Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:021525 (albumin)
 60,984 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum-25-hydroxy-vitamin-D (25-OHD) nephrotic syndrome (N.S.) without renal insufficiency (urinary protein excretion greater than 3-5 g/24 h/1-73 m2; glomerular filtration-rate greater than 80 ml/min/1-73 m2). Serum-25-OHD levels were low in patients with N.S. (mean 19 nmol/1, range 4-41 nmol/1), compared with a normal range of 25-200 nmol/1. Serum-concentrations of Gc-globulin--the binding protein for vitamin D and its metabolites (D.B.P.)--were significantly (P less than 0-001) lower in patients with N.S. (mean 340 mg/1, range 190-480 mg/1) than in non-proteinuric controls (mean 440 mg/1, range 376-510 mg/1, measured by radial immunodiffusion). In contrast to non-proteinuric urine, urine of all N.S. patients contained a large amount of 25-OHD-binding capacity; D.B.P. could be detected in all N.S. urines after concentration. Scatchard analysis of the urine demonstrated the presence of a low-affinity and a high-affinity binding protein (tentatively identified as albumin and D.B.P.). These results suggest an acquired deficiency of circulating 25-OHD in N.S. secondary to urinary loss of protein-bound 25-OHD. The biological relevance of the low 25-OHD levels is unknown. There was no clinical evidence of osteomalacia (X-ray, serum-alkaline-phosphatase); however, slightly elevated serum-parathyroid-hormone (P.T.H.) levels would be compatible with borderline vitamin-D depletion.
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PMID:25-hydroxy-vitamin-D in nephrotic syndrome. 6 93

Serum lipoproteins of 25 patients with uncomplicated renal diseases were studied with polyacrylamide gel block electrophoresis. (1) In the nephrotic syndrome (or nephrotic phase of nephritis), marked increases of chylomicrons, pre-beta lipoprotein or beta lipoprotein and decreases of alpha lipoproteins were detected in the most of the patients. Qualitative change was also frequent as in the glomerulonephritis. (2) In the renovascular hypertension, metabolism of serum lipoproteins was involved also. The principal abnormality was in alpha lipoproteins including the lipid-loaded albumin. Marked increases of alpha lipoproteins, to the level equal to or more than beta lipoprotein, was detected in 2 of 3 patients studied in this period. Surgical correction of abnormal physiology had resulted in a return to a normal lipoprotein profile. (3) In the glomerulonephritis confirmed by biopsies, serum lipoprotein abnormalities were detected more frequently than in the reported past studies as analyzed with the method employed in this study. Qualitative as well as quantitative abnormalities were in beta lipoprotein and alpha lipoproteins in the early and middle phase of the disease process. Gross qualitative change occured frequently. Furthermore, lipoprotein abnormalities in renal diseases were reversible; i.e., when the disease had ameliorated or was corrected surgically, the lipoprotein profile returned to the normal or near-normal profile. In conclusion, the results of the present study indicated that serum lipoprotein disorders are involved in the disease process of three major clinical entities of the renal diseases.
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PMID:Studies on serum lipoproteins in renal diseases. 19 63

The extent and nature of furosemide (F) binding to human albumin (HA) and to the plasma of 6 children with nephrotic syndrome were studied by equilibrium dialysis at 37 degrees C and pH 7.4 with 14C-F. At a total concentration of 3.4 mug/ml (therapeutic range), the unbound fraction of F to 4 gm per 100 ml HA was 2.79 plus or minus 0.35. The degree of binding was relatively constant from 1.8 to 36 mug/ml of F concentration. The percentage of unbound F doubled when total concentration of the drug was increased more than 130 times (1.8 to 245 mug/ml). F has two classes of binding sites (n1 = 1.42, k1 = 5.07 times 10-4 M-minus 1; n2 = 3.4, k2 = 1.58 times 10-4 M-minus 1); interaction with HA involves hydrophobic, ionic, and hydrogen forces. Acetylsalicylic acid (ASA), acetazolamide, diazoxide, phenylbutazone, sulfisoxazole (S), and tolbutamide (T) decreased F binding. Combinations of ASA, S, and T exerted a strong additive displacing effect. The binding of the F metabolite (4-chloro-5-sulfamoylanthranilic acid, CSA) was studied at 1.3 and 2.6 mug/ml. The unbound fraction was 5 times that of F. CSA did not influence F binding. Studies with plasma of 7 healthy adults showed that albumin is the only plasma protein responsible for F binding. The plasma albumin concentration range of the children with nephrotic syndrome was 0.6 to 2.1 gm per 100 ml. There was some correlation between albumin concentration and binding of F (2.8 to 9.6% unbound); this corresponded with findings with HA. Albumin concentrations lower than 2 gm per 100 ml seemed to influence the extent of the unbound fraction of F considerably.
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PMID:Furosemide binding to human albumin and plasma of nephrotic children. 23 96

Dimer and polymer albumin was detected in the urine of a proportion of pantients with a nephrotic syndrome. Most of it was present as S-S bonded dimer and polymer; co-polymers, however, with IgG and alpha (1) anti-trypsin could be demonstrated. It is suggested that albumin polymerizes after it has passed the glomerular membrane. Albumin dimer was associated mainly with minimal change disease and early membranous glomerulopathy in patients, who in general responded well to therapy.
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PMID:Polymeric albumin in the urine of patients with nephrotic syndrome. 30 62

