Nephrotic syndrome in Namibian children

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dc.contributor.authorVan Buuren, A. J.en_ZA
dc.contributor.authorBates, W. D.en_ZA
dc.contributor.authorMuller, N.en_ZA
dc.date.accessioned2011-03-18T14:59:28Z
dc.date.available2011-03-18T14:59:28Z
dc.date.issued1999
dc.descriptionThe original publication is available at http://www.samj.org.za
dc.descriptionCITATION: Van Buuren, A. J., Bates, W. D. & Muller, N. 1999. Nephrotic syndrome in Namibian children. South African Medical Journal, 89(10):1088-1091.
dc.description.abstractBackground and objectives. Patterns of nephrotic syndrome vary between regions and countries, and influence approaches to management. In the mid-1970s the University of Stellenbosch became involved in providing tertiary care to Namibia, including a paediatric nephrology service. The aim of this study was to document the clinical, pathological and outcome features of nephrotic syndrome in Namibian children. Subjects. Seventy black Namibian children with nephrotic syndrome were managed from 1975 to 1988. Sixty-eight renal specimens (67 biopsies and 1 autopsy specimen) were evaluated. Results. Twenty-nine of the 70 children (41.4%) were hepatitis B virus (HBV) carriers, of whom 25 (86.2%) were male. Of the 29, 26 had predominantly membranous glomerulonephritis (MGN), 1 mesangiocapillary glomerulonephritis (MCGN), and 1 focal segmental glomerulosclerosis (FSGS); 1 child in advanced renal failure was not biopsied. Five children (7.4%) showed minimal change disease (MCD), 11 (16.2%) FSGS and 15 (22.1%) diffuse mesangial proliferative glomerulonephritis (DMP). The remaining 10 children showed diffuse glomerulosclerosis (6), MCGN (3) and endocapillary proliferative GN (1). Four of the 5 children with MCD went into remission on immunosuppressive treatment. Of the 15 with DMF, 4 improved spontaneously and only 1 of those treated did not improve. Only 2 of those with FSGS improved on treatment. The children with HBV-associated MGN and MCGN were offered symptomatic rather than specific treatment. Thirteen children presented with degrees of chronic renal failure. Eight are known to have died, 3 of relentless nephrotic syndrome and 4 (of whom 3 were HBV carriers) of end-stage renal failure. One child died of penicillin anaphylaxis. Conclusions. The pattern of nephrotic syndrome in black Namibian children differed greatly from the non-African pattern elsewhere in that MCD was uncommon and HBV-associated GN was the most common single group. The most frequent pattern of HBV-associated GN was MGN with some mesangiocapillary features showing marked male predominance. MCD and DMP were potentially treatable and could only be identified by biopsy. HBV carrier rates exert a major influence on the proportions of morphological subgroups of nephrotic syndrome in children. As these HBV carrier rates alter in future due to the influence of vaccination and urbanisation, the relative size of nephrotic subgroups seems likely to alter.
dc.description.versionPublisher’s version
dc.identifier.issn2078-5135 (online)
dc.identifier.issn0256-9574 (print)
dc.identifier.urihttp://hdl.handle.net/10019.1/7853
dc.language.isoen
dc.publisherHealth & Medical Publishing Group
dc.rights.holderSouth African Medical Journal
dc.subjectPediatric nephrologyen_ZA
dc.titleNephrotic syndrome in Namibian childrenen_ZA
dc.typeArticle
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