Efficiency of Utilization of Urea Nitrogen for Albumin Synthesis by Chronically Uraemic and Normal Man

1975 ◽  
Vol 48 (5) ◽  
pp. 379-390 ◽  
Author(s):  
R. Varcoe ◽  
D. Halliday ◽  
E. R. Carson ◽  
P. Richards ◽  
A. S. Tavill
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Significant Positive Correlation ◽  
Normal Subjects ◽  
Nitrogen Utilization ◽  
Urea Synthesis ◽  
Absolute Rate ◽  
Albumin Synthesis ◽  
Urea Nitrogen ◽  
Urea Metabolism

1. The relation between endogenous urea metabolism and albumin synthesis has been studied in ten patients with chronic renal failure and in four normal subjects, after single intravenous injections of [14C]urea, [15N]urea and 125I-labelled albumin. 2. The rate of urea synthesis was determined from the dynamics of plasma [14C]urea specific radioactivity and the rate of urea metabolism was estimated from the relative rates of urea synthesis and urea appearance in urine and body water. Deconvolution analysis of plasma [15N]albumin enrichment and 125I-labelled albumin radioactivity yielded the cumulative incorporation of 15N into total exchangeable albumin and enabled calculation of the absolute rate of urea nitrogen utilization for albumin synthesis. 3. Although the mean absolute rate of urea degradation in uraemic patients (3.7 mmol/h) was higher than in normal subjects (2.3 mmol/h) there was no significant positive correlation between urea degradation and plasma urea concentration. 4. In uraemic subjects, there was a significant positive correlation between urea synthetic rate and urea degradation rate. 5. The rate of utilization of urea nitrogen for albumin synthesis was low, but was very much higher in uraemic subjects (mean 83.8 μmol/h) compared with normal subjects (mean 6.4 μmol/h), as was the provision by urea of the nitrogen required for albumin synthesis in uraemic subjects (2.37%) compared with normal subjects (0.13%). 6. The efficiency of utilization of urea nitrogen for albumin synthesis was higher in the uraemic patients (1.3%) than the normal subjects (0.2%), and was higher in those patients with chronic renal failure who received a 30 g protein diet than those on 70 g of protein. A significant negative correlation was noted between efficiency of urea nitrogen utilization and the rate of synthesis of albumin. 7. These studies suggest the presence of a mechanism for the conservation of urea nitrogen in chronic renal failure which is unrelated to the extent of urea degradation, and which can only be partly explained by the higher proportion of intraluminal gut nitrogen derived from urea.

Evidence for an Increased Generation of Prostacyclin in the Microvasculature and an Impairment of the Platelet α-Granule Release in Chronic Renal Failure

1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Clotting ◽  
Normal Subjects ◽  
Chronic Uraemia ◽  
Wall Interaction ◽  
End Stage ◽  
Granule Release

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.

Fluorescent substances in uremic and normal serum.

1985 ◽  
Vol 31 (12) ◽  
pp. 1988-1992 ◽  
Author(s):  
M Shaykh ◽  
N Bazilinski ◽  
D S McCaul ◽  
S Ahmed ◽  
A Dubin ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Normal Subjects ◽  
Normal Serum ◽  
Gel Chromatography ◽  
Intense Fluorescence

Abstract We measured the fluorescence, at various excitation (Ex) and emission (Em) wavelengths, of serum ultrafiltrates and fractions of serum resolved by chromatography on Sephadex G15, studying both normal subjects and patients in chronic renal failure requiring hemodialysis. We found hitherto undescribed fluorescence at Ex 380 nm/Em 440 nm and Ex 400 nm/Em 460 nm, the intensity being greatly increased in patients with chronic renal failure in comparison with normal subjects (p less than 0.005). This fluorescence persisted unaltered when serum was filtered through membranes having cutoffs ranging from 10 000 to 500 Da. Each serum fraction resolved by gel chromatography demonstrated a characteristic fluorescence, which was generally much more intense in uremics. The most intense fluorescence (Ex 380 nm/Em 440 nm and Ex 400 nm/Em 460 nm) was emitted in the higher-Mr fractions.