The published specifications of the acceptable limits of the maximum plasma volume to be "harvested" by plasmapheresis from one individual per year vary from 10-15 liters in Europe to 50-60 liters in the United States. To answer the question which of these widely diverging precepts is appropriate, the effects of plasmapheresis on serum protein levels and their relationship to albumin metabolism, the accepted safeguards for the donation of whole blood, and the disease known as the nephrotic syndrome are considered. A living person who cosents to his bodily integrity being violated for the benefit of others must be protected not only against the generation of manifest illness by such violation, but also against any prolonged deviation from the normal state of his body. It is concluded that plasmapheresis donors should not deliver more than 10 to 15 liters of plasma per year, as now recommended by European authorities. Not more than 500 ml of plasma should be withdrawn per session, and the interval between two such sessions should not be less than 2 weeks.
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PMID:Volume limitations of plasmapheresis. 32 Jul 64

Digitoxin in 97% bound to serum albumin and digoxin only to the extent of 24%. Hypoalbuminaemia significantly changes the protein binding of digoxin in Kwashorkor serum and the binding of digitoxin in patients with chronic active hepatitis and the nephrotic syndrome. Sprue patiens with normal albumin values have normal binding of digitoxin. Preliminary data in patients with thyrotoxicosis and myxoedema show digitoxin binding within the normal range. The effect of uraemia per se on digitoxin binding is controversial as both normal and slightly decreased values have been reported. In uraemic patients on treatment with haemodialysis, heparin administration has been shown to be a powerful serum binding displacing agent for both digitoxin and digoxin, the mechanism probably being a heparin-induced release of free fatty acids. Patients with a significant decrease in serum protein binding of digitoxin or digoxin should be maintained on a total serum concentration lower than usually considered within the therapeutic range.
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PMID:Protein binding of cardiac glycosides in disease states. 32 8

Plasma and urinary antithrombin III (AT-III) was measured in 15 cases of nephrotic syndrome. Plasma AT-III correlated well with serum albumin, but poorly with proteinuria, whereas urinary AT-III correlated well to proteinuria. The plasma AT-III level had a mean similar to 25 healthy controls, but the range was significantly wider. A case with nephrotic syndrome and left renal vein thrombosis is reported. The urinary output of AT-III rose and the plasma level fell with the activity of the disease. Although AT-III and albumin have similar molecule weight, their renal clearance was found to be different. It is suggested that urinary loss of AT-III plays a role in the hypercoagulable state sometimes found in the nephrotic syndrome.
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PMID:Antithrombin III and the nephrotic syndrome. 47 63

The main coagulation and fibrinolysis proteins have been studied in 22 children with nephrotic syndrome. Some anomalies such as the increase of fibrinogen and of Factors II, V, VII + X concentrations and the decrease of antithrombin III concentration could induce an hypercoagulability. Other anomalies such as the high alpha 2 macroglobulin concentration and the frequently low plasminogen concentrations could induce a decrease of the plasma fibrinolytic activity. The consequences of the low alpha 1 antitrypsin levels are probably less important. The fast alpha 2 antiplasmin levels have been found variable in the different patients. Practically, it appears that most children with plasma albumin levels less than 15-17 g/l have antithrombin III levels less than 23 mg/dl (70% of normal), which appears to result in a high risk of thrombosis (11).
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PMID:[Coagulation and fibrinolysis proteins in nephrotic syndromes in children]. 53 78

Micropuncture studies were carried out in surface nephrons of rats with nephrotoxic-serum (NTS)-induced nephrotic syndrome during a period of active sodium and water retention. It was found that hydrostatic pressure and tubular diameter were increased in the proximal tubules (13.4 +/- 0.2 vs. 10.4 +/- 0.2 mm Hg; 31.3 +/- 0.9 vs. 18.4 +/- 0.7 mu), whereas pressure and tubular diameter were normal in the distal tubules. Single nephron glomerular filtration rate (SNGFR) was decreased and fractional reabsorption of fluid was markedly increased in the proximal tubules (74.1 vs. 61.7%). The increased pressure gradient between the proximal and distal tubules suggests a condition of increased resistance to flow between the proximal and distal tubules. Microinfusion of proximal tubules with an isotonic "equilibrium" solution led to little or no rise in intratubular pressure in normal rats but it led to a significant rise in nephrotic rats. When proximal tubules of normal rats were infused with a solution containing 100 mg/100 ml albumin, pressure rose to levels observed in nephrotic rats. The mechanism of the increased resistance to flow appeared to be related, therfore, to the presence of protein in the tubular fluid. Sodium retention in the nephrotic animals might be attributed to the reduction in GFR. In other types of renal disease in animals and man with comparable or greater reductions in GFR, sodium retention does not occur, however, and fractional excretion of sodium in the urine is increased in proportion to the reduction in GFR. Thus, the rise in proximal fractional reabsorption secondary to impaired fluid flow could be an important factor in the sodium retention of this disease.
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PMID:A micropuncture study of renal sodium retention in nephrotic syndrome in rats: evidence for increased resistance to tubular fluid flow. 54

The authors have studied the effect of the infusion of sodium poor albumin on the primary nephrotic syndrome edema in children. The albumin dose used was 1 g per kilo, administered intravenously during four hours. A variable weight loss of 5.7% to 8.3% related to the initial weight was observed. The urinary volume increased considerably during the study period, as well as the urinary sodium excretion and creatinine clearance. The study of the relation of the urinary Na/K suggests that the secondary hyperaldosteronism is blocked by the albumin infusion probably due to an increase in the intravascular volume. They have concluded that the administration of sodium poor albumin whether or not associated to diuretics is effective in controlling the Primary Nephrotic Syndrome edema in children.
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PMID:[The effect of albumin and furosemide administration in children with primary nephrotic syndrome (author's transl)]. 59 31


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