The Effect of Aluminium Hydroxide Orally on Calcium, Phosphorus and Aluminium Metabolism in Normal Subjects

1976 ◽  
Vol 51 (4) ◽  
pp. 407-414 ◽  
Author(s):  
J. M. Cam ◽  
V. A. Luck ◽  
J. B. Eastwood ◽  
H. E. de Wardener
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Aluminium Hydroxide ◽  
Normal Subjects ◽  
The Other ◽  
Calcium Balance ◽  
Phosphorus Balance ◽  
Calcium Phosphorus ◽  
Aluminium Hydroxide Gel ◽  
Plasma Phosphorus

1. Five normal subjects were given 100 ml of aluminium hydroxide gel per day for 28 days. 2. The phosphorus balance became more positive in one subject, less negative in two and changed from negative to positive in the other two subjects. This was accompanied by a rise in the concentration of the fasting morning plasma phosphorus. Calcium balance did not change. 3. The normal subjects absorbed 0·3–3·6 mmol of aluminium/day, which is significantly less than that absorbed by five patients with chronic renal failure, three of whom were studied before, and two after, the observations on the normal subjects had been completed. 4. In a further five normal subjects on 100 ml of aluminium hydroxide gel/day the 08.00 hours concentration of plasma phosphorus did not fall, though there was a fall at 11.00, 14.00 and 17.00 hours.

The Effect of Aluminium Hydroxide on Calcium, Phosphorus and Aluminium Balances, the Serum Parathyroid Hormone Concentration and the Aluminium Content of Bone in Patients with Chronic Renal Failure

1972 ◽  
Vol 43 (4) ◽  
pp. 519-531 ◽  
Author(s):  
E. M. Clarkson ◽  
V. A. Luck ◽  
W. V. Hynson ◽  
R. R. Bailey ◽  
J. B. Eastwood ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Aluminium Hydroxide ◽  
Plasma Calcium ◽  
Aluminium Content ◽  
Serum Parathyroid Hormone ◽  
Calcium Phosphorus ◽  
Aluminium Hydroxide Gel ◽  
Plasma Phosphorus

1. Eight patients with chronic renal failure (creatinine clearance 4·9–22·0 ml/min) were given 75–150 ml of aluminium hydroxide gel (‘Aludrox’) daily for 20–32 days. 2. In all patients there was a decrease in plasma phosphorus. The phosphorus balance became more negative in four and less positive in one, remained unchanged in two, and became positive in one. 3. Patients absorbed 100–568 mg of aluminium daily. In two of three patients the content of aluminium in the iliac bone increased but not above normal values. 4. The concentration of parathyroid hormone was decreased by aluminium hydroxide therapy in three patients in whom there was an increase in plasma calcium and in one other patient in whom plasma calcium did not change.

The Effect of Aluminium Hydroxide on Calcium, Phosphorus and Aluminium Balances and the Plasma Parathyroid Hormone in Patients with Chronic Renal Failure

1971 ◽  
Vol 41 (2) ◽  
pp. 5P-6P ◽  
Author(s):  
R. R. Bailey ◽  
J. B. Eastwood ◽  
E. M. Clarkson ◽  
V. A. Luck ◽  
W. V. Hynson ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Aluminium Hydroxide ◽  
Calcium Phosphorus

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.

scholarly journals Familial Atypical Hemolytic Uremic Syndrome with Positive pS1191L (c.3572C> T) Mutation in CFH A Single-Center Experience

2019 ◽  
Author(s):  
Fadime ERSOY DURSUN ◽  
Gözde YESIL ◽  
Hasan DURSUN ◽  
Gülşah SASAK
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Family History ◽  
Hemolytic Uremic Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Gene Mutations ◽  
Factor H ◽  
The Other ◽  
History Of ◽  
Uremic Syndrome

