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  • 1
    ISSN: 1432-2307
    Keywords: Amyloidosis ; Urinary sediment ; Light-microscopy ; Immunofluorescence ; Electron-microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Urinary sediment of 11 patients with amyloidosis and 12 without (with proteinuria or in good health) have been studied by different morphological techniques. By light microscopy, an amyloid-related substance was occasionally demonstrated both in patients with amyloidosis and in control subjects. Immunofluorescence (IF) showed substance A (amyloid component) to be present in some cases of amyloidosis and in controls. On electron-microscopy, fibrils with characteristic appearance of amyloid substance were found in some cases of amyloidosis (4 out of 11), but were also found in controls. It therefore seems difficult to establish the diagnosis of amyloidosis by microscopic studies of the urinary sediment.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Furosemide was administered for seven days to normal rats. Urinary kallikrein excretion showed a biphasic response during the seven consecutive days of study. During the initial three days only the kininogenase activity showed a significant increase without any variation in the excretion of the immunoreactive kallikrein. The specific urinary kininogenase activity was therefore enhanced. After three days of furosemide administration, both the urinary kininogenase activity and urinary immunoreactive kallikrein were augmented. The urinary specific kininogenase activity was that time no more different when compared to the basal value. Considering the delay time of three days, this second part of the response could be a mineralocorticoid mediated effect. In this respect, kidney level of immunoreactive and kininogenase activity of kallikrein are also increased after seven days of furosemide administration. However the short lasting increase in urinary specific kininogenase activity observed during the initial three days is due to a change in the ratio active versus inactive kallikrein without any variation of total kallikrein. It is possible that this immediate response results of a direct effect of furosemide acting either on the preferential excretion of the active form or on the activation of the prokallikrein in the urine.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 74 (1982), S. 347-354 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The localization of amyloid P-component (AP) staining was studied by immunofluorescence in renal biopsies from 106 patients with various nephropathies and from 3 patients with normal kidneys. Linear staining was observed along the glomerular basement membranes (GBM) of normal kidneys. In amyloidosis, AP was always present in the glomeruli. In arteriolar walls, AP was present in numerous cases with varied intensity. No fixation was observed along tubular basement membranes. The possible modification of the permeability of GBM, related to a possible modification of the electrical charge of the filtration barrier, can be supposed.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The localization of β2-microglobulin (β2m) was studied in renal biopsies from 18 patients with pathological transplanted kidney using immunofluorescence and electron-immunohistochemical techniques; the renal biopsies of 4 cases with normal kidneys were used as controls. Using immunofluorescence, β2m was not observed in the normal kidneys, β2m was found in the glomeruli (7 cases) and the tubular epithelium (16 cases) of the transplanted kidneys. Using immunoelectron microscopy, some labelling of the normal kidneys was observed mainly along the cell coat of foot processes and in tubular-epithelial lysosomes. In the glomeruli of transplanted kidneys, particularly in cases of acute or chronic rejection, β2m was most frequently localized on the outer layer of the basement membrane and along the cell coat of foot processes. The brush border of the proximal tubules and the lysosomal structures were intensely labelled. Although immunoelectron-microscopy studies are unable to discriminate between the localization of β2m in normal and transplanted kidneys, these findings nevertheless suggest the glomerular filtration of β2m and its metabolism in the tubular epithelium.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Histochemistry and cell biology 97 (1992), S. 293-301 
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary During the course of chromate-induced acute renal failure (ARF), urinary kallikrein excretion (UKE), a serine protease of distal tubule origin in the normal animal was decreased but tissue kallikrein concentration (TK) was increased, suggesting intracellular accumulation. Severe morphological lesions were observed in proximal tubular cells which showed brush border damage, numerous vesicles, necrosis and liquefaction of cytoplasmic material. Less marked changes were also present in distal tubules: large apical vacuoles and swollen mitochondria. Compared to normal rats, using the peroxidase-anti-peroxidase (PAP) method for light microscopy, greater kallikrein immunoreactivity was detected along the apical pole in distal tubules, on the membrane and in the cytoplasm as well as in the glomerulus. By immunoelectron microscopy, kallikrein was found in the connecting apical area, along the luminal, basolateral and basement membranes, in some vesicles, in Golgi apparatus and on ribosomes bound to endoplasmic reticulum. In the glomerulus, kallikrein was observed along the luminal surface of endothelial cell. After 14 days a progressive recovery of renal function, tissue morphology and UKE towards control values was observed. The presence of immunoreactive kallikrein in the glomerulus observed only during ARF confirmed the previous demonstration of kallikrein mRNA in the glomerulus. The cellular accumulation results more likely from a dysfunction of a general secretory mechanism due to cell membrane alteration than from a specific inhibition of kallikrein production and secretion.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular histology 25 (1993), S. 772-777 
    ISSN: 1573-6865
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Treatment of rats with cisplatin (4 mg kg-1body wt i.p. injection) induced variations of urinary kallikrein excretion (UKE). Three phases were observed: a transient increase of UKE one day after injection, followed by a decrease up to 10 days suggesting an altered biosynthesis and a recovery phase with return to normal control values, 21 days after injection. Early morphological lesions were observed in proximal tubule cells on day 1; severe changes and tubular necrosis were observed in the following days. Less marked changes were also present in distal tubules but the vacuolated and desquamated cells appeared in the lumen of the tubules. By immunocytochemical methods, kallikrein was observed in connecting tubule cells, but also in some proximal tubule cells and along the endothelial side of the glomerular basement membrane and urinary space of glomeruli. An intense labelling was present in desquamated epithelial cells in dilated lumen of tubules. This study provides evidence of the presence of immunoreactive kallikrein in the glomerulus, already reported during acute failure, and confirms the use of urinary kallikrein measurements as a useful non-invasive index to assess a possible nephrotoxic effect at the distal level.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular histology 25 (1993), S. 664-669 
    ISSN: 1573-6865
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The renal origin of kallikrein is now clearly established. However, the presence of kallikrein in urine raises questions about a possible physiological role of this enzyme at the urinary level. We have already demonstrated the presence of kallikrein-like substance in rat ureter. For establishing the continuity of the presence of kallikrein-like substance along the urinary tract we have studied the localization of immunoreactive kallikrein-like substance in urinary bladder of the normal rat by immunohistochemical methods for light- and electron-microscopy, using an antibody against rat urinary kallikrein. By light microscopy, kallikrein-like substance was found to be associated with the lamina propria, which is the connective tissue component which constitutes one layer of the bladder wall. Weak staining was present in the smooth-muscle layer. By immuno-electron microscopy, kallikrein-like substance was localized in fibroblasts which were present in the connective tissue and which penetrated into the layer of smooth muscle; immunoreactivity was observed in endoplasmic reticulum, Golgi apparatus and free polyribosomes. Immunolabelling was demonstrated in no other part of the wall bladder and in no other cellular component. The continuity of the presence of kallikrein-like substance from the kidney to the urinary bladder gives new indications concerning the significance of this system in renal physiology.
    Type of Medium: Electronic Resource
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