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Biomedical subjects

J Churg

Publications and source records attributed to J Churg.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effect of IgA deposits on the glomerular mesangium in Berger's disease.

In mesangial IgA glomerulonephritis (Berger's disease), the immunoproteins appeared to gain access from the capillary lumen to the mesangium via endothelial fenestrae or via channels between the endothelial cells. The deposits are transported into the deeper mesangium by a process of inhibition or diffusion, with the matrix acting as the head. There are no true channels or grooves in the mesangial matrix for the transport of the immunoproteins. The contractility of the glomerular myoid fibrils may account for the movement of deposits to the hilus for possible removal. There was partial dissolution of the deposits in the mesangial matrix accompanied by loosening of the matrix. No evidence was found for any significant intracellular phagocytosis and digestion. The mesangial deposits directly or indirectly stimulated the cellular hypertrophy and hyperplasia and increased deposition of mesangial matrix. This was accompanied by formation of collagen fibrils within the thickened matrix and led to atrophy of the mesangial cells and sclerosis of the glomeruli.

Adolescent↗
PubMed1983

Fibrillary renal deposits and nephritis.

Fibrillary renal deposits and nephritis. The authors have studied 8 patients whose glomeruli contain abundant fibrils in their mesangial matrix and basement membranes. Although the location of these fibrils is very similar to that of amyloid, they are about twice the size of amyloid fibrils, averaging 20 nm in width, and fail to react as amyloid does with special stains. Immunofluorescence-microscopic studies are usually positive with antiserums to IgG, often IgM, and in some cases IgA, and also kappa and lambda light chains, C3, and C4. The fibrils are associated with diffuse mesangial widening and increased mesangial matrix strands. Although peripheral glomerular capillary walls appear to be spared initially, their eventual involvement leads to glomerular capillary collapse and glomerular obsolescence. Crescent formation occurred in 5 cases, focally in 3 and diffusely in 2. Tubular basement membrane involvement was seen in 1 case. These patients exhibit hematuria, and proteinuria, and often hypertension and renal insufficiency. Proteinuria was in the nephrotic range in 3 patients in whom involvement of glomerular capillary basement membranes was extensive. Unless electron microscopy is applied to renal biopsies, these cases may be considered to represent mesangiocapillary or rapidly progressive glomerulonephritis, or amyloidosis. The nature of these fibrils is as yet not determined. It is likely that they have been called "atypical amyloidosis" in the past.

Adult↗
PubMed1982

Histochemical study of Hurler's disease by the use of peroxidase-labelled lectins.

Peroxidase-labelled lectins specific for various carbohydrate residues were used as histochemical reagents in the investigation of Hurler's syndrome. Peanut lectin was used to detect terminal D-galactose, wheatgerm lectin for N-acetyl-D-glucosamine, soybean lectin for N-acetyl-D-galactosamine, Tetragonolobus lotus lectin for alpha-L-fucose and Bandeiraea S. lectin for alpha-D-galactose. It was found that Kupffer cells in the liver and splenic reticulo-endothelial cells contain acid mucopolysaccharides which bind lectins in paraffin sections after appropriate fixation. The pattern of lectin binding suggests that such cells contain significant amounts of D-galactose, L-fucose, N-acetyl-D-galactosamine and N-acetyl-D-glucosamine. It is likely that the last named carbohydrate is present as a polymer. Neurones contain a different carbohydrate, rich in galactose and fucose but poor in N-acetyl-D-glucosamine. This compound is resident to lipid extraction. Hepatocytes, as a rule, do not react with lectins, most likely because of loss of the more soluble mucopolysaccharides during fixation. The results are consistent with the biochemical data of Hurler's syndrome and indicate that lectins can be a useful tool for the investigation of the cytochemistry of storage disorders.

Child↗
PubMed1982

Cell coat of podocytes in patients with nephrotic syndrome.

Renal biopsies from 23 patients with the nephrotic syndrome and five patients with slight or no proteinuria were examined for the presence of cell coat of podocytes by light and electron microscopy. Of those with nephrotic syndrome, five had minimal change disease, nine focal glomerular sclerosis, six membraneous nephropathy and three amyloidosis. Colloidal iron and phosphotungstic acid stains were used for the demonstration of anionic and neutral polysaccharide components of the cell coat. On light microscopy, the colloidal iron reaction showed a reduction in intensity of the stain in glomeruli of patients with massive proteinuria, as compared to those with slight or no proteinuria. On electron microscopy, only the cell coat lining the surface of the foot processes disappeared parallel to the loss of these structures, while the coat covering the surface facing the urinary space remained unchanged with both stains.

Cell Membrane↗
PubMed1982

Lectin-peroxidase conjugate reactivity in normal human kidney.

