Comparison of Radioisotope Methods for the Measurement of Phosphate Absorption in Normal Subjects and in Patients with Chronic Renal Failure

1981 ◽  
Vol 60 (1) ◽  
pp. 55-63 ◽  
Author(s):  
K. Farrington ◽  
M. N. Mohammed ◽  
S. P. Newman ◽  
Z. Varghese ◽  
J. F. Moorhead
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Extracellular Fluid ◽  
Normal Subjects ◽  
Rapid Phase ◽  
Deconvolution Analysis ◽  
Phosphate Absorption ◽  
Transplant Patients ◽  
Rate Of Absorption ◽  
Intestinal Phosphate Absorption

1. Intestinal phosphate absorption was measured in normal subjects, in patients with chronic renal failure, and in post-transplant patients, by a double isotope technique involving oral administration of 32P and simultaneous intravenous injection of 33P with subsequent deconvolution analysis. 2. By this technique intestinal phosphate absorption has been shown to have two components: an initial rapid phase, which is completed by 3 h, and a slower more prolonged phase, which continues beyond 7 1/2 h. 3. Phosphate malabsorption has been demonstrated in chronic renal failure and transplant patients, which is accounted for by impairment of the initial rapid phase of absorption. 4. Results obtained by deconvolution analysis have been compared with other estimates of phosphate absorption obtained from analysis of 32P radioactivity curves alone. 5. The fractional hourly rate of absorption and the plasma 32P radioactivity at 60 min corrected for extracellular fluid volume provided the best approximations to the result obtained by deconvolution analysis, with respect to both the maximal rate of phosphate absorption and cumulative percentage phosphate absorption.

Effect of 2′-phosphophloretin on renal function in chronic renal failure rats

2004 ◽  
Vol 287 (1) ◽  
pp. F48-F56 ◽  
Author(s):  
B. E. Peerce ◽  
L. Weaver ◽  
R. D. Clarke
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Chronic Renal Failure ◽  
Matched Control ◽  
Urine Osmolality ◽  
Serum Phosphate ◽  
Urine Protein ◽  
Phosphate Absorption ◽  
Intestinal Phosphate Absorption ◽  
Serum Pth

Hyperhosphatemia and secondary hyperparathyroidism are common and severe complications of chronic renal failure. Therapies to reduce serum phosphate have been shown to reduce serum parathyroid hormone (PTH) and slow the progression of renal failure. The effect of the inhibitor of intestinal phosphate absorption, 2′-phosphophloretin (2′-PP), on serum and urine chemistry, renal histology, and cardiac structure in the uremic rat model of renal failure, 5/6 nephrectomy (5/6 NX), was examined. The effect of 2′-PP on serum phosphate, serum PTH, serum total Ca2+, and ionized Ca2+, Ca2+ × Pi product, urine protein, urine osmolality, and creatinine clearance in 5/6 NX rats was examined. Uremic rats in chronic renal failure were gavaged daily with 25 μM 2′-PP. Over the course of a 5-wk experiment, serum chemistry in untreated uremic rats, 2′-PP-treated uremic rats, and age-matched control rats with normal renal function was determined twice a week. Urine creatinine, urine osmolality, urine phosphate, and urine protein were determined once a week from 24-h collections. 2′-PP reduced serum phosphate 40 ± 3% compared with a 17% increase in untreated uremic control rats. 2′-PP did not alter total serum Ca2+. During 5-wk experiments, serum PTH increased 65 ± 25% in untreated uremic rats and decreased 70 ± 7% in uremic rats treated with 25 μM 2′-PP. Creatinine clearance decreased 20% in untreated uremic rats compared with a 100% increase in 2′-PP-treated uremic rats. Urine protein decreased and urine osmolality increased in uremic rats treated with 2′-PP. The mechanism of the effect of 2′-PP on serum phosphate was inhibition of intestinal phosphate absorption. 2-PP inhibited intestinal phosphate absorption 50% without altering dietary protein absorption or intestinal Ca2+ absorption. Over the course of the 5-wk treatment with 2′-PP, uremic animals treated with 2′-PP had a 2–4% weight gain/wk, similar to the weight gain seen in age-matched control rats with normal renal function.

scholarly journals Intestinal phosphate absorption in a model of chronic renal failure

2007 ◽  
Vol 72 (2) ◽  
pp. 166-173 ◽  
Author(s):  
J. Marks ◽  
L.J. Churchill ◽  
S.K. Srai ◽  
J. Biber ◽  
H. Murer ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Phosphate Absorption ◽  
Intestinal Phosphate Absorption

Abnormal erythrocyte choline transport in patients with chronic renal failure

1991 ◽  
Vol 80 (2) ◽  
pp. 137-141 ◽  
Author(s):  
F. C. Fervenza ◽  
D. Meredith ◽  
J. C. Ellory ◽  
B. M. Hendry
Keyword(s):  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Chronic Renal Failure ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Normal Subjects ◽  
Choline Transport ◽  
Maintenance Haemodialysis ◽  
Control Subjects ◽  
Transplant Patients ◽  
The Mean

