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Biomedical subjects

D Chevet

Publications and source records attributed to D Chevet.

At least 19 recordsLinked to original sources
PubMed1994

Interleukin 10 induces B lymphocytes from IgA-deficient patients to secrete IgA.

We have previously shown that human B lymphocytes cultured in the CD40 system, composed of an anti-CD40 mAb presented by a CD32-transfected fibroblastic cell line, proliferate but do not secrete antibodies. However, the addition of particles of Staphylococcus aureus Cowan (SAC) induces B cell differentiation even in the absence of exogenous cytokines (CD40/SAC system). Additionally, B lymphocytes cultured in the CD40 system in the presence of human IL-10, produce IgM, IgG, and IgA, and Ig levels are further increased by SAC. Here, we have studied the capacity of peripheral blood lymphocytes from patients with IgA deficiency (IgA-D) to secrete Igs, particularly IgA after CD40 triggering. Peripheral blood mononuclear cells (PBMNC) from IgA-D patients cultured in the CD40/SAC system produced IgM and IgG, but not IgA. The addition of IL-10 to the cultures, enhanced the production of IgM and IgG and most strikingly induced the production of high amounts of IgA. The addition of IL-10 to PBMNC from IgA-D patients activated through CD40 alone resulted in the production of IgA. Thus, SAC and anti-CD40 mAb stimulate B cells to differentiate into cells secreting IgG and IgM whereas IL-10 plays a central role in inducing B cells from IgA-D patients to differentiate into IgA secreting cells.

Adolescent↗
PubMed1991

[Extracapillary glomerulonephritis].

Extracapillary glomerulonephritis is characterized by cell proliferation within the urinary space of 50% of the glomeruli, where it covers more than 50% of the filtration chamber, associated with acute or rapidly progressive renal failure. It is a model of curable human renal failure. Extracapillary cell proliferation is an elementary lesion which may complicate any glomerulopathy and many systemic diseases, or appear to be primary. Its clinical manifestations may be extremely marked in some systemic diseases, but they may be minimal and delay a diagnosis which rests entirely on renal biopsy. An early renal biopsy commands the prognosis which depends on the finding of young cellular crescents that respond to treatment before fibrous transformation sets in. Experiments in animals and man suggest that cell proliferation results from rupture of the capillary walls and from the production of polymerized fibrin in the urinary space. This is followed by a cascade of reactions, with increased synthesis of local mediators issued from resident and invasive glomerular cells. These data constitute the basis of modern therapies, such as emboli of methylprednisolone, plasma exchange and immunodepressive drugs, aimed not only at a possible aetiological treatment but also at the cell proliferation itself. The use of such treatments, whose risks must be carefully weighted, has transformed the prognosis of extracapillary glomerulonephritis, since almost 50% of the cases the kidneys survive at 5 years.

Glomerulonephritis, Membranoproliferative↗
PubMed1990

Impairment of jacalin binding to serum IgA in IgA nephropathy.

A test was set up to analyze the direct binding of serum IgA to the lectin jacalin. Under the testing conditions, jacalin bound to both IgA subclasses and reacted similarly with monomeric and polymeric IgA. A jacalin index was defined to quantify serum IgA binding to this lectin. The jacalin index appeared significantly lower in IgA nephropathy than in controls. This may be related to abnormal IgA glycosylation, which could explain, at least in part, the mesangial deposition responsible for the renal disease.

Adolescent↗
PubMed1990

Linkage study of a large family with autosomal dominant polycystic kidney disease with reduced expression. Absence of linkage to the PKD 1 locus.

We describe a large three generation family with autosomal dominant polycystic kidney disease (PKD). Ultrasonographic screening of 60 family members revealed 20 individuals, whose age ranged from ten to eighty years, with one or several cysts in only one kidney and 7 individuals with cysts in both kidneys. Transmission of unilateral cysts seems to be autosomal dominant, although there are some generation gaps. Linkage studies with several markers of the PKD1 locus on the short arm of chromosome 16 showed no linkage with the disease. Lod scores for linkage between the disease and the most informative marker 3'HVR were computed using different penetrance models and several hypotheses concerning the clinical status of individuals with unilateral renal cysts. Results varied from Z = 1.31 to Z = -21.47 (theta = 0). Smith's test of heterogeneity gave a conditional probability of non-linkage between 0.9 and 1.0. We conclude that this family presents a form of autosomal dominant PKD with reduced penetrance and no linkage to the PKD1 locus on the short arm of chromosome 16. Other hypotheses, such as the existence of two distinct hereditary diseases in this large family, or neomutation in one branch of the family associated with a high frequency of isolated renal cysts, are also considered.

