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Biomedical subjects

J C Davin

Publications and source records attributed to J C Davin.

At least 55 records · Page 3Linked to original sources
PubMed1987

Anti-alpha-galactosyl antibodies and immune complexes in children with Henoch-Schönlein purpura or IgA nephropathy.

Episodes of hematuria in IgA nephropathy or Henoch-Schönlein purpura are frequently associated with microbial infections. Some of those infectious agents bear alpha-galactosyl residues on their cell surface. These observations prompted us to determine, by passive hemagglutination, the titers of natural anti-galactosyl antibodies in the serum of children presenting with Henoch-Schönlein purpura (10 cases) or IgA nephropathy (7 cases). Antibody titers of normal subjects (103 cases), children with a pharyngitis of unknown etiology (7 cases), and children exhibiting mesangial IgA deposits but no hematuria at the time of testing (6 cases) ranged from 1:20 to 1:80. Elevated titers (greater than 1:80) were observed in nine of 11 patients with mesangial IgA deposits and micro- or macroscopic hematuria, in nine of 19 children with other evolutive glomerular diseases (5 cases of acute glomerulonephritis and 4 cases of minimal change disease), and in most subjects presenting with a M. pneumoniae (4/5 cases) or a E. Coli (4/5 cases) infection. Antibody titers decreased after incubation of normal and pathological sera with D-galactose (10 mM) or with alpha-galactosyl-glucoside (10 mM), but not with D-glucose (10 mM). The anti-alpha-galactosyl antibodies purified, by affinity chromatography, from sera of 10 normal children, 10 pathological controls and four children with mesangial IgA deposits without hematuria belonged to IgG class. In contrast, both IgG and IgA anti-alpha-galactosyl antibodies were detected in six of six patients with mesangial IgA deposits and hematuria. The IgA content of immune complexes detected in those patients decreased after incubation of sera with alpha-galactosyl-glucoside, but not with D-glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Urinary excretion of neutral proteinases in nephrotic rats with a glomerular disease.

A proliferative glomerulonephritis was induced in rats pre-immunized with rabbit IgG by injecting intravenously a sub-nephrotoxic dose of rabbit anti-glomerular basement membrane (GBM) IgG (A rats). Most rats (80%) developed a severe proteinuria (greater than 100 mg/24 hr) within two to five days after the injection of anti-GBM IgG. At the same time, microscopic examination of the kidneys revealed a glomerular infiltration by mononuclear phagocytes and a prominent decrease in the intensity of the colloidal iron reaction in glomeruli. A non-proliferative glomerular disease was induced in another group of rats (B rats) by intraperitoneal administration of aminonucleoside of puromycin. A marked proteinuria (greater than 100 mg/24 hr) occurred after six days in 90% of animals. Histochemical studies then revealed a decrease in staining intensity of glomeruli for polyanion. No glomerular hypercellularity was noted. In normal rats and in non-proteinuric A or B rats, the 24 hour urinary excretion of neutral proteinases ranged from 1.4 to 7.8 units (mean value +/- SEM, 4.69 +/- 0.60, N = 11), that of laminin ranged from 100 to 3,900 ng (mean value +/- SEM, 1,154 +/- 325, N = 10), and that of type IV collagen ranged from 160 to 420 ng (mean value +/- SEM, 306 +/- 26.5 ng, N = 8). In proteinuric rats from groups A (N = 11) and B (N = 9), the 24 hour urinary excretion of neutral proteinases significantly increased (mean values +/- SEM, 38.55 +/- 8.66 U for A rats and 42.17 +/- 7.92 U for B rats) and ran parallely with that of proteins, laminin and type IV collagen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Relation between biological IgA abnormalities and mesangial IgA deposits in isolated hematuria in childhood.

Indications for renal biopsies in isolated hematuria in childhood remain difficult to define. Their limitation to patients presenting with either a macroscopic or a familial hematuria [Trachtman et al. 1984] bears the potential risk of missing the diagnosis of IgA-associated nephropathies (Berger disease and Henoch-Schönlein nephritis) which may manifest themselves by microscopic hematuria only. In order to reevaluate the association between biological IgA abnormalities and mesangial IgA deposits, iterative and concomitant determinations of IgA plasma levels, of IgA immune complexes and of IgA production by lymphocytes in vitro have been performed over a one-year period in two groups of hematuric children presenting with mesangial IgA deposits (14 cases) or not (13 cases). The incidence of positivity of each test was significantly higher in the former group of patients than in the latter. However, the best discrimination between both groups was observed when the three tests were repeated and/or considered together (97% vs 15% of positivity). In Berger disease and Henoch-Schönlein nephritis, IgA immune complexes were the only IgA abnormality more frequently detected in patients presenting with hematuria than in patients presenting with no hematuria at the time of testing. It is proposed to add IgA abnormalities to macroscopic or familial hematuria as indications for renal biopsies in isolated hematuria in childhood.