Abstract Background: Atypical hemolytic uremic syndrome is a condition characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury, which can exhibit a poor prognosis. Gene mutations play a key role in this disease, which may be sporadic or familial. Methods: We studied, 13 people from the same family were investigated retrospectively for gene mutations of familial atypical hemolytic uremic syndrome after a patient presented to our emergency clinic with atypical hemolytic uremic syndrome and reported a family history of chronic renal failure. Results: The pS1191L mutation in the complement factor H gene was heterozygous in 6 people from the family of the patient with atypical hemolytic uremic syndrome. One of these people was our patient with acute renal failure and the other two are followed up by the Nephrology Clinic due to chronic renal failure. The other 3 persons showed no evidence of renal failure. The index case had a history of 6 sibling deaths; two of them died of chronic renal failure. Plasmapheresis and fresh frozen plasma treatment was given to our patient. When patient showed no response to this treatment, eculizumab therapy was started. Conclusions: The study demonstrated that a thorough family history should be taken in patients with atypical hemolytic uremic syndrome. These patients may have familial type of the disease and they should be screened genetically. Eculizumab should be the first choice in the treatment with plasmapheresis. It should be kept in mind that the use of eculizumab as prophylaxis in post-transplant therapy is extremely important for prevention of rejection.

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.

scholarly journals Protein-to-creatinine urinary in the early diagnosis of renal injury in canine pyometra

2019 ◽  
Vol 39 (3) ◽  
pp. 186-191
Author(s):  
Marcos C. Sant’Anna ◽  
Guilherme F. Martins ◽  
Karina K.M.C. Flaiban ◽  
Luiz G.C. Trautwein ◽  
Maria I.M. Martins
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Injury ◽  
Renal Damage ◽  
Systemic Disease ◽  
The Other ◽  
Control Group ◽  
Creatinine Ratio ◽  
Renal Lesions ◽  
Tubular Cells

ABSTRACT: Kidney disease that affects bitches with pyometra may lead patients to develop chronic renal failure even after pyometra treatment. Therefore, several studies have sought to clarify the gaps in the understanding of the pathogenesis of renal injury in pyometra. Identification of early detection markers for renal damage, which can predict and identify the prognosis of the disease, is very important. Proteinuria analysis can diagnose kidney damage, since proteins such as albumin are not filtered through the glomerulus and those that undergo glomerular filtration are almost completely reabsorbed by tubular cells. The objective of this study was to evaluate whether the urinary protein-to-creatinine ratio (UPC) can detect renal injury in bitches with pyometra before development of azotemia. For this, 44 bitches with pyometra were divided into two groups: bitches with azotemic piometra (A, n=15, creatinine >1.7) and bitches with non-azotemic pyometra (NA, n=29). The two groups were compared to the control group (CG, n=12), which had no signs of systemic disease. All animals underwent blood and urine tests. Leukocytosis was more evident in bitches in the A group than in the other groups. This shows that the inflammatory response may be associated with the pathogenesis of renal injury. The median UPC in bitches with pyometra was significantly higher than in the CG, with a median above the reference values. In conclusion, the UPC can be used in bitches with pyometra to detect renal damage before the development of azotemia. It has been suggested that the UPC of bitches with pyometra should be followed through during the postoperative period so that permanent renal lesions secondary to pyometra can be diagnosed and treated properly before the development of azotemia.

Endogenous vasopressin regulates Na-K-ATPase and Na+-K+-Cl− cotransporterrbsc-1 in rat outer medulla

2002 ◽  
Vol 282 (2) ◽  
pp. F265-F270 ◽  
Author(s):  
Claudia A. Bertuccio ◽  
Fernando R. Ibarra ◽  
Jorge E. Toledo ◽  
Elvira E. Arrizurieta ◽  
Rodolfo S. Martin
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atpase Activity ◽  
Receptor Antagonist ◽  
The Other ◽  
Outer Medulla ◽  
Physiological Conditions ◽  
Increased Activity ◽  
Expression And Activity

Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V2-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 ± 1.5 to 3.7 ± 0.8 in controls ( P < 0.05) and from 19.0 ± 0.8 to 2.9 ± 0.5 μmol Pi · mg protein−1 · h−1 in moderate CRF rats ( P < 0.05). CRF was associated with a significant increase in Na-K-ATPase activity ( P < 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 ± 21.5% compared with controls ( P < 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 ± 9.5 and 105.3 ± 10.9%, respectively ( P < 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 ± 6.5 and 30.0 ± 6.9%, respectively ( P < 0.05), and was not influenced by CRF (95.7 ± 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.

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.

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