[Idiopathic membranous glomerulopathy with immunologic tubular involvement].
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Biomedical subjects
Publications and source records attributed to N Mandalenakis.
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The authors report the results of a histological and ultrastructure study of a case of a protuberant dermatofibrosarcoma evolving for the last 25 years with 27 relapses. Histologically the tumour is dermic, non-encapsulated, invading the hypodermis right from the beginning and mainly made up of fusiform cells which often have a storiform appearance and proliferate in a varying degree of collagenous stroma which includes an oedematous or myxoid component. During the course of the evolution of this tumour, there were zones of cystic degeneration, but in the last 10 relapses in 1978 and 1979, we noted the predominance of cellular and compact zones with an increase in the number of mitoses. The ultrastructure study showed tumour cells containing a fairly well developed endoplasmic reticulum in the cytoplasm, a prominent Golgi apparatus and some pinocytic vesicles. Some of the cells also contained lysosomes and phagolysosomes, whereas others contained cytoplasmic filaments and contractile elements. The nuclei were in general elongated and irregular. Sometimes the cytoplasmic membrane was covered by an amorphous substance with a membranoid appearance. Between the cells sometimes there were junctions of the tight kind. In conclusion, the authors consider that this tumour has the histological characteristics of a protuberant dermatofibrosarcoma and at the ultrastructure level, it is made up of cells which put it in the group of myofibroblastic and histiocytic proliferating lesions.
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A most unusual case of chronic membranoproliferative glomerulonephritis with nodule formation is reported in an elderly man in whom it was possible to document many episodes of acute oilguric and hemorrhagic glomerulonephritis and a syndrome resembling acute rheumatic fever. Severe renal failure necessitating peritoneal dialysis occurred on three occasions. Renal function returned to near preexacerbation levels in each episode. Although there was strong clinical evidence for streptococcal hypersensitivity, convincing laboratory documentation was lacking. The histologic and immunopathologic findings changed comparatively little during the several exacerbations. Impairment in fibrinolytic and coagulation activities by circulating macromolecular complexes is postulated for the induction and perpetuation of the glomerular injury.
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