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Biomedical subjects

D Droz

Publications and source records attributed to D Droz.

At least 91 records · Page 5Linked to original sources
PubMed1989

[Pulmonary hemorrhage and rapidly progressive glomerulonephritis ("pulmonary-renal" syndrome)].

The association lung hemorrhages and crescentic glomerulonephritis caracterises severe clinical disorders where specific diagnosis is required for initiating the apropriate therapy. Goodpasture's syndrome and systemic vasculitis, mainly Wegener's granulomatosis, are the most frequent etiologies of these syndromes. The detection of circulating auto-antibodies directed against glomerular basement membrane in Goodpasture's syndrome, or against neutrophil cytoplasmic constituents in Wegener's granulomatosis, provides at the present time, helpful specific diagnostic tests making these disorders more readily identifiable.

Anti-Glomerular Basement Membrane Disease↗
PubMed1987

Hemodialysis-associated amyloidosis and beta-2 microglobulin. Clinical and immunohistochemical study.

The beta-2 microglobulin type of amyloidosis was identified in articular and para-articular tissues of 14 patients with non-amyloid nephropathies undergoing long-term hemodialysis. Ten patients had carpal tunnel syndrome, 13 had juxta-articular radiolucent cysts (complicated by spontaneous fractures of the femoral neck in three), and six had destructive arthropathies of the large joints of the limbs. Massive amyloid deposits were found in the synovium, capsule, ligaments, articular cartilage, and/or bone. They were characterized by Congo red-induced green birefringence that was sensitive to potassium permanganate treatment. They reacted with anti-beta-2 microglobulin antiserum, whereas they did not react with antibodies directed against AA protein, prealbumin, or immunoglobulins. These data suggest that the potentially disabling arthropathy of hemodialysis is due to amyloid lesions. The persistently elevated plasma beta-2 microglobulin levels may play a role in the pathogenesis of this recently recognized complication, and if so, this complication should be preventable.

Aged↗
PubMed1987

Immunohistochemical characterization of renal amyloidosis.

Forty-five renal biopsies with amyloidosis were studied by light microscopy with Congo red staining and action of potassium permanganate and by immunofluorescence with antihuman tissue A component antiserum antilight and heavy chains of immunoglobulins antisera. The patients were classified on the basis of concordance between immunohistochemical characterization by immunofluorescence and the results of Congo red staining after potassium permanganate treatment. Thus, 37 of 45 cases (82%) were classified by immunohistochemical characterization (15 with AL amyloidosis and 22 with AA amyloidosis) when the amyloid type could be hypothetized in only 31 of these cases (66%) on the basis of clinical criteria. This study suggests that the association of these two technics is more reliable than clinical data alone in distinguishing between AA and AL amyloidosis.

Amyloidosis↗
PubMed1987

Long-standing spontaneous clinical remission and glomerular improvement in primary IgA nephropathy (Berger's disease).

Of the 244 cases of IgA nephropathy diagnosed at Necker Hospital before 1981, 9 patients (3.7%) developed spontaneous clinical remission of long duration. Three of these 9 patients presented with gross hematuria, while in the others the disease was discovered by the finding of proteinuria at routine urinalysis. During the disease course 5 patients had recurrent episodes of gross hematuria, lasting several years in 4. At the time of the first biopsy all patients had hematuria and permanent proteinuria. In 1 patient, renal biopsy showed only an increase in mesangial matrix while in the others segmentary lesions were observed, affecting less than 30% of the glomeruli in 6. Diffuse mesangial deposits of IgA were present in all. During the follow-up, proteinuria and microscopic hematuria gradually decreased and completely disappeared within 4-14 years after the onset of the disease. A repeat biopsy performed during remission in 4 patients showed, in 3, an improvement of glomerular lesions and a significant decrease in IgA mesangial deposits in parallel with clinical recovery. As in other types of 'primary' glomerulonephritis, these data indicate that the initial disorder in IgA nephropathy may be spontaneously reversible even after a long course of the disease.

Biopsy↗
PubMed1987

Relationship between the integrity of Bowman's capsule and the composition of cellular crescents in human crescentic glomerulonephritis.

