The Prognostic Implications of Changes in Albumin Following LVAD Implantation
Dipika GopalThomas C. HanffJeremy A. MazurekE. Wilson GrandinJessica HowardRhondalyn Ford-McLeanJoyce WaldMichael AckerLee R. GoldbergPavan AtluriKenneth B. MarguliesJ. Eduardo RameEdo Y. Birati
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Hypoalbuminemia
Serum Albumin
Albumin consists of 50% of the total plasma protein and it is very important protein in the animal's body. Hypoalbuminemia can occurs due to various conditions, such as loss of protein nephropathy, loss of enteropathic proteins, chronic and acute diarrhea or heavy bleeding as well as malnutrition and malabsorption conditions. This study aims to determine the effect of human serum albumin 20% infusion to increase albumin blood level in hypoalbuminemia dogs. Animals used in this study were 5 dogs whose results showed the levels of albumin below normal limits or hypoalbuminemia. Dogs with hypoalbuminemia will be infused with human serum albumin (HSA) 20% through intravenous for ± 4 hours. Then, these dogs blood will be drawn days after infusion to screen for albumin levels. The results obtained in the form of examination data of albumin blood levels in the blood before and after infusion will be analyzed with paired T-test. The results showed an increase of albumin level significantly from an average of 1.98 ± 0.356 to 2.28 ± 0.257(P <0.05). This study shows the presence of human albumin serum through intravenous infusion was able to increase albumin levels in dogs with hypoalbuminemia.
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Better knowledge of albumin kinetics is needed to define the indications for albumin use in clinical practice. This study involved two approaches: the synthesis rate and transcapillary escape rate of albumin were measured simultaneously at different levels of plasma albumin concentration in relation to acute inflammation and surgery; and two different tracers were compared to determine plasma volume and the transcapillary escape rate. Healthy volunteers (n = 10), patients with acute inflammatory abdominal disease (n = 10), and patients undergoing elective pancreatic resection (n = 10) were studied. The albumin synthesis rate was measured by the incorporation of deuterium-labeled phenylalanine. Plasma volume and the transcapillary escape rate were assessed using 123I-labeled and 125I-labeled albumin. A 50 % elevated de-novo albumin synthesis rate was seen in patients with acute inflammation and marked hypoalbuminemia, while patients with marginal hypoalbuminemia before the start of surgery had a normal albumin synthesis rate. The transcapillary escape rate was elevated intraoperatively during the reconstructive phase of pancreatic surgery, when plasma albumin was decreased but stable. In acute inflammation with marked hypoalbuminemia, the transcapillary escape rate was no different from normal. 123I-labeled and 125I-labeled albumin were found exchangeable for plasma volume determinations, but could be used only in groups of patients for the transcapillary escape rate. This observational study illustrates the limited information contained in albumin plasma concentrations to reflect albumin kinetics. On the contrary, single measurements of the synthesis rate and/or transcapillary escape rate of albumin obviously cannot explain the plasma level of albumin or the changes seen in plasma albumin concentration. www.clinicaltrials.gov , study number NCT01686776 . Registered 13 September 2012.
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Hypoalbuminemia, without any apparent cause, is occasionally seen in elderly patients. Eleven patients (6 with plasma albumin of over 3 gm% and 5 with plasma albumin of 3 gm% or less), who had no evidence of liver disease or nephrosis and whose dietic history suggested that they were taking adequate amounts of protein were investigated, using 131I human serum albumin. None were acutely ill and their age ranged from 70 to 86 years. It was found that elderly subjects with plasma albumin level of 3 gm% or less had significantly reduced albumin pools and an increased fractional catabolic rate. It is suggested that this may be due to an impairment of the control of degradation in these patients. There was no increased gut loss of albumin in 3 hypoalbuminemic patients investigated with 131I-PVP.
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In four patients with hypoalbuminemia due to the nephrotic syndrome, the removal rate of sulfobromophthalein (BSP) was rapid with less than 1 per cent dye retention at 45 minutes. After partial correction of the hypoalbuminemia by intravenous infusion of salt-poor human albumin, dye retention was 4 to 9 per cent at 45 minutes. This reciprocal relation between BSP removal rate and plasma albumin level appears to reflect the degree of dye binding in the plasma that governs the rate of BSP extraction by the liver. The accelerated dye disappearance associated with hypoalbuminemia may have clinical implications in patients with chronic parenchymal liver disease, in whom a low plasma albumin may tend to minimize the extent of BSP retention that would prevail if the albumin level were normal.
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The mechanisms leading to hypoalbuminemia in sepsis were explored by measuring plasma volume, albumin distribution, plasma albumin transcapillary escape rate (TER), and efflux (TER × albumin intravascular pool). These parameters were quantified in infected rats, injected intravenously with live Escherichia coli, and pair-fed and well-fed rats using an injection of 35 S-albumin and measuring plasma and whole body albumin concentrations. Animals were studied on days 1, 6, and 10 after infection. In pair-fed rats, neither albumin distribution nor exchange rate between the intra- and extravascular compartments was modified. The increase of plasma volume after infection partly explained hypoalbuminemia. Infection resulted in a reduction of the total albumin pool of the body all along the experimental period, indicating a net loss of the protein. Albumin TER (%/day) was significantly increased 1 and 6 days after infection, but the absolute efflux was increased only on day 1. Normal values were observed on day 10. Therefore, an accelerated plasma efflux contributes to hypoalbuminemia only during the early period of sepsis. During this phase, the protein was retained in the extravascular space where it was probably catabolized. Later on, other factors are probably involved.
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Abstract Hypoalbuminemia is associated with inflammation. Despite being addressed repeatedly in the literature, there is still confusion regarding its pathogenesis and clinical significance. Inflammation increases capillary permeability and escape of serum albumin, leading to expansion of interstitial space and increasing the distribution volume of albumin. The half‐life of albumin has been shown to shorten, decreasing total albumin mass. These 2 factors lead to hypoalbuminemia despite increased fractional synthesis rates in plasma. Hypoalbuminemia, therefore, results from and reflects the inflammatory state, which interferes with adequate responses to events like surgery or chemotherapy, and is associated with poor quality of life and reduced longevity. Increasing or decreasing serum albumin levels are adequate indicators, respectively, of improvement or deterioration of the clinical state. In the interstitium, albumin acts as the main extracellular scavenger, antioxidative agent, and as supplier of amino acids for cell and matrix synthesis. Albumin infusion has not been shown to diminish fluid requirements, infection rates, and mortality in the intensive care unit, which may imply that there is no body deficit or that the quality of albumin “from the shelf” is unsuitable to play scavenging and antioxidative roles. Management of hypoalbuminaemia should be based on correcting the causes of ongoing inflammation rather than infusion of albumin. After the age of 30 years, muscle mass and function slowly decrease, but this loss is accelerated by comorbidity and associated with decreasing serum albumin levels. Nutrition support cannot fully prevent, but slows down, this chain of events, especially when combined with physical exercise.
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