1. Erythrocyte choline transport has been studied in nine patients on maintenance haemodialysis for chronic renal failure, six patients on continuous ambulatory peritoneal dialysis, 31 patients with renal transplants and in nine normal control subjects. 2. The mean maximum rate of choline influx (Vmax., measured at an extracellular choline concentration of 250 μmol/l) was 66.7 (sd 14.1) μmol h−1 l−1 cells in patients on haemodialysis, 87.8 (sd 18.5) μmol h−1 l−1 cells in patients on continuous ambulatory peritoneal dialysis and 30.5 (sd 4.9) μmol h−1 l−1 cells in control subjects. The increase in choline flux in patients on haemodialysis and patients on continuous ambulatory peritoneal dialysis compared with control subjects was highly significant (P < 0.001). 3. Renal transplant patients showed variable values for the Vmax. of choline influx (range 17.7-71.7 μmol h−1 l−1 cells). The values showed a signifcant negative correlation with creatinine clearance and this correlation correctly extrapolated to the maximum choline flux in normal subjects and in patients on dialysis. 4. The kinetics of choline transport have been studied in erythrocytes of patients on haemodialysis and control subjects in ‘zero-trans’ conditions after depletion of intracellular choline. The mean Vmax. in these conditions was 38.4 (sd 4.6) μmol h−1 l−1 cells in patients on haemodialysis compared with 14.2 (sd 3.7) μmol h−1 l−1 cells in control subjects. The mean Km under ‘zero-trans’ conditions was 19.4 (sd 2.4) μmol/l in patients on haemodialysis and 7.4 (sd 1.4) μmol/l in control subjects. These differences were significant (P < 0.001).

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.

Disturbed lipoprotein composition in non-dialyzed, hemodialysis, continuous ambulatory peritoneal dialysis and post-transplant patients with chronic renal failure

2006 ◽  
Vol 44 (1) ◽  
Author(s):  
Elżbieta Kimak ◽  
Andrzej Książek ◽  
Janusz Solski
Keyword(s):  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Chronic Renal Failure ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Healthy Subjects ◽  
Linear Regression Analysis ◽  
Multivariate Linear Regression Analysis ◽  
Post Transplant ◽  
Transplant Patients ◽  
Lipoprotein Composition

AbstractStudies were carried out in 183 non-dialyzed, 123 hemodialysis, 81 continuous ambulatory peritoneal dialysis and 35 post-transplant patients and in 103 healthy subjects as a reference group. Lipids and apolipoprotein (apo)AI and apoB were determined using Roche kits. An anti-apoB antibody was used to separate apoB-containing apoCIII and apoE-triglyceride-rich lipoprotein (TRL) in the non-high-density lipoprotein (non-HDL) fraction from apoCIIInonB and apoEnonB in the HDL fraction in four groups of patients with chronic renal failure (CRF) and healthy subjects. Multivariate linear regression analysis was used to investigate the relationship between triglyceride (TG) or HDL-cholesterol (HDL-C) concentrations and lipoproteins. Dyslipidemia varied according to the degree of renal insufficiency, the type of dialysis and therapy regime in CRF patients. Lipoprotein disturbances were manifested by increased TG, non-HDL-C and TRL concentrations, and decreased HDL-C and apoAI concentrations, whereas post-renal transplant patients showed normalization of lipid and lipoprotein profiles, except for TG levels and total apoCIII and apoCIIInonB. The present study indicates that CRF patients have disturbed lipoprotein composition, and that hypertriglyceridemia and low HDL-C concentrations in these patients are multifactorial, being secondary to disturbed lipoproteins. The method using anti-apoB antibodies to separate apoB-containing lipoproteins in the non-HDL fraction from non-apoB-containing lipoproteins in HDL can be used in the diagnosis and treatment of patients with progression of renal failure or atherosclerosis. The variability of TG and HDL-C concentrations depends on the variability of TRL and cholesterol-rich lipoprotein concentrations, but the decreases in TG and increases in HDL-C concentrations are caused by apoAI concentration variability. These relationships, however, need to be confirmed in further studies.

A Study on the Distribution of Body Fluids after Rapid Saline Expansion in Normal Subjects and in Patients with Renal Insufficiency: Preferential Intravascular Deposition in Renal Failure

1983 ◽  
Vol 64 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Hendrik A. Koomans ◽  
Anton B. Geers ◽  
Peter Boer ◽  
Jan C. Roos ◽  
Evert J. Dorhout Mees
Keyword(s):  
Renal Failure ◽  
Blood Volume ◽  
Plasma Volume ◽  
Extracellular Fluid ◽  
Normal Subjects ◽  
Distribution Volume ◽  
Fluid Distribution ◽  
Severe Renal Failure ◽  
Control Value ◽  
Stage Renal Disease

1. The effect of rapid intravenous infusion of 25 ml of isotonic sodium chloride solution (saline)/kg body weight on extracellular fluid volume (ECFV, 82Br distribution volume), plasma volume (131I-labelled albumin distribution volume) and blood volume (from plasma volume and packed cell volume) was studied in nine normal subjects and a group of 11 patients with end-stage renal disease (ESRD). 2. Immediately after the infusion, the increases in ECFV were equal in the two groups but the increases in plasma and blood volumes were significantly larger in the patients with ESRD. .3. Ninety minutes after the end of the infusion, the blood volume/ECFV ratio was significantly decreased from the control value in the normal subjects, but slightly increased in the patients with ESRD. 4. It is concluded that in severe renal failure the control of fluid distribution is changed in a way which leads to a preferential distribution of rapidly infused saline into the intravascular compartment.

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.

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.

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