Mechanism of hypoalbuminemia in the 7/8-nephrectomized rat with chronic renal failure

1982 ◽  
Vol 243 (4) ◽  
pp. F372-F378 ◽  
Author(s):  
G. A. Kaysen ◽  
J. B. Watson
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Serum Albumin ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Albumin Concentration ◽  
Serum Albumin Concentration ◽  
Albumin Synthesis ◽  
Plasma Volume Expansion ◽  
Albumin Clearance

Hypoalbuminemia has been observed consistently in patients and experimental animals with chronic renal failure (CRF). A defect in albumin synthesis, catabolism, or distribution has been invoked as the cause, but there is no agreement as to which, if any, of these disorders results from the uremic state. We studied albumin homeostasis in 7/8-nephrectomized rats with CRF. Serum albumin concentration was lower in CRF (29.6 +/- 4.59 mg/ml) than in sham-operated control rats (36.3 +/- 4.3 mg/ml). Albumin synthesis, determined directly by measuring incorporation of 14CO2 into arginine in albumin, was increased in CRF rats as was total albumin clearance, measured using 125I-albumin disappearance. Rats with CRF were albuminuric. Albumin synthesis was increased by the amount necessary to replace urinary losses, but net albumin catabolism was the same as in control animals. Albuminuria was prevented by addition of excess tryptophan to the diet. Total albumin clearance and albumin synthesis were the same in these tryptophan-fed CRF animals as in CRF sham-operated animals, but these CRF rats were still hypoalbuminemic (33.6 +/- 5.27 vs. 36.3 +/- 4.3 mg/ml). Rats with CRF were plasma volume expanded. Institution of a low-sodium diet at the time of partial nephrectomy prevented plasma volume expansion and albuminuria as well. Serum albumin concentration, albumin distribution, pool sizes, and total albumin clearance remained the same as in CRF sham-operated animals. Hypoalbuminemia in CRF rats is due to two factors. Plasma volume expansion with pool dilution contributes 40% of the decrease and external albumin losses resulting from albuminuria contribute the other 60%. Albumin synthesis, catabolism, and distribution are intact.

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.

Albumin metabolism in fasted subjects during late pregnancy

1991 ◽  
Vol 81 (2) ◽  
pp. 161-168 ◽  
Author(s):  
O. Samson Olufemi ◽  
Paul G. Whittaker ◽  
Dave Halliday ◽  
Tom Lind
Keyword(s):  
Serum Albumin ◽  
Plasma Volume ◽  
Late Pregnancy ◽  
Whole Body ◽  
Albumin Concentration ◽  
Serum Albumin Concentration ◽  
Body Protein ◽  
Control Subjects ◽  
Synthetic Rate ◽  
Fractional Synthetic Rate

1. Albumin fractional synthetic rate was determined in five non-pregnant subjects and five normal pregnant subjects in late gestation after an overnight fast by simultaneous prime and intravenous infusion of two precursor amino acids, [15N]glycine and l-[1-13C]leucine, with additional priming of the large but, slowly turning over, urea pool with [15N2]urea. 2. The two tracers yielded similar values of albumin fractional synthetic rate: 6.1 and 6.0%/day in nonpregnant subjects and 7.3 and 7.6%/day in pregnant subjects, for glycine and leucine, respectively. While plasma volume was greater and serum albumin concentration was significantly reduced during pregnancy, the calculated intravascular albumin mass was significantly increased in pregnant subjects. 3. The amount of albumin synthesized in the intravascular compartment was significantly greater at 8.8 and 9.5 g/day in pregnant subjects compared with 6.4 and 6.3 g/day in non-pregnant control subjects (glycine and leucine methods, respectively). Calculated whole-body protein turnover using glycine was not different between the two subject groups, but leucine flux was higher in pregnant subjects. Partitioning of nitrogenous products in urine revealed that pregnant subjects excreted less urea, less ammonia and less creatinine than the non-pregnant control subjects. 4. These findings suggest that whereas the serum albumin concentration decreases during pregnancy secondary to the large increase in plasma volume, there is an increase in albumin synthesis such that total intravascular albumin mass is increased in late pregnancy.

