Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/133939
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dc.titleThe pathology of mesangial IgA nephritis with clinical correlation
dc.contributor.authorSinniah, R.
dc.contributor.authorJavier, A.R.
dc.contributor.authorKu, G.
dc.date.accessioned2016-12-20T08:41:42Z
dc.date.available2016-12-20T08:41:42Z
dc.date.issued1981
dc.identifier.citationSinniah, R., Javier, A.R., Ku, G. (1981). The pathology of mesangial IgA nephritis with clinical correlation. Histopathology 5 (5) : 469-490. ScholarBank@NUS Repository.
dc.identifier.issn03090167
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/133939
dc.description.abstractOf 710 patients in whom renal biopsies with immunofluorescence, light and electron microscopic and clinical data were available, 239 had idiopathic mesangial IgA nephritis. In these 239 cases IgA was found alone in 45.7%, accompanied by IgG in 50.1%, IgM in 21.4%, C3 in 82.4% and fibrin in 37.2%. Serum immunoglobulin levels including IgA were not significantly raised, and complement C3 activation was via the alternative pathway. There was a wide range of glomerular lesions with minor change, minor change with focal and segmental lesions including sclerosis and mesangial cell hypercellularity, diffuse mesangial cell proliferation and, infrequently, diffuse sclerosing glomerulonephritis. The glomerular lesions were related to the stage, duration and severity of the disease. There was also a wide variability of clinical presentations, with asymptomatic and symptomatic microscopic haematuria-proteinuria, macroscopic haematuria, recurrent proteinuria, nephrotic syndrome, acute nephritis, hypertension, and uncommonly as acute renal failure and potassium losing nephritis. No aetiological agent was found, and both the streptococcus and HB[s]Ag could not be identified. The disease(s) was the commonest type of primary glomerulonephritis (33.7%) in Singapore, another geographic area in addition to Japan and France, where this lesion has an apparent high incidence.
dc.typeArticle
dc.contributor.departmentPATHOLOGY
dc.description.sourcetitleHistopathology
dc.description.volume5
dc.description.issue5
dc.description.page469-490
dc.description.codenHISTD
dc.identifier.isiutNOT_IN_WOS
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