Parathyrin radioimmunoassay: diagnostic utility of antisera produced against carboxyl-terminal fragments of the hormone from the human.

1978 ◽  
Vol 24 (3) ◽  
pp. 451-454 ◽  
Author(s):  
F P Di Bella ◽  
J M Kehrwald ◽  
K Laakso ◽  
L Zitzner
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Guinea Pigs ◽  
Normal Subjects ◽  
Terminal Region ◽  
Diagnostic Utility ◽  
Human Origin ◽  
Widespread Availability ◽  
Carboxyl Terminal

Abstract Antisera directed toward the carboxyl-terminal region of human parathyrin (parathyroid hormone), for use in daignostically applicable radioimmunoassays of the hormone in serum, are scarce, largely because of the lack of suitable immunogens of human origin. We produced four antisera in goats and guinea pigs by immunization with recently discovered carboxyl-terminal fragments of human parathyrin extracted from parathyroid tumors. Here, we report results of radioimmunoassays of nearly 200 normal and pathological sera with one of these antisera; we observed almost complete differentiation between concentrations of parathyrin in serum of healthy normal subjects and patients with primary, secondary (due to chronic renal failure), or "ectopic" hyperparathyroidism (due to nonparathyroid cancer). The availability of a new immunogen should now make possible the deliberate production of large quantities of diagnostically applicable parathyrin antisera directed toward the carboxyl-terminal region of human parathyrin. This should, in turn, lead to more widespread availability of this useful radioimmunoassay.

Origin of Glycosylated Hemoglobin Al in Chronic Renal Failure

1983 ◽  
Vol 6 (2) ◽  
pp. 77-82 ◽  
Author(s):  
S. De Marchi ◽  
E. Cecchin ◽  
C. Camurri ◽  
P. Quaia ◽  
A. Raimondi ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Urea Nitrogen ◽  
Serum Ferritin ◽  
Serum Iron ◽  
Urea Nitrogen ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Blood Ph

In chronic renal failure both HbAI and HbAlc levels have been reported to be elevated. In order to investigate the causes of such increase we measured HbAI (cation-exchange chromatography), blood urea nitrogen, arterial blood pH, plasma bicarbonate, phosphatemia, serum iron and serum ferritin before dialysis in 60 uremic patients receiving long term hemodialysis. The increased levels of HbAI do not correlate with glucose intolerance, phosphatemia, blood urea nitrogen, time averaged concentration of urea, serum iron and serum ferritin. On the contrary the presence of a highly significant correlation between HbAI and arterial blood pH (p < 0.001) and between HbAI and plasma bicarbonate (p < 0.001) seems to emphasize a major role for acidosis in increasing the HbAI levels in uremic patients on long term hemodialysis.

Plasma β-Thromboglobulin And Platelet Factor 4 In Patients With Chronic Renal Failure And Effect Of Hemodialysis

1981 ◽  
Author(s):  
Y Endo ◽  
M Mamiya ◽  
K Takahashi ◽  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Statistical Significance ◽  
Normal Subjects ◽  
Statistical Correlation ◽  
Platelet Factor 4 ◽  
Cellulose Membrane ◽  
Heparin Infusion ◽  
Platelet Factor ◽  
The Difference

