UMLS:C0033687 - FACTA Search

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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The parietal epithelium of Bowman's capsule has been analyzed by enzyme cytochemistry in kidneys of mice (C57BL/6J) from birth to 50 days of age. There is a greater tendency for cells in the central portions of the capsular crescent to be cuboidal in post-pubertal males than in pre-pubertal mice of either sex or in post-pubertal females where they are generally squamous; moreover, these heightened capsular cells have a distinct microvillous border. Cytochemical procedures were selected which might confirm the morphological suggestion that the cuboidal parietal epithelium possesses an absorptive capacity. The oxidoreductase activity of the mitochondria of the cuboidal cells of this layer is comparable to that of the columnar cells of the proximal convoluted tubule. The cytochrome oxidase activity of the mitochondria in both of these segments of the nephron is intense. This is in sharp contrast to the unreactive mitochondria in the squamous cells of the parietal epithelium. Furthermore, a striking heterogeneity in the degree of cytochrome oxidase activity is evident in the mitochondria of the cuboidal parietal cells as well as in the cells of the proximal tubules. In the former cells, active mitochondria were generally found near microvilli at the apical ends and in the areas of the basal infoldings whereas those in a central position were more frequently unreactive. The brush border of the cuboidal capsular epithelium had prominent alkaline phosphatase and aminopeptidase activities as has previously been observed in other brush borders. Functional capacity corresponding to the morphological and cytochemical specialization of the cuboidal capsular cells was demonstrated by their uptake of horseradish peroxidase. This exogenous protein tracer could be seen in apical vacuoles and phagosomes in the cuboidal parietal epithelium. The cytochemical resemblance of the cells of this epithelium to those of the proximal convoluted tubules suggests a similar involvement in resorption and perhaps in active transport. A possible relationship of this differentiation of the capsular epithelium to the proteinuria normal for adult male mice is discussed.
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PMID:Cytochemical correlates of structural sexual dimorphism in glandular tissues of the mouse. I. Studies of the renal glomerular capsule. 17 Dec 42

A human proximal renal tubular epithelial antigen (designated HRTE-1) was isolated and purified from a crude tubular preparation (Fx1A) by a process of salt fractionation, DEAE anion-exchange chromatography, and Sephadex G-200 gel filtration. Utilizing 125I-HRTE-1 and a rabbit antiserum specific for the proximal tubular brush border, as determined by immunofluorescent microscopy, a radioimmunoassay by competitive protein-binding was developed. HRTE-1 was demonstrated in serum and urine and in extracts of a variety of body organs. A range of concentrations for normal random urine samples and 24-hr urine excretion rates were determined. Random urine samples from 36 patients with a variety of functional and pathologic renal disorders were assayed for the HRTE-1 antigen. Twenty-three of 24 patients with either chronic nephropathy or pre-renal azotemia had normal urinary antigen concentrations, despite wide differences in urine flow rates, the degree of existing renal function, and the amount of proteinuria. Ten of 12 patients with acute tubular necrosis, however, had statistically abnormal HRTE-1 concentrations (high in eight patients, undetectable in two). These findings suggest that HRTE-1 antigen can be detected in both normal and pathologic urines, that altered antigen concentrations can be documented in at least one renal disorder, and that quantitation of HRTE-1 in urine may have clinical value as a marker of acute rubular injury.
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PMID:Radioimmunoassay for urinary renal tubular antigen: a potential marker of tubular injury. 36 38