Serum Albumin Concentration on Admission as a Predictor of Morbidity and Mortality in Patients With Burn Injuries

2021 ◽  
Author(s):  
Nilmar G Bandeira ◽  
Marcus Vinícius V S Barroso ◽  
Marcos Antônio A Matos ◽  
Alexandre L M Filho ◽  
Adson A Figueredo ◽  
...  
Keyword(s):  
Renal Failure ◽  
Serum Albumin ◽  
Pulmonary Infection ◽  
Severity Index ◽  
The Body ◽  
Burn Injuries ◽  
Morbidity And Mortality ◽  
Albumin Concentration ◽  
Serum Albumin Concentration ◽  
Severe Burn Injuries

Abstract Efforts have been made to determine new predictors of morbidity and mortality in patients with severe burn injuries. This prospective cohort study aimed to determine the association of serum albumin concentration on admission and renal failure, pulmonary infection, sepsis, and death in patients with burn injuries. We included 141 patients, aged &gt;18 years, who were admitted to our institution between April and August 2018. Among them, 59.1% were male and 83.8% had burns covering &lt;20% of the body surface area. Scalds were the most common cause of burns (34.8%). Twelve patients died, of whom eight (66.6%) had an Abbreviated Burn Severity Index (ABSI) ≥8. Patients with serum albumin ≤2.2 g/dL had a higher mortality rate than those with &gt;2.2 g/dL (odds ratios [OR]: 18.7; 95% confidence interval [CI]: 4.9 to 70.8). Serum albumin ≤2.2 g/dL was also significantly associated with pulmonary infection (OR: 13.1, 95% CI: 3.8 to 45.7), renal failure (OR: 30.2, 95% CI: 7.4 to 122.3), and sepsis (OR: 16.9, 95% CI: 4.9 to 58.3). Serum albumin concentration cut-points and ABSIs were determined to be death predictors using areas under the receiver operating characteristic curves (AUCs). The AUCs with albumin or ABSI alone were 0.89 (95% CI: 0.79 to 0.98) and 0.92 (95% CI: 0.87 to 0.96), respectively. The AUC including both albumin and ABSI was 0.96 (95% CI: 0.90 to 0.98), indicating that the combination is a better death predictor than either measure alone. We confirmed that burn patients with a serum albumin concentration ≤2.2 g/dL on admission have substantially increased morbidity and mortality.

scholarly journals Effects of Changing Plasma Volume, Serum Albumin Concentration, and Plasma Osmolality on Renal Function in Cirrhosis

1967 ◽  
Vol 53 (2) ◽  
pp. 229-239 ◽  
Author(s):  
Randolph M. McCloy ◽  
William P. Baldus ◽  
Frank T. Maher ◽  
W.H.J. Summerskill
Keyword(s):  
Renal Function ◽  
Serum Albumin ◽  
Plasma Volume ◽  
Plasma Osmolality ◽  
Albumin Concentration ◽  
Serum Albumin Concentration

scholarly journals Acute suppression of albumin synthesis in systemic inflammatory disease: an individually graded response of rat hepatocytes.

1992 ◽  
Vol 40 (2) ◽  
pp. 201-206 ◽  
Author(s):  
P E Ballmer ◽  
K Ballmer-Hofer ◽  
F Repond ◽  
H Kohler ◽  
H Studer
Keyword(s):  
Serum Albumin ◽  
Rat Hepatocytes ◽  
Immunoperoxidase Technique ◽  
Albumin Concentration ◽  
Phase Reaction ◽  
Serum Albumin Concentration ◽  
Albumin Synthesis ◽  
Clear Trend ◽  
Systemic Inflammatory Disease

The effects of an inflammatory insult on albumin of the rat liver were investigated at the cellular level and were correlated with serum albumin concentration. After SC injection of turpentine, the livers were perfused and fixed in vivo; serial liver sections were stained using a streptavidin-ABC-immunoperoxidase technique with an antibody to rat albumin. Albumin and total protein were measured at intervals after turpentine injection in whole livers and in serum. Fibrinogen was determined in plasma only. Twenty-four hours after turpentine injection serum albumin had dropped by 25% and was at 50% of its initial value at Day 3. Serum fibrinogen increased 2.4-fold within 24 hr and decreased thereafter. Liver homogenates showed no significant changes in albumin concentration. Immunohistochemically, all hepatocytes stained positive for albumin in normal animals. During inflammation, the immunostainable albumin content vanished entirely in a majority of all hepatocytes while remaining unchanged in other cells, thus producing a strikingly patchy staining pattern. No signs of resumption of albumin accumulation in depleted hepatocytes were seen after 8 days, despite a clear trend towards normalization of serum albumin concentration. These results suggest that individual hepatocytes differ widely in their response to agents that suppress albumin synthesis in an acute-phase reaction.