We have reported that jS-thromboglobulin (β-TG) and platelet factor 4 (PF4) increased in chronic renal failure. The purpose of the current study is to reveal a correlation between plasma β-TG (Amersham Corp. England) and renal function, a correlation between plasma β-TG and PF. (Abbott Lab., USA) and the effect of hemodialysis on patients with chronic renal failure.Significantly increased levels of plasma β-TG (76.8±25.5 ng/ml, p<0.01) were observed in 24 patients with chronic renal failure (BUN>20mg/dl), compared to normal subjects (13.2±5.6ng/ml). The increase in β-TG was highly correlated with BUN (r=0.651, p<0.01), creatinine (r=0.778, p<0.01) and creatinine clearance (r=-0.723, p<0.01). Although plasma PF4 (normal 5.0±2.0ng/ml) increased also, no statistical significance could be found. Statistical correlation between β-TG and PF4 was not found in these patients. This reason is thought to Be due to the difference of molecular weight (PF. 8000MW, β-TG 36000MW) and half-life (PF4 30min,β-TG 100min) The high levels of β-TG (89.4±3.4ng/ml) showed a further increase (109.4±5.8ng/dl, p<0.01) after dialysis. This is thought to be due to hemoconcentration, because of no adhesion of platelet to cellulose membrane but about 20% elevation in mean of other blood factors such as RBC, WBC, platelet, fibrinogen etc. The PF4 levels (before, 7.7±1.3ng/ml) which increased at 15min (55.2±19.6ng/ml, p<0.01) and 1 hr (23.7±8.4ng/ml, p< 0.01) are thought to be due to the influence of heparin infusion. The change in PF4. was not accompanied by the change in β-TG. During hemodialysis the decrease of other platelet functions such as adhesiveness, aggregation induced by ADP, collagen and PF3remained unchanged.

Inhibitors of the Fibrinolytic Enzyme System in Renal Disease

1970 ◽  
Vol 39 (5) ◽  
pp. 549-557 ◽  
Author(s):  
N. B. Bennett ◽  
D. Ogston
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Damage ◽  
Enzyme System ◽  
Normal Subjects ◽  
Plasminogen Activation ◽  
Significant Elevation ◽  
Normal Range ◽  
Marked Inhibition ◽  
Serum Inhibitor

1. Levels of serum inhibitor of plasminogen activation, anti-plasmin and plasminogen activator were measured in normal subjects and patients with active glomerulonephritis and chronic renal failure. 2. Patients with active glomerulonephritis all had grossly elevated levels of serum inhibitor of plasminogen activation and significant elevation of anti-plasmin. The majority of activator levels lay at the lower end of the normal range. 3. Patients with chronic renal failure had significantly elevated levels of serum inhibitor of plasminogen activation and anti-plasmin, but the changes were less marked than in those with active glomerulonephritis. Activator levels were consistently reduced. 4. The marked inhibition of fibrinolysis in active glomerulonephritis may be a factor in the persistence of glomerular fibrin and ultimately in perpetuation of renal damage. The changes in the fibrinolytic system in chronic renal failure may determine the development of the serosal exudates characteristic of that condition.

A radioimmunoassay for bone Gla protein (BGP) in human plasma

1987 ◽  
Vol 114 (3) ◽  
pp. 410-416 ◽  
Author(s):  
Julia S. Johansen ◽  
J. E. Mølholm Hansen ◽  
Claus Christiansen
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Human Plasma ◽  
Biochemical Marker ◽  
Normal Subjects ◽  
Bone Gla Protein ◽  
Low Concentrations ◽  
Metabolic Bone ◽  
The Mean ◽  
Bone Physiology

Abstract. To study the value of bone Gla protein (BGP) as a biochemical marker of normal bone physiology and metabolic bone disorders, we have developed a radioimmunoassay (RIA) for the detection of BGP in human plasma. Antibodies were generated in rabbits immunized with purified calf BGP conjugated to thyroglobulin. Human plasma BGP reacted identically with the calf BGP standard, thus demonstrating the suitability of the assay to measure plasma BGP levels in man. The RIA is sensitive, accurate, and technically simple. Plasma BGP levels were determined in normal subjects (N = 35) and in patients with hypothyroidism (N = 10), hyperthyroidism (N = 22) and chronic renal failure (N = 35). The mean (± 1 sem) concentration of plasma BGP in normal subjects was 1.27 ± 0.07 nmol/l. Plasma BGP was significantly increased in patients with hyperthyroidism, 4.04 ± 0.78 nmol/l (P < 0.001) and chronic renal failure, 10.17 ± 2.47 nmol/l (P < 0.001). Low concentrations were found in patients with hypothyroidism, 0.74 ± 0.11 nmol/l (P <0.01). Our studies indicate that plasma BGP provides a useful technique in the diagnosis of patients with bone disease.

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