Biomedical subjects
Publications and source records attributed to P Mahieu.
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The urinary excretion of inorganic arsenic and of its less toxic metabolites [monomethylarsonic acid (MMA) and dimethylarsinic acid (DM)] has been followed-up in five cases of acute oral intoxication by As2O3. In addition to supportive therapy all patients were given BAL. The proportion of the three species of urinary arsenic (inorganic, MMA, DMA) changes markedly with time. During the first 2 to 4 d after the intoxication, arsenic is excreted mainly as its unmetabolized inorganic form but this is rapidly followed-up by a progressive increase of the proportion excreted as MMA and DMA. The time at which the majority of arsenic is excreted as its organic metabolites depends on the severity of the intoxication but in all the cases, more than 95% of th excreted arsenic is in the organic form after 9 d, the dimethylated derivative being preponderant. Speciation of arsenicals in urine might be useful to determine the duration of BAL treatment.
C3H, CBA (H-2k) and NZB (H-2d) mice were immunized with dog insoluble glomerular (GBM) or tubular basement membrane (TBM). The titre of circulating antibodies was sequentially determined and their specificity was analysed using various soluble antigenic fractions. Glomerular and tubular deposits were studied on serial biopsies by direct immunofluorescence. After elution from whole kidneys, IgG fixation on normal mouse kidney sections was analysed by indirect immunofluorescence. After immunization with insoluble GBM, animals from all three strains develop antibodies mainly directed against collagenous antigenic determinants shared by GBM and TBM. After immunization with insoluble TBM, the antibodies are directed in NZB mice against non-collagenous TBM-specific determinants, in C3H mice against collagenous determinants and in CBA mice against both types of antigenic determinants. Thus the ability to respond to the various antigens of GBM and TBM is genetically determined and does not depend only on the major histocompatibility complex.
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Two immune sera have been raised in sheep against rabbit glomerular and tubular basement membranes, respectively (GBM and TBM). Their specificity was investigated by immunoabsorption and radioimmunoassay, and their nephrotoxicity was studied by injecting them into New Zealand rabbits. Both antisera reacted in vitro collagen and noncollagen-related glycopeptides. However, while the anti-GBM antiserum reacted preponderantly with GBM and TBM collagen which probably represent the antigen(s) shared by the two basement membranes, the anti-TBM antiserum was directed preferentially against the noncollagenous component of rabbit TBM. The anti-GBM antiserum induced in rabbits a diffuse extracapillary glomerulonephritis with linear fixation of autologous IgG and C3 along the GBM. The anti-TBM antiserum also induced an extracapillary glomerulonephritis but in addition a focal tubular atrophy was seen and autologous IgG and C3 were fixed along both GBM and TBM and glucosuria frequently occurred. These results suggested that the glomerular lesions induced by the two antisera were due to anticollagen antibodies while the tubulointerstitial lesions were due to antibodies directed against the noncollagenous portion of TBM.
A case associating asbestosis and clinical lupus erythematosus (SLE), both diagnosed according to standard criteria, is described. It is suggested that such an association may bear some analogy to the well-known 'Caplan-Collinet' syndrome, associating silicosis and rheumatoid arthritis.
The sera of 24 patients presenting with Good-pasture's syndrome, and of 30 normal blood donors were tested for the presence of anti-basement membrane (BM) antibodies, by a radioimmunological method, using two highly purified BM antigens, i.e. the type IV (BM) procollagen and a non-collagenous glycoprotein (laminin) isolated from the BM matrix secreted by a murine tumor. In marked contrast to the normal sera, the sera from 20 out of 24 patients presenting with Goodpasture's syndrome exhibited high anti-laminin and/or anti-type IV procollagen antibody levels. The other sera did not react with both BM antigens tested. The antibody titers varied according to the antigens used the sera tested. Kidney eluates from 4 "positive" patients also contained significant amounts of anti-laminin and anti-type IV procollagen antibodies. The data demonstrate that, in Goodpasture's syndrome, the pathogenicity of circulating and kidney-fixed anti-BM antibodies is not related to the chemical nature of the BM antigens triggering the immune response only. They suggest a polyclonal rather than a monoclonal stimulation in this disease.
A rapidly progressive glomerulonephritis with definitive anuria was observed after solvent inhalation in two young women, aged 22 and 17 years. In both cases the renal biopsy specimen showed diffuse epithelial crescents in all glomeruli, with linear deposits of IgG along the glomerular basement membrane (GBM). High circulating anti-GBM antibody levels were found in sera by indirect immunofluorescence and radioimmunoassay. No anti-alveolar basement membrane antibodies were detectable by immunofluorescent microscopy in one patient. It is suggested that the solvent inhalation resulted in a chemical alteration of the alveolar basement membrane giving rise to anti-basement membrane antibodies, some of which may have cross-reacted with the GBM and initiated the glomerulonephritis.
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