Antigen-Antibody Complex↗
PubMed1986

Elevated antigalactosyl antibody titers reflect renal injury after gold or D-penicillamine in rheumatoid arthritis.

Titers of circulating antigalactosyl antibodies (a-Gal Ab) were assessed by passive hemagglutination using rabbit red blood cells in 40 normal subjects, in 14 patients with immunodeficient states, in 47 patients with active rheumatoid arthritis (RA), and in 15 patients with an Henoch-Schönlein disease (HS). Titers of controls ranged from 1:16 to 1:64. All immunodeficient patients exhibited very low titers (1:1). On the contrary, the existence of an enhanced humoral immune response status, as observed in RA, was not reflected by a parallel increase of a-Gal Ab titers. However, in this disease, a strong relationship existed between titers exceeding control values (greater than 1:64) and the prior occurrence of renal injury under gold or D-penicillamine therapy. Lastly, the discovery of elevated titers (greater than 1:64) in HS only when renal involvement occurred further suggests that such antibodies reflect a renal injury.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Sequential measurements of the reticulo-endothelial system function in Henoch-Schönlein disease of childhood. Correlations with various immunological parameters.

Different immunological parameters were studied in 16 children suffering from Henoch-Schönlein purpura. The following results were observed during the acute phases in some patients: (1) an increase in C3d plasma levels; (2) the presence of circulating immune complexes (CIC); (3) an increase in IgA plasma levels and (4) an impairment of the reticuloendothelial system (RES) function assessed by an in vitro and an in vivo test. After the acute phase, all the altered parameters were almost normalized in recovering patients. On the contrary, all 5 patients with persistent urinary findings or relapsing purpura continued to present increased IgA plasma levels and/or CIC and/or impaired RES function. Our results therefore show that, in Henoch-Schönlein disease of childhood, a correlation exists between persisting clinical signs and persisting high IgA plasma levels, CIC and RES function impairment.

Acute Disease↗
PubMed1985

Electron microscopic studies in a long-term follow-up of a case of congenital nephrotic syndrome.

A boy presenting with a severe congenital nephrotic syndrome diagnosed by histological analysis at the age of 3 weeks was biopsied again 7 years later. The ultrastructural glomerular basement membrane abnormalities depicted in the first biopsy were no longer present in the second one. The number of completely hyalinized glomeruli was not significantly decreased. The GFR remained normal, but a moderate persistent, non-selective proteinuria (800 mg/24 h) was noted without oedema. The patient however developed a progressive perceptive deficit of hearing.

Basement Membrane↗
PubMed1983

A Rothmund-Thomson case with hypertension.

An unusual association of Rothmund-Thomson syndrome and hypertension is described. The histologic studies showed large narrowing and calcification of arteries at renal biopsy, thickenings of glomerular basement membranes and nodules of subendothelial basement membrane lamellae in arterioles by means of electron microscopy. The mechanisms of these morphologic alterations are discussed with regard to disturbances of collagenous and fundamental substances of metabolism.

Cataract↗
PubMed1983

Studies on the glomerular filtration barrier and on the urinary excretion of basement membrane glycoproteins during the accelerated model of nephrotoxic serum nephritis.

A proliferative glomerulonephritis was induced in rats preimmunised with rabbit IgG by injecting a sub-nephrotoxic dose of rabbit anti-rat GBM IgG. All the rats developed a severe proteinuria within 2-5 days after the injection of anti-GBM IgG. At the same time, many mononuclear phagocytes infiltrated the glomeruli, the colloidal iron staining of the glomerular filtration barrier was altered, and the urinary excretion of laminin and of neutral proteinase strongly increased. However, the pattern and intensity of staining of different collagenous and non-collagenous BM glycoproteins were not modified, as shown by indirect immunofluorescence microscopy. The existence of a direct significant correlation between the proteinuria and the laminin urinary excretion, and between the latter and the urinary neutral proteinase activity suggests that lysosomal proteinase of mononuclear phagocytes may be involved in the damage of the GBM during the course of this experimental glomerulonephritis.

Animals↗