The role of circulating immune complex deposition versus in situ complex formation in membranous nephropathy is controversial. Passive Heymann nephritis in rats resembles membranous nephropathy in man and was induced by injection of sheep antibody to rat proximal tubular epithelial cell brush border antigen (anti-Fx1A). Minutes after injection of 1 ml. of anti-Fx1A, subepithelial immune deposits were seen by immunofluorescence and electron microscopy, and proteinuria appeared within 5 days. The effects of alterations in the dose of administered antibody, corticosteroid therapy, and vasoactive amine blockade on the development of subepithelial deposits and consequent proteinura were studied. Variation of the dose of anti-Fx1A from 0.25 ml. to 1 ml. resulted in a progressive increase in the size and number of glomerular capillary wall deposits, but no alterations in their distribution. Only those rats which received 1 ml. became proteinuric within 5 days. Corticosteroid therapy and vasoactive amine blockade, begun 24 hours prior to the induction of passive Heymann nephritis and continued until termination of the study 5 days later, had no effect on the amount or site of immune complex formation, nor on the extent of proteinuria as compared to untreated controls. In contrast, in rats with unilateral proteinuria produced by the selective perfusion of one kidney with aminonucleoside of puromycin 7 days prior to the induction of passive Heymann nephritis, there was a marked reduction of subepithelial deposits in the perfused kidney as compared to the nonperfused contralateral kidney. In this model of membranous nephropathy, systemic factors play little role in the development of subepithelial deposits, whereas local factors are critical. These findings are consistent with the hypothesis that subepithelial immune deposits form locally.
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PMID:Determinants of glomerular localization of subepithelial immune deposits: effects of altered antigen to antibody ratio, steroids, vasoactive amine antagonists, and aminonucleoside of puromycin on passive Heymann nephritis in rats. 37 41

Scanning electron microscopy (SEMy), supplemented with light microscopy and transmission electron microscopy, was used to study aminonucleoside nephrosis in rats. The visceral epithelium undergoes dramatic restructing in response to aminonucleoside nephrosis. Due in part to an accumulation of intracellular vacuoles, kidney podocytes swell in size. Podocyte major processes lose their many pedicles and slit pores and form close junctions (80 A) with adjacent podocytes. Although no prominant pores opening into the urinary space are found in the visceral epithelium, there is evidence that podocyte vacuoles may rupture and thereby release protein into the urinary space. Many parietal cells also increase in size, accumulate intracellular vacuoles and come into very cose proximity to the visceral epithelium. Casts of PAS-positive, electron-dense material fill the lumina of many uriniferous tubules. Although most proximal tubules exhibit an extensive loss of brush border, no significant changes in other kidney microprojections or cilia were noted. Transmission electron and light microscopy of nephrotic kidneys reveal considerable changes in proximal and distal tubules including a reduction in mitochondria, in cell height, in electron density of the cytoplasmic matrix, in lateral and basal plasmalemma infolds, enlarged euchromatic nuclei, dilated lumens, and accumulation of PAS-positive cytoplasmic granules. SEMy of kidney needle biopsies from patients with proteinuria reveal that SEMy is useful for evaluating glomerular changes in man.
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PMID:Scanning electron microscopy of the nephrotic kidney. 80 6

Ultrastructural changes in the visceral epithelium and proximal tubules of rats were studied by scanning and transmission electron microscopy during the onset and progression of puromycin aminonucleoside nephrosis (PAN)-induced proteinuria. These changes were compared with those that occur during a similar degree of proteinuria induced by intraperitoneal injections of albumin. With the onset of proteinuria and oliguria, PAN rats exhibit loss of podocyte pedicels and podocyte major processes, an increase in pinocytotic activity, and an accumulation of cytoplasmic vacuoles and granules of variable size, shape, and electron density. Loss of podocyte pedicels involves a gradual decrease in pedicel height beginning at the pedicel tip and progressing down the pedicel arm, formation of nublike protrusions and interpedicel microbridges (35 to 45 nm. in width and 40 to 60 nm. in length) along the pedicel's base, the merging of microbridges to form more extensive regions of interpedicel contact, and a gradual broadening and retraction of pedicels. In response to hyperalbuminemia-induced proteinuria, kidney podocytes exhibit reactions during PAN, however, the podocyte pedicels, slit pores, and major processes of rats with hyperalbuminemia-induced proteinuria remain discrete. The loss of pedicels and major processes during PAN, therefore, apparently results from the effects of puromycin aminonucleoside per se rather than from the proteinuria associated with this disease. The proximal tubules of rats with hyperalbuminemia-induced proteinurea exhibit the same characteristic changes as PAN rat proximal tubules (i.e., loss of brush border, dilated lumina, abnormally thin walls, and accumulation of periodic acid-Schiff positive electron-dense luminal casts and cytoplasmic protein absorption droplets). The significance of these ultrastructural findings during PAN and hyperalbuminemia-induced proteinurea are discussed in terms of the etiology of PAN.
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PMID:A scanning and transmission electron microscopic comparison of puromycin aminonucleoside-induced nephrosis to hyperalbuminemia-induced proteinuria with emphasis on kidney podocyte pedicel loss. 83 33

