[Electron microscopic observations on disseminated intravascular coagulation in rat kidney induced by liquoid].
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Biomedical subjects
Publications and source records attributed to J Ormos.
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Twenty percutaneous renal transplant biopsies and 20 removed allografts were investigated ultrastructurally. Most of the detected alterations were of a degenerative or regenerative nature and not specific of rejection. The most interesting phenomenon was the tubulitis, namely, the migration of the interstitial inflammatory cells (IC) through the tubular basement membrane (BM) and the invasion of the tubular epithelium in this way. Tubular epithelial cells (TEC) in the vicinity of IC were often necrotic. The composition of cells invading the tubules corresponded to those infiltrating the interstitium. The distal tubule was more frequently infiltrated than the proximal tubule. The TEC were always in very close contact with the BM. The invading IC were in direct contact with the inner surface of the BM only while passing through it. IC that passed the BM were immediately separated from it by a thin epithelial layer. The tubular ultrastructural changes did not reveal substantial differences between the various rejection types, except for the pronounced thickening and lamellation of the BM in chronic rejection.
Hematuria (HU) of tubular origin is described on the basis of ultrastructural investigations of two rejected human renal allografts. The red blood cells (RBC) got into the interstitium through the walls of the damaged intertubular capillaries, and, via ruptures of the tubular basement membrane (BM), they may pass from the interstitium into the tubular lumen, causing HU. Rupture of the tubular BM may develop owing to the enzymes released by interstitial inflammatory cells or to the difference in the interstitial and intratubular pressures. Some of the RBC already in the tubular lumen may penetrate between the epithelial cells and even between the epithelium and the BM, probably because of the locally increased intraluminal pressure. If the RBC reach the BM, the epithelial cells produce a new, thin BM above them, with disintegration of the outer older one, and, thus, the RBC may pass into the interstitium again. This phenomenon is called the tubulointerstitialis circulation of RBC.
This ultrastructural study is based on nine cases of adenoid cystic carcinoma arising from the salivary glands. Electron microscopically, the tumors consisted of five cell types: relatively differentiated intercalated duct cells, secretory cells, undifferentiated cells, cells of a squamous nature, and myoepithelial cells. Special attention was paid to the characteristic extracellular substances noted by light microscopic examination of these tumors. The hyaline material of the pseudocysts contained not only mucopolysaccharide granules but also fingerprint-like structures formed by replicated basement membrane. Some of these structures had a dense core, probably composed of mucopolysaccharide granules. Cell islands surrounded by elasticlike material also were found. The true lumina were usually filled with membranovesicular structures originating from fragments of the lining cells, mainly those with squamous differentiation. These membranovesicular structures included electron-dense rods, filamentous whorls, and structures displaying periodicity.
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A study of 196 renal biopsies was carried out by electron microscopy. In 78 cases concretions were detected, which x-ray microanalysis (EDAX) proved to be calcium phosphate deposits. Concretions always occurred in damaged basement membranes, especially in the basement membranes of Bowman's capsules and of proximal convoluted tubules. They were frequently also found in sclerotic foci. Both nephrotic syndrome (through hypercholesterolaemia) and progressive sclerotic processes seem to play a role in the pathogenesis of concretion formation. Concretions are considered to represent early dystrophic calcification.