[Immunologic aspects of infections of the urinary tract].
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Biomedical subjects
Publications and source records attributed to K Matousovic.
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In two patients with glomerulonephritis (GN) IgG and C 3 were visualized in ultrastructure by means of HRP-conjugated antisera. The first patient had an acute postinfectious extra-intracapillary GN lasting for about two months with granular fluorescence of anti-IgG, -C 3, and -C 1q. Electron microscopy revealed widespread endothelial defects, a well-pronounced polymorphonuclear stasis, and typical perimembranous "humps". These deposits reacted with HRP-anti-C 3 but the ultrastructural proof of IgG was negative. A weak and sporadic reaction of both these conjugates was seen in the swollen mesangial matrix while intraluminal plugs of coagulated plasma and extracapillary exudates yielded a dense coarse reaction product. In the second patient (allograft, three years after transplantation) the membranous and proliferative probably recurrent GN with nephrotic syndrome showed massive perimembranous deposits in the late involution stage. Granular fluorescence of the main Ig classes and of C 3 was sporadic or absent. In the ultrastructural immunoenzyme assay, too, the residues of deposits failed to react with HRP-anti-IgG or -C 3 and the mesangial matrix harboured only sporadic foci of faint positivity; however, dense product was again seen in capillary plasmatic "microthrombi". The discrepancy between immunofluorescence microscopy and immunoenzyme histochemistry, noted also by others in experimental glomerulopathies, may reflect the instability and dynamic properties of immune deposits with an early loss of antibody reactivity and a more protracted though not persistent local activation of complement. In light microscopy, fluorescent granules may correspond not only to the sites of immune deposition but also to accidental intracapillary plasma precipitates.
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The acute effect of 20 mg i. v. furosemide on the excretion fraction (EF) of osm, Na, K, and urea was investigated in groups of 32 patients with chronic renal disease and 20 with renal allograft. In renal patients furosemide elicited comparably high increment (delta) of EF osm, Na, and K in both the stage of renal insufficiency and at normal Cin. In transplant patients, the delta EFosm increased in linear relationship to increasing Cin. The different response seems to be attributable to the significance of the correlation of delta EFk to delta EFosm, resp., delta EFNa. The results indicate that in transplant patients the acute effect of furosemide on tubular transport of solutes increases with increasing GFR. This finding could be explained by the influence on potassium excretion.
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