[Acute reversible renal insufficiency induced by ketoprofen].
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Biomedical subjects
Publications and source records attributed to F Ducret.
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A prospective randomised trial was carried out in 14 patients with severe 'idiopathic' acute crescentic glomerulonephritis. The mean percentage of crescents was 78 per cent and 11 patients were anuric at presentation. Eight patients received pulses of methylprednisolone, immunosuppressive drugs and anticoagulants and six the same therapeutic regimen plus plasma exchanges for one to two months. Mean follow-up was 22 months. Recovery was statistically better in the PE+ group (p less than 0.02), but for discontinuation of dialysis, the difference is significant only at two months (p less than 0.02), perhaps because of the small number of patients. For this reason and because all pathological subgroups cannot be analysed separately, this study is continuing.
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The development of membranous glomerulonephritis in a 51 year old patient suffering from rheumatoid arthritis suggested drug toxicity, and particularly of a recently developed anti-inflammatory agent, diclofenac. The toxicity is discussed in relationship to the biochemical and pharmacological properties of the molecule, the therapeutic setting and the positivity of serological tests for rheumatoid arthritis in this particular case.
Two HLA identical brothers with mesangial IgA glomerulonephritis are reported. Patient 1 developed gross hematuria at age 12 and required chronic hemodialysis at age 20. Patient 2 presented at age 21 with gross hematuria and normal renal function, the follow up period is only 9 months. Neither of these patients had nerve deafness, ocular defects or complement abnormalities. The family history did not support a diagnosis of classical hereditary nephritis, but a genetic linkage is strongly suggested by the identical HLA phenotypes of these brothers (A10 - A32 - B13 - B35). The B35 antigen has previously been suspected to be linked to this disease. These observations strongly support the hypothesis of an aberrant, genetically controlled, immune response, in patients with mesangial IgA glomerulonephritis.
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Suicidal attempt using beta-blockers are rare. Overdose by the ingestion of a large number of tablets rarely exceeds the high therapeutic doses suggested for the treatment of certain resistant cases of hypertension. The case described is that of a 65-year-old patient who took 800 mg of propanolol. Observation of plama levels showed that the half-life propanolol in the case of overdose is prolonged: 8.6 hours in this case, with a maximum plasma level of 1536 ng/ml. Plasma renin activity levels were low during the phase of intoxication and showed evidence of a rebound effect at its end. Treatment is above all that of the circulatory insufficiency produced: isopropylnoradrenaline or glucagon. Indications for extra-renal dialysis should take into account knowledge concerning the pharmacokinetics of these drugs and their prolonged physiological action.
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The clinical association between glomerulonephrtis (GN) and malignant hematological disease is very rare. We report, in a 24 years old male, the occurrence of an apparently idiopathic nephrotic syndrome with minimal change glomerular lesions. This GN was in fact closely related to the progression of a stage 2A of Hodgkin's disease, following an infectious mononucleosis contracted one year ago. The nephrotic syndrome responded well to the therapy by Prednisone and Chlorambucil, and the complete remission persisted after eradication of Hodgkin's disease and despite early treatment discontinuation. Renal vein thrombosis, renal amyloidosis and renal interstitial infiltration with malignant cells were ruled out. Immunofluorescent and electron microscopy examination of the renal biopsies were consistent with, but not demonstrative of, an immune complex nephritis. Because of the chronological succession of infectious mononucleosis, Hodgkin's disease, and GN, we are stressing the possible oncogenic and immunogenic role of the Epstein-Barr virus.
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