This study was designed to evaluate the occurrence and the type of proteinuria in 82 children with vesico-ureteric reflux (VUR) with or without renal scars. The urinary excretion of the high molecular weight protein albumin was taken as an index of glomerular alterations and the excretion of retinol-binding protein (RBP), beta 2-microglobulin and brush border antigens (BBA) (measured by monoclonal antibody-based enzyme-linked immunosorbent assay) was taken as an index of tubular alterations. All such markers were increased in children with VUR and were related to the degree of renal function. Patients showing reduced creatinine clearance had very high levels of albuminuria, microproteinuria and BBA, with all these variables reciprocally correlated. In children with normal renal function however, only microproteins (not albumin or BBA) were slightly increased, thus indicating an isolated tubular defect without involvement of the proximal segment of the tubule. However, microprotein excretion did not correlate with the grade of scarring (99mtechnetium-dimercaptosuccinic acid scan), both RBP and beta 2-microglobulin excretion being normal in 75% of children with radioisotopic signs of renal lesions but increased in 17% of children without scars. Therefore, tubular proteinuria identifies different groups of children with VUR but is not related to renal scarring. Prospective studies will define the usefulness of proteinuria as a reliable indicator of renal outcome.
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PMID:Urinary excretion of brush border antigens and other proteins in children with vesico-ureteric reflux. 131 Nov 86

FK506 is a recently-developed immunosuppressive drug. The aim of the present work was to investigate the effects of FK506 in experimental autoimmune glomerulonephritis (active Heymann nephritis) in rats. Active Heymann nephritis was induced in female Lewis rats by two immunizations with the homologous brush border vesicles (BBVs) at day 0 and day 28 (groups I, II, V, and VI). Rats of groups III and IV received the third immunization at day 56. In rats of groups I and III, FK506 was injected (1 mg/kg/day IM) from day 0 for 14 days. In rats of groups II and IV, significant proteinuria was observed (group II, 112.8 mg/16 hours; group IV, 55.4 mg/16 hours) at the time the rats were killed (day 84). Coarse subepithelial immune deposits (IDs) were found in these rats. In contrast, urinary protein excretion remained within normal range (less than 3.0 mg/16 hours) in groups I and III rats, and tiny subepithelial IDs were only occasionally seen. Circulating anti-BBV antibody levels were markedly lower in group I and III rats than in those of groups II and IV during the period between day 14 and day 56. To investigate the effects of FK506 on the proteinuric rats, FK506 (1 mg/kg/day, IM) was administered every day for 2 weeks beginning on day 56 (group V).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of a new immunosuppressive agent, FK506, in rats with active Heymann nephritis. 137 Dec 98