The carbohydrate histochemistry of normal human kidney has been investigated by the use of four peroxidase-labeled lectins at the light and electron microscopic level. The results show that the lectin of Lotus tetragonolobus, specific for l-fucose, binds exclusively to the proximal convoluted tubules of the nephron. While peanut and soybean lectins, specific for D-galactose and N-acetyl-D-galactosamine, respectively, are confirmed to the collecting ducts, wheat germ lectin, specific for sialic acid and N-acetyl-D-glucosamine, stains several parenchymal structures, including the glomerular capillary wall, particularly its podocyte cell coat. Sialidase digestion reveals strong binding sites for peanut and soybean lectin in the glomeruli. At the ultrastructural level most of the binding is shown to be on the podocyte surface and within the lamina rara externa of the basement membrane. The technique represents a potentially very useful tool for the study of various pathological states in the kidney.

Acetylgalactosamine↗
PubMed1982

Patterns of renal injury in systemic lupus erythematosus: light and immunofluorescence microscopic observations.

Light and immunofluorescent microscopic patterns of lupus nephritis in 203 biopsies, 1 nephrectomy, and 20 autopsies from 179 patients were analyzed. The latest World Health Organization (WHO) classification was used. Seventy patients had diffuse lupus nephritis, 43 mesangial, 19 membranous, 19 focal, and 16 minimal change; 2 patients had advanced sclerosing nephritis. Nine patients were difficult to classify by light microscopy, but 3 of these could be classified with the help of immunofluorescence microscopy. Strict definition, especially of category III (focal and segmental lupus nephritis) is important, since this lesion has a tendency to heal, and patients with few immune deposits outside the segmental lesions have a rather good prognosis. Category V (membranous lupus nephritis) should probably be limited to membranous lesions with pure subepithelial deposits or with subepithelial and mesangial deposits, while membranous changes associated with diffuse or focal proliferative lesions are better classified as Category IV (diffuse lupus nephritis). It was observed that steroid treatment reduces the amount of deposits, especially those in the subendothelial and mesangial locations. The amount of proliferation is also reduced, but in a considerable proportion of cases, it is replaced by sclerosis. Therefore, interpretation of biopsy patterns must take prior therapy into consideration. Immunofluorescence findings in the glomeruli correlated quite well with light microscopic patterns. Active interstitial inflammation, which is most common in diffuse lupus nephritis, was only observed in the presence of tubulointerstitial immune deposits. Acute arteritis was much more common in autopsy than in biopsy specimens pointing to its ominous nature. It was concluded that combined examination of biopsies by light and immunofluorescence microscopy as well as electron microscopy, and strict categorization of lesions are valuable diagnostic and prognostic aids. Their usefulness is considerably enhanced if certain clinical data, such as prior therapy are taken into consideration.

Antigen-Antibody Complex↗
PubMed1982

Focal segmental lupus nephritis.

Nineteen renal biopsies and one autopsy from fifteen patients with focal segmental lupus nephritis were examined by light and electron microscopy, and seven biopsies also by immunofluorescence microscopy. Histopathologic data were correlated with clinical course. Patients were selected on the basis of strict histologic criteria, and had to have a minimum of 2 years clinical follow-up after biopsy. All patients were treated with steroids. It could be demonstrated by light and electron microscopy that segmental lesions go through several stages of evolution, starting with mesangial proliferation, followed by necrosis and terminating as a nodule composed mainly of collagen. The necrotic lobule sometimes contains electron dense deposits, but no wire loop lesions. Prognosis was generally good with an average of 6.3 year survival of 86%. Factors contributing to outcome include number of involved glomeruli, amount of mesangial deposits outside the segmental lesions, and the presence of vasculitis. The pathogenesis of segmental lesions probably differs from that of diffuse lupus nephritis, constituting a localized reaction, independent of immune deposits in the remainder of the glomerulus, and with a considerable tendency to heal, particularly when treated with steroids.

Adolescent↗
PubMed1981

Morphologic and clinical correlates in renal amyloidosis.

Morphologic studies and clinical correlations were undertaken in 59 patients with renal amyloidosis. Spicularly arranged amyloid deposits in the glomerular capillary wall were found in all clinical groups but were more frequent and more extensive in primary amyloidosis and multiple myeloma. The severity of proteinuria correlated with the presence of spicules and podocyte destruction rather than with the amount of amyloid in the glomerulus. The spicules were associated with morphologic and clinical evidence of rapid amyloid deposition and a fulminant clinical course. The absence of spicules and the presence of extensive new basement membrane material may produce basement membrane thickening, lamination, and double capillary wall contours, which are associated with mild proteinuria and, rarely, resolution of amyloidosis. Nodular or mixed nodular-diffuse patterns of glomerular amyloid deposits were more frequent in patients with secondary amyloidosis and a longer clinical course. Renal failure generally corresponded to severe glomerular amyloidosis and tubular atrophy. However, a relatively precipitous, usually irreversible decrease in renal function frequently occurred in patients with renal amyloidosis and did not always have a morphologic explanation. The duration of life from the time of biopsy no death in patients with primary amyloidosis (nine months) was markedly shorter than in those with secondary amyloidosis (more than 50 months).

