Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Splenectomised calves in metabolism cages were infected with Babesia bovis. During the infection, urine samples were collected and analysed for electrolytes, proteins, kinin, and urinary kallikrein. During the later stages of the infection there were significant reductions in urinary volume, water intake, urinary kinin, kallikrein, and electrolytes. Proteinuria was detected from 3--8 days postinfection of which 15--20% was haemoglobin and most of the remainder was albumin (70--75%). Fibrin degradation products, fibrinogen-like products, and haptoglobin were not detected. Degeneration of cortical tubules was detected by histological studies. As these tubules produce urinary kallikrein it seems probable that diminished glomerular blood flow and hence glomerular filtration rate are due to decreased production of this enzyme.
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PMID:Acute Babesia bovis infections: renal involvement in the hypotensive syndrome. 49 8

In order to evaluate the effect of measles on proteins carrying vitamin A, we have examined 58 children with measles (24 have been seen again 2 weeks later) and 52 healthy controls of similar age and nutritional status. During the course of fever we have observed a high urinary excretion of urea and creatinine with proteinuria while the hydroxyproline index is significantly lower than in the controls. Irrespective of the nutritional status the plasma levels of albumin, prealbumin and R.B.P. are consistantly low. Two weeks later, while the albumin level has decreased, the other parameters are aiming towards normal values. The higher levels of prealbumin and R.B.P. suggest a reactivation of the hepatic protein synthesis. The urinary excretion of R.B.P. has not changed significantly during measles. We have observed rather high urinary losses of R.B.P. in the controls. The low levels of plasma prealbumin possibly do not allow the complete binding of the R.B.P.
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PMID:[Variations of various plasma (albumin, prealbumin, retinol binding protein), and urinary parameters during measles in Senegalese children]. 57 74

Following nephroangiography with an ionic contrast medium (metrizoate) proteinuria occurred in 25 of 28 patients, reaching its maximum with 1/2 to 24 hours. It fell to preangiographic values within 6 days. The degree of proteinuria varied but was massive, i.e. more than 10 g albumin/g creatinine, in 9 patients. The underlying mechanism is a marked, reversible increase in glomerular permeability.
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PMID:Proteinuria following nephroangiography. I. Clinical experiences. 60 12

The urinary excretion of a glomerular basement membrane-like antigen was quantitated in 19 adult normal subjects and in 15 patients with febrile proteinuria by means of rocket immunoelectrophoresis. In the normal persons the excretion averaged 59 (S.D.8.9) U/24 hours' creatinine clearance. An increased excretion was demonstrated in 80% of the patients. There was a significant relation between the urinary excretions of albumin and protein in the patients with febrile proteinuria. The basement membrane antigen was also demonstrated in normal human serum, liver and placenta. No unusual basement membrane antigen could be demonstrated in the urine from patients with febrile proteinuria.
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PMID:Urinary excretion of basement membrane antigen in normal persons and patients with febrile proteinuria--quantitated by means of rocket immunoelectrophoresis. 66 1

Antithrombin III (AT II/III) was determined immunologically and by means of a heparin cofactor assay in plasma samples and 24-hour urine of 15 patients with various degrees of proteinuria, being predominantly of glomerular origin. In urine the AT II/III concentrations were significantly correlated to the concentrations of albumin, plasminogen and IgG. One third of the patients had AT II/III plasma levels below the normal range. The plasma levels showed a significant inverse correlation to the AT II/III and albumin clearance rates. Similarily, the plasminogen concentrations in plasma were decreased in two thirds of the patients, being inversely correlated to the renal plasminogen clearance values. It is proposed that AT II/III deficiency in the nephrotic syndrome is an important pathogenetic factor in venous thrombosis.
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PMID:Acquired antithrombin III deficiency in patients with glomerular proteinuria. 68 89

Antithrombin III levels were studied in relation to the occurrence of thromboembolism in 48 patients with various degrees of proteinuria. Nine of these patients had clinical signs of thrombosis, including four with renal vein thrombosis. In eight of these nine patients, antithrombin III concentrations were below 70 per cent. There was a significant negative correlation between the antithrombin III concentration and the urinary protein excreation (P less than 0.001). Antithrombin III was found in the urine of 32 of 42 patients. There was a significant correlation between the renal clearance and the degree of antithrombin III serum deficiency (P less that 0.001). The clearance and serum level of albumin closely paralleled these changes. We conclude that thrombosis in patients with severe proteinuria is associated with a deficiency of antithrombin III due to urinary excretion of this protein.
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PMID:Acquired antithrombin III deficiency and thrombosis in the nephrotic syndrome. 70 21

