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Dive into the research topics where Anthony E. Seymour is active.

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Featured researches published by Anthony E. Seymour.


Pathology | 1980

Vascular IgA deposits in clinically normal skin of patients with renal disease

Aileen J. Thompson; Y-L. Chan; Andrew J. Woodroffe; A. R. Clarkson; Anthony E. Seymour

&NA; Direct immunofluorescent tests for IgA deposits were done on biopsies of normal appearing skin from 49 patients with proven renal disease and 7 healthy individuals, in order to evaluate the method in the diagnosis of IgA nephropathy. Many of the 28 patients with IgA nephropathy had high levels of IgA deposition, often accompanied by notable deposits of IgM, Clq and fibrin, and less frequently by C3 and IgG, in small vessels of the superficial dermis. However, some of the 21 patients with other renal diseases had heavy deposits of IgA, limiting the usefulness of the test as a diagnostic aid.


Springer Seminars in Immunopathology | 1982

Mesangial IgA nephritis

Andrew J. Woodroffe; A. R. Clarkson; Anthony E. Seymour; Jane D. Lomax-Smith

SummaryCurrent data suggest that mesangial IgA nephritis is mediated by the mesangial deposition of soluble antigen-IgA class antibody complexes from the circulation. It is likely that common infectious gut flora and dietary antigens contribute to the immune complex load. Defects in antigen exclusion at the mucosa, in the control of IgA production, and in immune complex clearance are postulated to account for each of the recognized clinical syndromes. As yet no effective treatment is available, and a detailed analysis of the mediation pathways will be required before prevention or therapy can be attempted.


Pathology | 1985

IgA nephropathy--accumulated experience and current concepts.

Jane D. Lomax-Smith; Andrew J. Woodroffe; A. R. Clarkson; Anthony E. Seymour

&NA; Primary IgA nephropathy is the most common form of glomerulonephritis in Australia. The condition presents in a variety of ways, but commonly with synpharyngitic hematuria, most often in young men in the third and fourth decades. The course of the disease is indolent but there is progression to renal failure in up to one quarter of cases. Renal biopsy morphology is variable but the essential immunofluorescence finding is diffuse mesangial IgA staining of greater intensity but often in association with other immunoglobulins. C3 is usually also present. Mesangial cellularity is increased in some two‐thirds of cases, one third being of a minor focal or variable extent and one‐third diffuse. Focal segmental lesions, hyaline nodules and vascular changes are frequent. Crescents are also often present. The etiology of the disease is uncertain but has been linked with HLA antigens, elevated serum IgA levels, IgA polymers, immune complexes and impaired T cell function. Secondary forms of mesangial IgA deposition occur with mucosal defects, hyperglobulinemia or impaired hepatobiliary clearance, and these may offer some insight into the immunopathogenesis of the primary disease.


Pathology | 1987

Mitomycin c associated hemolytic uremic syndrome

Sanjiv Jain; Anthony E. Seymour

&NA; Mitomycin C associated Hemolytic Uremic Syndrome (HUS) is a potentially fatal but uncommon condition that is not yet widely recognised. It consists of microangiopathic hemolytic anemia, thrombocytopenia and progressive renal failure associated with mitomycin C treatment and affects about 10% of patients treated with this agent. The renal failure usually develops about 8‐10 mth after start of mitomycin C treatment and the mortality is approximately 60% from renal failure or pulmonary edema. Renal lesions are similar to those seen in idiopathic HUS and include arteriolar fibrin thrombi, expanded subendothelial zones in glomerular capillary walls, ischemic wrinkling of glomerular basement membranes and mesangiolysis. The mechanism of action is postulated as mitomycin C‐induced endothelial cell damage. We describe the clinical course and pathological findings in a 65 yr‐old man with gastric adenocarcinoma who developed renal failure and thrombocytopenia while on treatment with mitomycin C and died in pulmonary edema.


Pathology | 1985

Glomerulonephritis: Approaches to Classification

Anthony E. Seymour

&NA; Glomerulonephritis has many mechanisms and may take a variety of patterns. Almost as many classifications of glomerulonephritis exist as there have been classifiers. None is perfect. Morphological classification of glomerulonephritis is inadequate alone but provides useful information about the pattern of response to the injurious mechanism and may allow accurate assessment of prognosis. In this paper some approaches to the classification of glomerulonephritis are discussed, the major categories are reviewed and a prognostic method of classification is proposed.


Kidney International | 1980

Immunologic studies in IgA nephropathy

Andrew J. Woodroffe; Alan A. Gormly; Peter E. McKenzie; Andrew M. Wootton; Aileen J. Thompson; Anthony E. Seymour; A. R. Clarkson


Australian and New Zealand Journal of Medicine | 1979

Serum immune complexes and disease.

Andrew J. Woodroffe; M. Foldes; P. E. McKenzie; Aileen J. Thompson; Anthony E. Seymour; A. R. Clarkson


Australian and New Zealand Journal of Medicine | 1980

GUT‐DERIVED ANTIGENS AND IMMUNE COMPLEXES IN IgA NEPHROPATHY

P.E. McKenzie; Alan A. Gormly; A. R. Clarkson; Anthony E. Seymour; A.O. Kwitko; D. J. C. Shearman; Andrew J. Woodroffe


Australian and New Zealand Journal of Medicine | 1980

IMMUNE COMPLEX (IgA) GLOMERULONEPHRITIS ASSOCIATED WITH CIRRHOSIS

A.A. Gornily; P.E. McKenzie; A. R. Clarkson; Anthony E. Seymour; J. Lorna‐Smith; D. Rowley; Andrew J. Woodroffe


Australian and New Zealand Journal of Medicine | 1980

CONTROLLED TRIAL OF PHENYTOIN THERAPY IN IgA NEPHROPATHY

A. R. Clarkson; Anthony E. Seymour; Andrew J. Woodroffe; P.E. McKenzie; Y‐L. Chan; A.M. Wootton.

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A.O. Kwitko

Royal Adelaide Hospital

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M. Foldes

Royal Adelaide Hospital

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