[The acute nephritic syndrome].
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Biomedical subjects
Publications and source records attributed to L Humair.
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In a group of 29 patients treated with digoxin for cardiac failure, only 16 showed increased calcium and potassium concentrations in saliva. There was no correlation in the 29 patients between serum digoxin levels and concentrations of salivary electrolytes. On the other hand, in 4 normal subjects treated with digoxin no change in salivary electrolytes was noted. It is concluded that modifications in salivary electrolytes seen in patients with cardiac failure treated with digitalis are not due to this drug. However, a retrospective clinical study showed a good correlation between clinical signs of cardiac failure and increased levels of salivary calcium, potassium and CaX Kproduct. It is suggested that this phenomenon is due to the well-known adrenergic stimulation in patients with cardiac failure.
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A 45-year old developed membranoproliferative GN seven years after acute hepatitis. He was found to be a chronic carrier of HBsAg, and glomeruli contained granular deposits of immunoglobulins (Ig), complement (C) and HBsAg. Six months later, HN persisted, but HBsAg has disappeared from glomeruli; Ig and C were still present. It was concluded that GN was probably due to a hepatitis B associated antigen, but not necessarily to HBsAg.
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The prognosis in patients with glomerulonephritis can now be established with some confidence. The major advance has been the use and interpretation of renal biopsies. The different histological varieties have their own evolution and prognosis. The clinical/pathological correlations assist the physician in determining the prognosis in patients with glomerulonephritis. On the clinical side, the most important observation is the simplest: proteinuria or hematuria may persist separately for many years without alteration of renal function. However, in patients with persistent proteinuria associated with hematuria the prognosis is poor, as the evolution is towards renal failure.
This study demonstrates that in systemic lupus erythematosus (SLE), the presence of immune complexes on the glomerular basement membrane (GEM) does not invariabley result in histological and/or functional lesions of the kidney. Among a group of 29 lupus patients, six subjects were selected for thorough investigation, because their renal function was normal or only slightly altered though they had suffered from SLE for 20 months to 18 years. All patients had antinuclear factor, anti-native-DNA antibody and a low level of complement; 3 had anti-denatured-DNA antibody, 2 had denatured DNA-anti-denatured-DNA circulating complexes and 3 had anti-RNA-protein antibody. Kidney biopsies disclosed either no histological lesion or minimal changes in five of them and diffuse proliferative glomerulonephritis in one. By contrast, using the immunofluorescent technique, granular deposits containing the third component of complement (C3) were found on the GBM of all patients; IgG was present in 5 cases, IgM in 3, fibrinogen in two cases and around the tubules of one. Electron microscopy confirmed the presence of subendothelial and mesangial deposits. Our results also showed a good correlation between the importance of deposits and the presence of denatured DNA-anti-denatured-DNA circulating complexes. From the data obtained in these 6 cases as well as in the 23 other patients of the group, 3 categories of lupus patients could be distinguished with regard to kidney involvement: 1) patients with insignificant histological lesions, no immune deposits and essentially normal function; 2) patients with definite histological lesions, immune deposits and renal insufficiency and 3) patients with few if any histological lesions and little functional impairment contrasting with important immune deposits. The resistance of some patients to the mephrotoxic effects of immune deposits shows that lupus nephritis depends on intricate pathogenic mechanisms and suggests that these are possible antagonized by "protective" factors.
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