Cell constituents of glomerular crescents still remain controversial. We examined cellular crescents in ten cases of crescentic glomerulonephritis (GN) using indirect immunoperoxidase technique and monoclonal antibodies against T cells (OKT3) and subsets: T helper/inducer cell (T4), T suppressor/cytotoxic cell (OKT8), T activated cell (IoT14 and IoT15); B cells (B1, B4, OKB2 and IoB3) and subsets (B2 and IoB1); monocytes/macrophages (LeuM3); DR Ag (I2) and renal native cells: podocytes (IoT5), Bowman's capsule (BC) parietal epithelial cell (OKB2, IoB3). Studied cases were 2 anti-glomerular basement membrane (GBM) GN, 4 immune complex GN, 3 vasculitis and 1 idiopathic GN. When the BC continuity was preserved almost all crescent cells were identified; they originated in majority from the BC parietal epithelium and ranged from 55 to 95 per cent. The other main constituents which represented 15 to 35 per cent of the crescent cells were monocytes (LeuM3+) and T-activated cells (IoT15+). In the interstitial infiltrate, which was mostly periglomerular, LeuM3+ cells and IoT15+ cells accounted for more than 70 per cent of the cell population. On the other hand, when BC were ruptured, mononuclear inflammatory cells, mainly LeuM3+ and IoT15+ cells accompanied by significant number of T4+ and T8+ cells, constituted the glomerular crescents. At this time, BC parietal epithelial cells were rarely identified (15 per cent). These findings strongly support the importance of BC integrity to discriminate the nature of crescent cells.

Antibodies, Monoclonal↗
PubMed1987

[Severe epithelio-exfoliative colitis in infants. Anatomical data].

Amongst the uncommon forms of congenital severe colitis, we wish to draw attention to a peculiar and probably previously never described condition that we propose calling provisionally, epithelio-exfoliative colitis. This condition appears to be characterized by the following features: its early beginning within the first weeks of life; the smooth, glossy appearance of the mucosa, without ulcerations visible to the naked eye; the prevalent degenerative changes of the epithelial cells which become vacuolated, break away prematurely from the basement membrane and finally exfoliate within the glandular lumens; the distension and rupture of the glands, the mucous contents of which intrude into the lamina propria and induce a localized, mild and non suppurative inflammatory reaction; accessory reactive traits: intense mucus production actively regenerating epithelium (high mitotic activity, syncytial cells) and increase of the cholinergic fibers within the lamina propria. Although patchily distributed, these lesions involve the colon exclusively. The cause of epithelio-exfoliative colitis is unknown. However, the ultrastructural studies and immunocytochemical investigations using anti-collagen IV, antilaminin, anti-fibronectin antibodies disclose in some glands localized thinning and rupture of the basement membrane. These data suggest a primary disorder within the molecular arrangement of either the basement membrane itself or the proteins which anchor the glandular cells to the basement membrane.

Colitis↗
PubMed1986

Role of antibodies directed against tubular basement membranes in human renal transplantation.

Direct immunofluorescence studies of graft biopsies from 662 renal transplant recipients demonstrated linear IgG deposition along tubular basement membranes (TBM) in 18 cases. In ten of them, circulating anti-TBM antibodies, whose detectable levels varied from 1/4 to 1/100, were demonstrated by indirect immunofluorescence on normal human kidneys. These antibodies reacted with every human kidney tested and in two cases, it could be demonstrated that they recognized the TBM of the patient's own end-stage kidney. Hence, they reacted as autoantibodies. Circulating anti-TBM antibodies were detected within the first 6 months after transplantation, remained present for an average of 3 months, and never recurred once they had disappeared. Serial biopsies demonstrated the loss of IgG linear fixation on TBM. Neither tubular nor interstitial injury was significantly associated with the presence of anti-TBM antibodies, and the transplant survival was not different in these patients who developed anti-TBM antibodies compared to our entire population of transplant biopsies.

Actuarial Analysis↗
PubMed1986

Characterization of mononuclear cell subsets in renal cellular interstitial infiltrates.

Indirect immunoperoxidase analysis using monoclonal antibodies (Mo Ab) was performed in 33 renal biopsies with interstitial cellular infiltration obtained from non-transplanted patients. We reviewed four acute interstitial nephritis (IN), three chronic IN, four granulomatous IN, four acute tubular necrosis, four vasculitis, seven primary glomerulonephritis and seven active lupus nephritis (LN). We used Mo Ab recognizing T and B cell markers [OKT3, OKT8, T4, B1, IOT14 (IL2 receptor)], HLA-DR related antigen (I2) and monocytes/macrophages (LeuM3). In all cases the interstitial cellular infiltrates were predominantly T cells, whereas the B cell population accounted for less than 20% of the infiltrate. LeuM3+ cells were present in 28 of 32 cases, usually in a lesser proportion than T cells. IOT14+ cells were exceptional. T4+/T8+ cells were clearly greater than one in three acute IN, three granulomatous IN, two LN and two vasculitis. The T8+ cell population predominated in one case of chronic IN related to a non-steroidal anti-inflammatory drug. In all the remaining cases T4+ and T8+ cells were equally present. Aberrant strong HLA-DR expression within tubular cells was noted in nine cases (4 LN) irrespective of the presence of tubular lesions. On the basis of the phenotypic analysis, our data do not support a specific pattern of the infiltrate in regard to a given etiology and thus cannot be used as a diagnostic tool. However, such analysis may aid in understanding the mechanisms of tissue injury.

