesis to replace losses. Thus, ESRD does not directly suppress albumin synthesis. The rate of albumin synthesis is inversely proportional to the serum concentration of one potential acute phase protein (alpha2 macroglobulin), and albumin concentration is inversely proportional to that of either C-reactive protein or serum amyloid A in both HD and PD patients. The cause of decreased albumin synthesis is primarily a response to inflammation (the acute phase response), although it is possible that inadequate nutrition may also contribute. The cause of the inflammatory response is not immediately evident. There is no evidence that shifts of albumin to the extravascular space or that dilution of the plasma by volume expansion plays any role in causing hypoalbuminemia in ESRD patients.

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