CARDIORESPIRATORY STATUS OF ERYTHROBLASTOTIC NEWBORN INFANTS: II. BLOOD VOLUME, HEMATOCRIT, AND SERUM ALBUMIN CONCENTRATION IN RELATION TO HYDROPS FETALIS

PEDIATRICS ◽  
1974 ◽  
Vol 53 (1) ◽  
pp. 13-23
Author(s):  
R. H. Phibbs ◽  
P. Johnson ◽  
W. H. Tooley ◽  
B. Bradley Johnson ◽  
D. Sudman ◽  
...  
Keyword(s):  
Blood Cell ◽  
Serum Albumin ◽  
Blood Volume ◽  
Plasma Volume ◽  
Red Blood Cell ◽  
Newborn Infants ◽  
Hydrops Fetalis ◽  
Albumin Concentration ◽  
Serum Albumin Concentration ◽  
Blood Volumes

We measured hematocrit and serum albumin concentration at birth and red blood cell and plasma volume soon after birth in prematurely born infants with erythroblastosis fetalis of varying severity and examined the realtionships between these variables and the presence and severity of hydrops fetalis. Blood volumes in most of these infants were similar to the established normals for newborn infants without erythroblastosis. There was no simple association between blood volume and the presence of hydrops. Nonhydropic and severely hydropic infants had, on the average, similar and normal blood volumes, while mildly hydropic infants had low blood volumes. Anemia correlated fairly well with severity of hydrops but almost a quarter of the infants with severe hydrops were only mildly anemic. Red blood cell volume decreased and plasma volume increased proportionally with the degree of anemia at birth. Thus, hydropic infants with severe anemia had large plasma volumes while those with milder anemia did not. On the other hand, hypoalbuminemia was common and correlated closely with severity of hydrops. We suggest that hydrops results at least in part from low plasma colloid osmotic pressure due to hypoalbuminemia.

Effects of Long-term Nitric Oxide Synthesis Inhibition on Plasma Volume Expansion and Fetal Growth in the Pregnant Rat

Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1019-1023 ◽  
Author(s):  
Sofía P. Salas ◽  
Fernando Altermatt ◽  
Mauricio Campos ◽  
Andrea Giacaman ◽  
Pedro Rosso
Keyword(s):  
Nitric Oxide ◽  
Fetal Growth ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Nitric Oxide Synthesis ◽  
Plasma Volume Expansion ◽  
Pregnant Rat ◽  
Synthesis Inhibition

scholarly journals Increased susceptibility of db/db mice to rosiglitazone-induced plasma volume expansion: role of dysregulation of renal water transporters

2013 ◽  
Vol 305 (10) ◽  
pp. F1491-F1497 ◽  
Author(s):  
Li Zhou ◽  
Gang Liu ◽  
Zhanjun Jia ◽  
Kevin T. Yang ◽  
Ying Sun ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Underlying Mechanism ◽  
Fluid Retention ◽  
Receptor Subtype ◽  
Fluorescent Nanoparticles ◽  
Peroxisome Proliferator ◽  
Plasma Volume Expansion

Thiazolidinediones (TZDs), which are synthetic peroxisome proliferator-activated receptor subtype-γ (PPARγ), agonists are highly effective for treatment of type 2 diabetes. However, the side effect of fluid retention has significantly limited their application. Most of the previous studies addressing TZD-induced fluid retention employed healthy animals. The underlying mechanism of this phenomenon is still incompletely understood, particularly in the setting of disease state. The present study was undertaken to examine rosiglitazone (RGZ)-induced fluid retention in db/db mice and to further investigate the underlying mechanism. In response to RGZ treatment, db/db mice exhibited an accelerated plasma volume expansion as assessed by hematocrit (Hct) and fluorescent nanoparticles, in parallel with a greater increase in body weight, compared with lean controls. In response to RGZ-induced fluid retention, urinary Na+ excretion and urine volume were significantly increased in lean mice. In contrast, the natriuretic and diuretic responses were significantly blunted in db/db mice. RGZ db/db mice exhibited a parallel decrease in plasma Na+ concentration and plasma osmolality, contrasting to unchanged levels in lean controls. Imunoblotting analysis showed downregulation of renal aquaporin (AQP) 2 expression in response to RGZ treatment in lean mice but not in db/db mice. Renal AQP3 protein expression was unaffected by RGZ treatment in lean mice but was elevated in db/db mice. In contrast, the expression of Na+/H+ exchanger-3 (NHE3) and NKCC2 was unchanged in either mouse strain. Together these results suggest that compared with the lean controls, db/db mice exhibited accelerated plasma volume expansion that was in part due to the inappropriate response of renal water transporters.

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