Amyloid↗
PubMed1981

Light- and electron-microscopic histochemistry of Fabry's disease.

A histochemical study was performed on light- and electron-microscopic level in a case of Fabry's disease. The patient underwent kidney transplantation for renal failure and died of heart failure 6 months later. Patient's tissues were studied at the light- and electron-microscopic levels with various embedding and staining techniques for lipids and carbohydrates. Two peroxidase-labeled lectins (from Ricinus communis and from Bandeiraea simplicifolia) known to have affinity for alpha- and beta-D-galactose, were strongly reactive with the storage material on frozen sections. The ultrahistochemical and extraction tests showed that the typical granules had a variable reactivity and morphologic characteristics in different cells, probably reflecting different composition. A small number of typical deposits were also observed in the transplanted kidney. This is the first reported case of recurrence of the storage disease in the allograft. Of interest was also the fact that the patient's blood inhibited normal alpha-galactosidase activity, suggesting a possible inhibitor-related mechanism in the pathogenesis of the recurrence.

Adult↗
PubMed1980

Ultrastructure of transplant glomerulopathy.

Thirty-one specimens of tissue were obtained from 15 renal allografts 3-96 months after transplantation and studied by light, electron and in some cases also by immunofluorescence microscopy. All patients had a degree of renal insufficiency and almost all had proteinuria and moderate hypertension; nephrotic syndrome was present in one and hematuria in two. On histological examination one patient showed cellular proliferation suggestive of glomerulonephritis (recurrent or de novo) and another patient had numerous crescents. The most frequent glomerular lesion was widening of the lamina rara interna with subendothelial accumulation of finely granular material, formation of new subendothelial basement membrane and deposition of microfibrils and fine filaments. The mesangial changes were mainly those of mesangiolysis and mesangial sclerosis with deposition of mesangial matrix and microfibrils, but little cellular proliferation. Fragmented red blood cells were seen in nearly half of the patients. In another seven patients the lesion resembled focal segmental glomerulosclerosis. This combination of changes termed transplant glomerulopathy leads to diffuse glomerular sclerosis. Arterial intimal thickening and occasionally also thrombosis produced ischaemic changes in the kidney and in the glomeruli and contributed significantly to the process of transplant rejection.

Arteries↗
PubMed1980

Mesothelioma in man and experimental animals.

Asbestos has been established as the cause of most cases of diffuse malignant mesothelioma occurring in the industrialized world. The morphology of mesothelioma may be complex, and the employment of chemical, histochemical and ultrastructural studies are often helpful in identification. Diagnostic difficulties may to some degree blur the extent of its prevalence and reliance on exposure history may not reveal its association with asbestos. Reference panels can be useful in assessing the former and analysis of lung tissue asbestos content may help to clarify the latter, especially in the low dose range. Electron microscopy may prove to be of assistance in this respect, possibly with particular attention to the peripheral areas of the lung. Animal experimentation has supported epidemiologic conclusions and revealed the phenomenon of fiber carcinogenesis. The morphology of mesothelioma in experimental animals is very similar to that in humans, including ultrastructural and biochemical features.

Animals↗
PubMed1980

The ultrastructure of mucoid "onionskin" intimal lesions in malignant nephrosclerosis.

The ultrastructure of mucoid "onionskin" intimal thickening in the intrarenal arteries was studied in 12 cases of malignant hypertension. The thickened areas were found to contain proliferating myointimal cells, basement membrane lamellas, and ruthenium-red--positive proteoglycans. The proteoglycans consisted of granules 15--35 nm in diameter and thin filaments about 3 nm thick. The filaments connected the granules to each other and to the basement membranes of the concentric lamellas, to the basement membranes of the endothelial and myointimal cells, and also to the cell surfaces. This arrangement imparted a loose meshwork pattern to the mucoid layer. The granulofilamentous material is considered to be a structural component of the pathologic lesion distinct from plasma insudation. The relationship between the intercellular substances and the myointimal cells is briefly discussed.

Arterioles↗
PubMed1979

Glomerular microfibrils in renal disease: a comparative electron microscopic study.

Microfibrils are a common component of connective tissue that have been described only rarely in the renal glomerulus. Structurally, microfibrils are fibrotubules with an average diameter of 12 nm, a lucid core, and a dark periphery. High resolution electron microscopy, including stereo microscopy performed on renal biopsy tissues, demonstrated the presence of microfibrils under the endothelium of the capillary walls and in the mesangium in several glomerular diseases. These diseases were characterized by widening of lamina rara interna or separation of the endothelium from the basement membrane, among them transplant glomerulopathy, focal segmental glomerulosclerosis (including a case associated with Marfan syndrome), preeclamptic toxemia, and less frequently hemolytic-uremic syndrome and malignant hypertension. The number of microfibrils generally correlated with the degree of subendothelial widening.

Basement Membrane↗