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Biomedical subjects

G Rostoker

Publications and source records attributed to G Rostoker.

At least 73 records · Page 4Linked to original sources
PubMed1990

[Frequency of painless myocardial ischemia during hemodialysis in 50 patients with chronic kidney failure].

The authors carried out a prospective study to determine the frequency of silent ischemia (SI) in 50 consecutive patients with end stage renal failure during dialysis by Holter monitoring. Twenty patients had SI (40%). This event was related to the number of cardiovascular risk factors (p = 0.0025), principally diabetes, smoking and the underlying renal disease (p = 0.018), and to a history of coronary artery disease (p = 0.0015). Two patients died during the nine months follow-up period and both had SI on Holter monitoring. Dialysis therapy in anaemic patients may predispose to and facilitate the detection of myocardial ischemia by the simultaneous interplay of hypotension, hypovolemia, hypoxia and tachycardia. The detection of these ischemic events may allow identification of a subgroup of dialysis patients with a high cardiovascular risk. The prognosis of these patients and best therapeutic approach require further study.

Adult↗
PubMed1989

Food allergy and idiopathic nephrotic syndrome.

Patients with the idiopathic nephrotic syndrome (INS) with steroid treatment failure, who did or did not have a history suggesting food intolerance, were systematically evaluated for food allergy. We evaluated 42 cases for sensitization to usual foods. The following results were obtained: skin tests (intradermal, Stallergenes Lab) were positive in 16 out of 42 cases; total serum IgE was elevated in 12 of 42 patients; specific IgE (RAST) was positive in eight of 42 patients; the basophil histamine release test (HRT) was positive in 20 of 42 patients. For each of these tests, the results in the INS patients with steroid treatment failure were significantly different from controls. The following exclusion or challenge tests were carried out. In seven cases, an elemental diet was used; proteinuria decreased in one case, but acceptance of the diet was poor in the other cases. In 27 cases, a limited diet with exclusion of one or several foods was used. A complete remission was induced by this diet in seven steroid-dependent INS cases, allowing steroids to be discontinued during a follow-up of one to five years. However, relapses were frequent. More recently, an oligoantigenic diet was prescribed for 10 days without modifying steroid therapy. In 13 INS patients (5 steroid-dependent, 3 steroid-resistant, and 5 multiple relapses), 24-hour urine protein was significantly reduced (P less than 0.05). Proteinuria decreased by more than half in nine patients, with complete disappearance in five cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens↗
PubMed1989

[Significance of IGA antigliadin antibodies during primary glomerulonephritis with mesangial IGA deposits].

The association of IgA anti-gliadin antibodies and IgA glomerulonephritis (IgA GN) was first reported in 1987 (Am J Nephrol, 1987, 7, 178-183) and has since been confirmed by other groups. We have developed a second generation ELISA (alkaline phosphatase, biotin-avidin) and used it to test 45 adult IgA GN, 34 idiopathic membranous nephropathy (MN), 31 idiopathic nephrotic syndrome (INS), and 11 idiopathic membranoproliferative glomerulonephritis (MPG) patients. IgA anti-gliadin antibodies were found in 24 IgA GN (53%), 1 MN (3%), 1 INS (3%), and 1 MGP (9%) patients. The presence of these antibodies in a patient with proteinuria strongly suggests IgA GN, with a sensitivity of 53%, a specificity of 96%, a positive predictive value of 88% and a negative predictive value of 77%. The presence of IgA anti-gliadin antibodies in IgA GN did not necessarily indicate coeliac disease because: a) neither IgG nor IgA anti-reticulin nor IgA anti-endomysium antibodies were found; b) intestinal absorption tests (folates, EDTA) were normal; c) biopsies of the small intestine were normal; and d) a gluten-free diet did not alter the evolution of the disease. Immunochemical analysis (footprinting after separation of the gliadins by rocket electrophoresis) showed the variability of the fractions recognized by the IgA antibodies from patients and controls, in addition to the absence of a typical profile. Gliadin does not have a lectin effect, since mannan and mannose did not inhibit the ELISA. Immunofluorescent labeling of human kidney with purified rabbit IgG anti-gliadin antibodies did not reveal a common epitope shared by gliadin and renal structures.(ABSTRACT TRUNCATED AT 250 WORDS)

Enzyme-Linked Immunosorbent Assay↗
PubMed1989

Serum IgG subclasses and IgM imbalances in adult IgA mesangial glomerulonephritis and idiopathic Henoch-Schoenlein purpura.

Serum IgG subclass levels were investigated in 27 IgA GN and HSP patients and 19 healthy paired controls using a panel of monoclonal antibodies. IgG1 and IgG2 were statistically lower than in the controls in both the non-nephrotic and nephrotic patients, and 80% of the non-nephrotic patients exhibited a partial deficiency for either IgG1, IgG2 or IgG3. Urinary losses of IgG only accounted for decreased levels of IgG4. Fifty-four percent of these patients exhibited decreased IgM levels. This IgG-IgM imbalance may increase the susceptibility of these patients to viral and bacterial infections of the upper respiratory tract and trigger the renal disease. These findings raise the hypothesis that this IgG-IgM imbalance might be involved in the etiopathogenesis of these diseases.

Adolescent↗
PubMed1989

[The hyper IgE syndrome (Buckley syndrome)].

An exceptional case is reported of hyper IgE syndrome and membranoproliferative glomerulonephritis with onset in 1964. Renal disease, symptoms of hyper IgE syndrome and level of serum IgE were improved by a long-term cyclosporine treatment (3/5 mg/kg/day) with a follow-up of 4 years. The characteristics of the hyper IgE syndrome, described by Buckley in 1972 are given and the respective roles of IgE-BF, IL4 and interferon in the mechanism of increase in serum IgE is discussed.

Cyclosporins↗