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PubMed1992

Involvement of activated periglomerular leukocytes in the rupture of Bowman's capsule and glomerular crescent progression in experimental glomerulonephritis.

BACKGROUND: In an experimental model of crescentic glomerulonephritis, we have investigated whether periglomerular leukocytes are involved in (a), the disruption of Bowman's capsule (BC), and (b) the progression of cellular crescents. EXPERIMENTAL DESIGN: Experimental crescentic glomerulonephritis was induced in inbred Sprague-Dawley rats using passive accelerated anti-glomerular basement membrane disease. Groups of 4 animals were sacrificed at 3, 7, 14, 21, and 28 days after administration of nephrotoxic serum. RESULTS: Periglomerular infiltration of macrophages and T cells was evident at day 3, although focal accumulation of activated mononuclear cells (IL-2R+) was not apparent in this area until day 14. BC rupture in some glomeruli was first evident at day 14, and this was seen in all 12 animals from days 14 to 28. Similarly, glomerular crescent formation was first apparent at day 14, and from days 14 to 28, 11 of 12 animals displayed crescent formation (25 to 74% crescentic glomeruli). Examination of glomeruli (> or = 200/animal) within periodic acid-Shiff stained sections found that BC disruption invariably occurred at sites of prominent focal periglomerular mononuclear cell infiltration. Monoclonal antibody labeling revealed that T cells and IL-2R+ cells were restricted to focal infiltrates at sites of BC rupture, whereas macrophages were more widely distributed throughout the periglomerular area. A key finding was that while BC disruption occurred in both the presence and the absence of crescent formation, it was always associated with prominent periglomerular leukocytic infiltration. In this model, most cellular crescents contained leukocytes (88.8 +/- 2.1%). In the presence of an intact BC, macrophages constituted the predominant leukocyte cell type within these crescents. However, when BC was ruptured, although the number of macrophages remained unchanged, a marked accumulation of both T cells and IL-2R+ cells occurred within crescents. Progressive fibrous organization of cellular crescents was observed only in those glomeruli in which BC was disrupted. CONCLUSIONS: The results suggest that: (a) activated periglomerular mononuclear cells may cause disruption of BC via a delayed-type hypersensitivity mechanism, (b) rupture of BC facilitates entry of activated periglomerular T cells and fibroblasts into Bowman's space leading to progressive fibrous organization of cellular crescents, and (c) disruption of BC may be a general mechanism of progressive glomerular damage mediated by periglomerular leukocytes irrespective of crescent formation.

Animals↗
PubMed1995

The parietal sheet of Bowman's capsule of rat renal glomerulus: a target of endothelin and PAF.

On the basis of intracellular calcium concentration ([Ca2+]i) measurements, we have previously reported that the parietal sheet of Bowman's capsule was sensitive to cholinergic agonists. The aim of the present work was to investigate whether this structure could be also a target of endothelin and platelet-activating factor (PAF), since we observed [Ca2+]i increases in response to both agonists in the glomerulus, but which were very different from that induced by carbachol. For this purpose, we measured [Ca2+]i on single microdissected parietal sheets, using a fura 2 microfluorescence technique and compared the effects of maximal concentrations of the three agonists (10(-7), 10(-8), and 10(-4) M for endothelin, PAF, and carbachol, respectively) under various experimental conditions. We observed that, like in the glomerulus, endothelin and PAF induced, in the parietal sheet, [Ca2+]i responses that differed in many respects from those found with carbachol. Thus, in the presence of 2 mM external calcium, 1) endothelin and PAF responses spontaneously declined to basal level, whereas a stationary plateau was observed after a sharp peak of [Ca2+]i with carbachol; 2) the magnitude of [Ca2+]i peak was smaller with endothelin and PAF than with carbachol; and 3) endothelin and PAF, but not carbachol, induced a homologous dose-dependent desensitization. Moreover, in the absence of external calcium, endothelin and PAF responses were smaller than carbachol response, although all three responses apparently resulted from release of calcium ions from the same internal pool. In additional experiments, we observed that, like carbachol, endothelin and PAF contracted the parietal sheet, which is only composed of myoepithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Electron microscopic studies on the myofibrils in the epithelial cells of the Bowman's capsule and of proximal tubules in rat renal cortex (first report).

