Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/134279
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dc.titleRenal glomerular lesions in patients with asymptomatic microscopic haematuria/proteinuria discovered on a routine medical examination
dc.contributor.authorSinniah, R.
dc.contributor.authorPwee, H.S.
dc.contributor.authorLim, C.H.
dc.date.accessioned2016-12-20T08:45:27Z
dc.date.available2016-12-20T08:45:27Z
dc.date.issued1975
dc.identifier.citationSinniah, R., Pwee, H.S., Lim, C.H. (1975). Renal glomerular lesions in patients with asymptomatic microscopic haematuria/proteinuria discovered on a routine medical examination. Annals of the Academy of Medicine Singapore 4 (2 sup) : 11-16. ScholarBank@NUS Repository.
dc.identifier.issn03044602
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/134279
dc.description.abstract145 patients were found during a routine medical examination to have asymptomatic microscopic hematuria. Kidney biopsy was performed and the predominant morphologic change on light microscopy was a diffuse mesangial proliferative glomerulonephritis (GN) (85%). In 80% of cases, there was deposition of immunoglobulins, mainly in the mesangium. The predominant immunoglobulin deposited was IgA (56.2%) and this was found in combination with IgG in 50.0% of all cases studied. Mucin IgA was negative in all cases investigated. Complement C3 was present in 67.8% of all cases studied whereas C1q was negative. Electron microscopy showed the deposits to be predominantly in the mesangium with lesser amounts in the subendothelium of the more severe cases. There were changes in the basement membranes of the capillary loops which may be secondary to the disease process. The changes seen on light and electron microscopy and immunofluorescent antibody studies in the cases with symptomatic microscopic hematuria and gross hematuria were similar to the patients with asymptomatic microscopic hematuria. All three conditions appear to be the spectrum of one disease process which is immunologically mediated. There was utilisation of IgA predominantly, with IgG, and the lesion is mediated through the complement pathway, activating C3 without the utilisation of Clq. Since the completion of this study, 5 patients have developed chronic renal failure indicative of the disease not having a benign course.
dc.typeOthers
dc.contributor.departmentPATHOLOGY
dc.description.sourcetitleAnnals of the Academy of Medicine Singapore
dc.description.volume4
dc.description.issue2 sup
dc.description.page11-16
dc.description.codenAAMSC
dc.identifier.isiutNOT_IN_WOS
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