The present study describes the development of membranous glomerulopathy (MGP) with high proteinuria in DZB rats exposed to mercuric chloride (HgCl2). IgG1 and IgG2a antibodies, eluted from glomeruli with subepithelial immune deposits, bind to the interface of the GBM and epithelial cells. High reactivity to GBM was demonstrated by ELISA and Western blotting, which could be absorbed for 30% by laminin or laminin-associated extracellular matrix components. No reactivity was found with type IV collagen, fibronectin, heparan sulfate proteoglycans, or tubular brush border antigens. Absorption to GBM removed the reactivity to renal antigens. Passively transferred eluted antibodies bind in a predominantly linear pattern along the GBM, causing focal ultrastructural transformations of the podocytes. These results suggest that this type of HgCl2-induced MGP, associated with epithelial cell injury and proteinuria, is caused by autoantibodies to basement membrane components which are located at the epithelial cell-basement membrane interface and may be involved in cell-matrix binding.
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PMID:Antigenic specificities of glomerular-bound autoantibodies in membranous glomerulopathy induced by mercuric chloride. 159 88

To investigate the antigenicity of glomerular cell products for the induction of Heymann nephritis (HN), eight Lewis rats were immunized with an isolated glomerular protein (GLP) with only limited tubular cell contamination. Four out of four rats immunized with 240 micrograms GLP showed proteinuria at week 12. Their kidney specimens taken at week 16 showed contiguous granular deposits of IgG along the glomerular basement membrane by direct immunofluorescence and corresponding electron-dense deposits; the findings were identical to those in classical HN induced by the brush border protein. By immunoprecipitation, IgG eluted from isolated glomeruli of rats that received 240 micrograms GLP precipitated only a 700 kd glycoprotein (gp 700) in GLP, whereas 330, 440, and 700 kd glycoproteins were precipitated in the crude preparation (Fx1A), which is derived mainly from renal tubules. Two different monoclonal antibodies (anti-gp 330 and 14C1) against gp 330 precipitated the antigens in the same fashion as the glomerular eluate. These data reveal that gp 700, gp 440, and gp 330 share epitopes and that the gp 700 is demonstrable both in the glomerulus and in tubular brush border but that gp 440 and gp 330 are present only in the brush border. In addition, glomerular gp 700 was shown to induce Heymann-type glomerulonephritis just as gp 330 did.
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PMID:Experimental membranous glomerulonephritis in rats induced with gp 700, a glomerular protein. 170 2

Passive Heymann nephritis (PHN), an experimental model of membranous nephropathy, is produced by Fx1A antiserum, which also reacts with antigens on the brush border (gp 330) and basolateral membrane (gp 90) of proximal tubules. We examined tubulointerstitial disease in PHN, identifying two distinct processes occurring on the luminal and basolateral membranes, respectively. Injected antibody bound diffusely to the tubular brush border from Day 1 to Day 7, followed by sloughing of microvilli and tubular-cell regeneration. Fine granular deposits of Fx1A antibody were present along the basolateral cell membrane by Day 1. These deposits rearranged in situ, enlarged, and became more focally distributed along tubular basement membranes (TBM). Interstitial inflammation, dominated by macrophages (Ia+, ED-1+) in association with a smaller number of T-cytotoxic cells (OX19+, OX8+) began by Day 3, reached peak intensity and persisted throughout the autologous phase (to Day 21). The distribution of focal clusters of interstitial macrophages predominately in association with TBM-immune deposits was demonstrated. Complement depletion prevented proteinuria but TBM deposits developed and the interstitial inflammation was unchanged. All aspects of the tubulointerstitial disease were amplified by a second injection of Fx1A antiserum. In vitro, Fx1A antibody bound to the surface of isolated proximal tubular epithelial cells and redistributed to form clusters of immune aggregates. Anti-Fx1A-induced cytotoxicity of tubular cells was demonstrated by prelabeling cells with 2'-7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. The degree of cytotoxicity was dependent on complement concentration and the duration of incubation at 37 degrees C. PHN induced by Fx1A antiserum causes tubular-cell injury following interactions with brush-border antigens and TBM immune-complex disease associated with interstitial inflammation. These findings may be relevant to the acute and chronic interstitial disease of human membranous nephropathy.
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PMID:The contribution of antibody-mediated cytotoxicity and immune-complex formation to tubulointerstitial disease in passive Heymann nephritis. 172 79

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