Adult↗
PubMed1986

Prophylactic use of OKT3 monoclonal antibody in cadaver kidney recipients. Utilization of OKT3 as the sole immunosuppressive agent.

We describe the first clinical trial of OKT3, a monoclonal anti-T-cell antibody, for prevention of kidney transplant rejection. 13 patients receiving a first cadaveric kidney transplant were randomly assigned to conventional treatment with azathioprine and high-dose steroids (7 patients) or to treatment with daily injection of OKT3 alone (6 patients). The first OKT3 injection resulted in a dramatic decrease in T3+, T4+, and T8+ cells, while patients simultaneously experienced fever, chills, and diarrhea. These symptoms did not recur with subsequent injections. All six OKT3-treated patients had a rejection necessitating introduction of steroids 12.8 +/- 2.9 days after surgery. Rejection was related to appearance of anti-OKT3 antibodies leading to disappearance of detectable OKT3 in the serum. Modulating (T3-, T4+ or T3-, T8+) cells were observed in all patients but were functionally inactive. As no rejection was observed before day 9 posttransplant, despite the lack of additional immunosuppressive agents, we conclude that OKT3 is a powerful, well-tolerated immunosuppressive agent. However, it is highly immunogenic and anti-OKT3 antibodies lead to loss of clinical effectiveness in this protocol. The use of OKT3 alone for prevention of kidney graft rejection cannot be recommended until a method for reducing the effects of anti-OKT3 immunization is developed.

Acute Disease↗
PubMed1986

Linear glomerular IgG fixation in renal allografts: incidence and significance in Alport's syndrome.

Twelve of 767 renal allograft recipients developed linear fixation of IgG along the glomerular basement membrane (GBM) by direct immunofluorescence technique. This was associated with linear fixation along the tubular basement membrane in 7 of them. Circulating anti-GBM antibodies were not detected by indirect immunofluorescence or radioimmunoassay in any patient whereas anti-TBM antibodies were found in 2 of 4 with linear TBM fixation. Among the 12 patients with linear GBM fixation, 5 had Alport's syndrome; the 7 others had various renal diseases, excluding anti-GBM nephritis. Among the 767 patients, 34 had Alport's syndrome or variants (i.e., 4.5%). The incidence of linear GBM fixation is much higher in Alport's syndrome than in other renal diseases. Linear GBM fixation was not clearly related to anti-GBM antibodies and was not accompanied by significant deterioration of graft function. These findings may be relevant, however, to the missing GBM antigen in Alport's syndrome.

Adult↗
PubMed1986

[Adult nephronophthisis: a single disease or 2 diseases?].

Six families including 27 patients with adult nephronophthisis were studied. The diagnosis was based on the evidence of heredofamilial chronic tubulointerstitial renal disease, not related to urologic abnormality, and progressing to renal failure in at least 2 members of each kindred. In two families, the mode of inheritance is compatible with recessive autosomal transmission; retinal heredodegeneration was found in both kindreds; mean age at end-stage renal failure (ESRF) was 22 years. In one additional case, kidney involvement is apparently sporadic, and associated with retinal changes and blindness. In one kindred, the mode of inheritance could not be determined. In the last 3 families, pedigrees are compatible with dominant autosomal transmission; retinal involvement was found in none; ESRF developed at a mean age of 47 years. Renal cysts were detected by ultrasonography in 9 of 12 patients; they were located at the cortico-medullary junction or in the medulla in 5 cases. Renal biopsy showed rather similar changes in the various kindreds. These results are compared with those already reported from 29 families with adult nephronophthisis.

Adolescent↗
PubMed1985

Clinical and histological resolution of systemic amyloidosis after renal cell carcinoma removal.

This report describes the case of a 62-year-old woman with systemic amyloidosis involving the kidneys and digestive tract, consecutive to a renal cell carcinoma. Within 3 years after tumor removal, both the nephrotic syndrome and protein loss enteropathy regressed. Histological examination showed the disappearance of the potassium permanganate-sensitive deposits within the digestive tract. This indicates that clinical remission of systemic amyloidosis may be associated with morphologic disappearance of amyloid deposits.

Amyloidosis↗