Two kinds of filaments in parallel arrangement have been observed in the basal part of the cytoplasm in the epithelial cells of a Bowman's capsule and in the epithelial cells of a proximal tubule of a glycerinated rat kidney. The first was thin and linear in shape, 55-70 A in diameter and exhibited arrow-head structures upon treatment with heavy meromyosin (HMM). The other was rod shaped, with thick filaments, 110-130 A in diameter, 0.14-0.16 micrometer in length, few in number scattered among the thin filaments. From the non-glycerinated kidney, bundles of fibers were attached to some electron-dense regions inside the cell membrane. In highly magnified pictures, two kinds of filaments could be observed. One kind was thin, attached to dense regions, and the other thick, and not attached to dense regions. It is conceivable that these filaments correspond to myofibrils from their characteristic electron microscopical features. An electron microscopical analogy detected in both smooth muscle cells and renal cells leads us to speculate that these thin and thick filaments consisted of actin and myosin respectively.

Animals↗
PubMed1987

The elasmobranch renal corpuscle: fine structure of Bowman's capsule and the glomerular capillary wall.

The fine structure of the renal corpuscle of the marine elasmobranch fish, the little skate (Raja erinacea), and two species of dogfish sharks, the spiny dogfish (Squalus acanthias) and the smooth dogfish (Mustelus canis), was studied by light microscopy and by transmission (thin sections, freeze-fracture replicas) and scanning electron microscopy. Bowman's capsule was lined by ciliated cells, similar to those of the first part of the tubule, at the urinary pole and squamous cells in the zone between urinary and vascular poles. At the vascular pole the visceral epithelial cells had some closely apposed cuboidal cell bodies with a few processes inserted along the basement membrane, but foot processes were absent. These cuboidal cells were continuous with podocytes, which had primary, secondary and tertiary processes from which the pedicels arose. An inconsistently present slit membrane bridged the pedicels at varying distance from the urinary space. Small maculae and large fasciae occludentes joined the podocytes and/or their processes among which gap junctions were observed. In the skate kidney, the podocyte plasma membrane facing the basement membrane contained orthogonal arrays of particles. The epithelial basement membrane of the glomeruli in all elasmobranchs was consistently thick. The mesangial cells were numerous and partially enveloped in a basement membrane; their long processes almost completely circumscribed the capillary walls. The mesangial matrix was abundant and consisted of loosely arranged collagen fibrils, microfibrils and occasional anchoring fibrils. The endothelial cells had irregularly distributed fenestrations of various sizes and lay on their discontinuous basement membrane which was separate from that under the epithelial cells. The filtration apparatus resembles that of immature mammals and lower vertebrates.

Animals↗
PubMed1987

Relationship between the integrity of Bowman's capsule and the composition of cellular crescents in human crescentic glomerulonephritis.

Cell constituents of glomerular crescents still remain controversial. We examined cellular crescents in ten cases of crescentic glomerulonephritis (GN) using indirect immunoperoxidase technique and monoclonal antibodies against T cells (OKT3) and subsets: T helper/inducer cell (T4), T suppressor/cytotoxic cell (OKT8), T activated cell (IoT14 and IoT15); B cells (B1, B4, OKB2 and IoB3) and subsets (B2 and IoB1); monocytes/macrophages (LeuM3); DR Ag (I2) and renal native cells: podocytes (IoT5), Bowman's capsule (BC) parietal epithelial cell (OKB2, IoB3). Studied cases were 2 anti-glomerular basement membrane (GBM) GN, 4 immune complex GN, 3 vasculitis and 1 idiopathic GN. When the BC continuity was preserved almost all crescent cells were identified; they originated in majority from the BC parietal epithelium and ranged from 55 to 95 per cent. The other main constituents which represented 15 to 35 per cent of the crescent cells were monocytes (LeuM3+) and T-activated cells (IoT15+). In the interstitial infiltrate, which was mostly periglomerular, LeuM3+ cells and IoT15+ cells accounted for more than 70 per cent of the cell population. On the other hand, when BC were ruptured, mononuclear inflammatory cells, mainly LeuM3+ and IoT15+ cells accompanied by significant number of T4+ and T8+ cells, constituted the glomerular crescents. At this time, BC parietal epithelial cells were rarely identified (15 per cent). These findings strongly support the importance of BC integrity to discriminate the nature of crescent cells.

Antibodies, Monoclonal↗
PubMed2001

Podocyte bridges between the tuft and Bowman's capsule: an early event in experimental crescentic glomerulonephritis.