Family↗
PubMed1990

Acute renal failure following collective intoxication by Cortinarius orellanus.

Twenty-six young men with no previous medical history all ingested mushroom soup, exclusively made with Cortinarius orellanus. They were hospitalized 10-12 days after the incident. On admission, 12 patients presented with acute tubulointerstitial nephritis with acute renal failure; 8 required haemodialysis. In addition to symptomatic treatment, 9 patients were given corticosteroids. In this group of 12 patients, 8 recovered rapidly, and the other 4 suffered from chronic renal failure for several months. In the other group of 14 patients, initial leukocyturia was observed in 12 cases, although renal function remained normal during a one-year follow-up. Hepatic acetylation and hydroxylation tests performed after 6 months in 22 patients did not provide any explanation for the strong individual sensitivity to the renal toxicity of this fungus.

Acute Kidney Injury↗
PubMed1990

[Anti-basement-membrane antibody mediated, rapidly progressive, glomerulonephritis. Diagnostic and therapeutic strategy based on a retrospective study of 14 cases].

Fourteen cases of anti-GBM antibody-induced RPGN were evaluated retrospectively in terms of renal function improvement and therapeutic risks. Nine men and 5 women (mean age: 55.3 years) were observed over a 9 year period; in three patients, hemoptysis was associated with renal disease (Goodpasture's syndrome). Most of these patients had received combinations of steroid therapy (ST), immunosuppressive drugs (IS) and plasma exchanges (PE). Age, duration of symptoms prior to diagnosis, initial renal function, therapeutic modalities and complications were assessed according to renal outcome: 9 patients (group A, "non-responders") remained on dialysis irrespective of the treatment administered; 5 patients (group B, "responders") recovered renal function. Complications, especially infections, were twice as frequent in group A. Two of the 4 recorded deaths were related to the disease or the treatment. Analysis of clinical and pathological values at the time of entry into the study for both groups indicated that oliguria/anuria, serum creatinine greater than 500 mumol/l and greater than 50% crescents, when associated, were factors predictive of poor renal outcome; in these patients, dialysis may be required except in cases of pulmonary hemorrhage. In all other patients, treatment with ST, IS and PE is recommended. Active hemoptysis necessitates pulse steroids or PE; if absent, further tests (carbon monoxide uptake, bronchoalveolar lavage, lung biopsy) are indicated before use of aggressive therapy.

Adrenal Cortex Hormones↗
PubMed1988

[Interstitial nephropathies in sarcoidosis. Effect of corticosteroid therapy and long-term evolution. Retrospective study of 22 cases].

Interstitial Nephritis (IN) with or without epithelioid granulomas is the most frequent form of renal impairment in sarcoidosis. Nevertheless, few studies have provided conclusions about its treatment and long-term outcome. We report 22 cases collected over a 20-year period in 9 nephrologic departments of the west of France. We discuss the criteria which permit sarcoidosis to be distinguished from other causes, particularly of IN drugs. Twenty patients were treated with corticoids. In 18 the result could be evaluated on at least 12 months. In 11 there was a decrease of plasma creatinine (Pc) and in 8 of these cases this decrease reached 50%. Of the 12 who were followed from 1 to 17 years, 4 obtained a reduction of Pc of at least 50%. These improvements occurred even in patients whose Pc was initially higher than 300 mumol/l. Only 2 patients reached end-stage renal failure and hemodialysis within the observation period, one as early as the first month, the other after 6 years. Five relapses were observed after stopping treatment but 4 responded again favorably upon resumption. Two patients who received no treatment at all nevertheless had stabilization or improvement of their renal function with a follow-up of 5 years for one case. It may be concluded that the long-term prognosis of sarcoidosis IN can be fairly good but there is no proof that it depends mainly on corticosteroid therapy.

Adrenal Cortex Hormones↗