To study some of the aspects of albumin homeostasis and proteinuria in PNS, the hepatic production of albumin is analyzed using semiquantitative immunofluorescent techniques, in biopsy specimens from nine subjects, free of hepatic or renal disease and nine patients with PNS, where renal biopsies were also made. Tissue sections 0.5 millimicron thick were cut. The hepatic synthesis of albumin, interpreted by the number of cells with specific fluorescence, was much higher in patients with PNS (p less than 0.001), and kept inverse relationship with serum albumin concentrations. Numberless droplets containing albumin were observed in the renal tissue indicating intense resorption and catabolism in the luminal and basal portions of the proximal convoluted tubules. Our findings indicate that, in PNS, albumin synthesis is substantially increased and hypoalbuminemia is caused by exaggerated renal excretion and catabolism.
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PMID:Hepatic synthesis and albumin distribution in the primary nephrotic syndrome (PNS). as demonstrated by immunofluoresce. 70 87

Direct measurements of the pressures and flows governing the formation of glomerular ultrafiltrate have been made possible in recent years by virtue of 1) the discovery of rats and monkeys possessing glomerular capillaries on the renal cortical surface, accessible to micropuncture, and 2) technological advances that permit measurement of intracapillary hydraulic pressure and assessment of the change in colloid osmotic pressure along the glomerular capillary network. Based on these direct measurements, evidence has been obtained to indicate that glomerular capillary hydraulic pressure and hence the net driving force for ultrafiltration are lower than previously believed. By the efferent end of the glomerular capillary network, net filtration of fluid ceases, owing to a reduction in the net driving force to zero. Evidence in the rat indicates that the process of ultrafiltration is highly dependent on glomerular plasma flow rate. Studies in rats with surface glomeruli have also made possible an assessment of the factors that govern the transport of macromolecules across the highly specialized capillary network. In addition to molecular size, transcapillary movement of macromolecules is influenced by the glomerular filtration rate, since total transport reflects the combined contributions of convection as well as diffusion. Molecular charge has also been found to be an important determinant of the transport of macromolecules, very likely contributing to the marked restriction to the transcapillary movement of albumin. This electrostatic restriction to the transport of polyanions such as albumin, by some fixed, negatively charged component(s) of the glomerular capillary wall, is markedly reduced in primary glomerular injury. Evidence indicates that glomerular injury results in loss of these fixed negative charges from the capillary walls, providing an attractive explanation for the enhanced filtration of albumin, and hence the proteinuria, observed in a variety of glomerulopathic states.
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PMID:Transport of molecules across renal glomerular capillaries. 77 68

Fifty patients with renal glomerular diseases entered a double-blind cross-over study on the effect of cyclophosphamide; 38 had received neither corticosteroids nor cytostatic drugs before joining the study. Cyclophosphamide was given for 4 months in doses decreasing from 3 to 1.5 mg/kg b.wt. Cyclophosphamide caused a 46% decrease in the 24-hour excretion of urinary protein and a decrease in serum creatinine within the normal range. Albumin, transferrin and IgA in urine, as well as albumin clearance and the sieving coefficient of albumin, changed parallel to the total urinary protein. The initial values of proteinuria and serum complement were of prognostic significance for the effect of cyclophosphamide in serum creatinine. We were unable to demonstrate a prognostic significance for the variables: clinical diagnosis, renal histology, arterial BP, initial values of serum creatinine and IgG, IgA and IgM in serum and urine. ESR appeared to be the most reliable acute phase reactant. No differences were found between the changes in renal histology during cyclophosphamide or placebo.
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PMID:Cytostatic treatment of glomerular diseases. III. A double-blind cross-over study of the effect of cyclophosphamide report from a copenhagen study group of renal diseases. 78 59

The urinary concentration of fibrin-fibrinogen degradation products (F.D.P.) was measured in 90 patients with proteinuria above 2 g/1 and correlated with proteinuria, differential protein clearances, serum urea and creatinine, and renal biopsy findings. There was a linear correlation (r equals 0-7; P less than 0-001) between the urinary F.D.P. excretion and the selectivity of the proteinuria such that patients with highly selective proteinuria excreted only small amounts of F.D.P. whereas those with non-selective proteinuria excreted much higher levels. There was a significant correlation between the urinary F.D.P. excretion and the urine:serum (U:S) ratio of IgG excretion but not with the U:S ratio or urinary excretion of albumin or transferrin. Sephadex G200 column chromatography of the concentrated urine in 26 cases showed that patients with highly selective proteinuria excreted predominantly F.D.P. of low molecular weight in the urine whereas those with non-selective proteinuria excreted mainly fibrinogen and products of high molecular weight. Hence the type and quantity of F.D.P. in the urine are determined primarily by the differential filtration of fibrinogen and the various degradation products from the plasma through the glomerular basement membrane, which in turn is determined by the "pore size" of the basement membrane. In clinical nephrology measurement of the urinary F.D.P. level provides a rapid and convenient means of estimating the differential protein clearance.
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PMID:Urinary fibrin-fibrinogen degradation products in nephrotic syndrome. 80 53


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