Although experimental crescentic glomerulonephritis starts with an endocapillary inflammation, the crescents themselves seem to originate from the proliferation of parietal epithelial cells (PEC). In this study, an attempt was made to disclose a link between the two processes by a morphologic analysis of early stages of the disease. Mice were immunized with rabbit IgG in complete Freund's adjuvant on day -6. At day 0, they received an intravenous injection of a rabbit antiglomerular basement membrane serum. On days 3, 6, and 10, the kidneys were fixed by vascular perfusion for examination by light and electron microscopy. On day 3, morphologic alterations affected mainly the endocapillary compartment; most podocytes appeared to be intact. On day 6, alterations of podocytes were widespread, including foot process effacement and prominent microvillous transformation, and some crescents were found. On day 10, crescents were found in 40% of glomeruli. The most surprising finding was podocytes that adhered to both the glomerular basement membrane and the parietal basement membrane, thus forming bridges between the tuft and Bowman's capsule. Those podocyte bridges were sparse on day 3 but were regularly encountered on days 6 and 10 in glomeruli without crescents and also as a component of crescents. They were interposed between PEC and later between the cells of a crescent without formation of junctional connection with these cells. It is proposed that the spreading of podocytes on the parietal basement membrane represents a lesion of the parietal epithelium and that this process initiates the proliferation of PEC to form a crescent.

Animals↗
PubMed1985

Cell proliferation within Bowman's capsule in mice.

Crescentic glomerulonephritis in man, irrespective of aetiology, indicates severe glomerular damage and carries a poor prognosis. The importance of the presence of macrophages in the development of glomerular crescents is well established, but the contribution of cellular proliferation in both macrophages and epithelial cells has received little attention. The purpose of this investigation was to develop a model of crescentic glomerulonephritis in mice, which will be suitable for cell kinetic studies. Preliminary studies are described, involving immunization with rabbit anti-mouse glomerular basement membrane (GBM) antiserum after pre-immunization with rabbit immunoglobulin G, both with and without treatment with a fibrinolytic inhibitor, Cyklokapron. Extensive glomerular damage, with crescent formation, was induced with four daily intravenous injections of rabbit anti-mouse GBM antiserum, after pre-immunization with rabbit IgG. The effect was shown to be dose dependent and was seen within 3 days of the last injection. Linear deposits of rabbit IgG were detected in all glomeruli by immunofluorescence and both linear and granular deposits of mouse IgG were also found. There was a significant increase in glomerular size and in the numbers of cells in Bowman's capsule (P less than 0.01), and increases in mitotic indices to 0.8 per cent were seen by day 13.

Animals↗
PubMed1977

Development of a lesion resembling diabetic nephropathy in a renal homograft.

One month following a cadaver renal transplant for obstructive uropathy, a 27-year-old man developed diabetes mellitus. Two years later, marked proteinuria and decreased renal function were detected. Eight months later, a second decline in function occurred. Light microscopy of graft biopsy specimens obtained after each decline in renal function showed increased mesangial cells and matrix, thickening of Bowman capsule, and tubular atrophy with basement membrane thickening. Vascular changes, interstitial infiltrate, and fibrosis were not prominent. Electron microscopic studies of the second biopsy specimen confirmed the light microscopic changes; subepithelial dense deposits were also detected. Immunofluorescent studies of both biopsy specimens demonstrated linear staining of glomerular and tubular basement membranes and Bowman capsule for IgG and albumin. Antikidney antibodies were not detected in the patient's serum. These observations suggest development of the diffuse form of diabetic nephropathy in a renal homograft following steroid-induced diabetes mellitus.

Adult↗
PubMed2004

An immunophenotypic comparison of metanephric metaplasia of Bowman capsular epithelium with metanephric adenoma, Wilms tumor, and renal development: a case report and review of the literature.

Metanephric metaplasia of the parietal epithelium of the Bowman capsule is a rare pathologic finding of unknown pathogenesis that has occurred in patients with widespread malignant neoplasms of various types. We report this finding in a 25-year-old woman with partial expression of the Carney triad who died of a disseminated gastrointestinal stromal tumor, specifically a gastric stromal sarcoma. The metaplasia involved both kidneys diffusely. It originated in the parietal epithelium of the Bowman capsule, extended into the proximal tubules, and focally surrounded the glomeruli in a semicircular manner Immunohistochemical analysis revealed that the cells of metanephric metaplasia expressed the Wilms tumor gene product, bcl-2 protein, and CD57 and cytokeratin 7 and keratin AE1/AE3 focally, but not CD56. This immunophenotype parallels that of metanephric adenoma, Wilms tumor, and nephrogenic rests and overlaps with antigen expression in certain periods of renal development.

Adenoma↗