Nephrotic syndrome in Namibian children

Citation
Aj. Van Buuren et al., Nephrotic syndrome in Namibian children, S AFR MED J, 89(10), 1999, pp. 1088-1091
Citations number
12
Categorie Soggetti
General & Internal Medicine
Journal title
SOUTH AFRICAN MEDICAL JOURNAL
ISSN journal
02569574 → ACNP
Volume
89
Issue
10
Year of publication
1999
Pages
1088 - 1091
Database
ISI
SICI code
0256-9574(199910)89:10<1088:NSINC>2.0.ZU;2-0
Abstract
Background and objectives. Patterns of nephrotic syndrome vary between regi ons 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 stud y was to document the clinical, pathological and outcome features of nephro tic syndrome in Namibian children. Subjects. Seventy black Namibian children with nephrotic syndrome were mana ged from 1975 to 1988. Sixty-eight renal specimens (67 biopsies and 1 autop sy 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 m embranous glomerulonephritis (MGN), 1 mesangiocapillary glomerulonephritis (MCGN), and 1 focal segmental glomerulosclerosis (FSCS); 1 child in advance d renal failure was not biopsied. Five children (7.4%) showed minimal chang e disease (MCD), 11 (16.2%) FSGS and 15 (22.1%) diffuse mesangial prolifera tive glomerulonephritis (DMP). The remaining 10 children showed diffuse glo merulosclerosis (6), MCGN (3) and endocapillary proliferative GN (1). Four of the 5 children with MCD went into remission on immunosuppressive treatme nt. Of the 15 with DMP, 4 improved spontaneously and only 1 of those treate d did not improve. Only 2 of those with FSGS improved on treatment. The chi ldren with HBV-associated MGN and MCGN were offered symptomatic rather than specific treatment. Thirteen children presented with degrees of chronic re nal failure. Eight are known to have died, 3 of relentless nephrotic syndro me and 4 (of whom 3 were HBV carriers) of end-stage renal failure. One chil d died of penicillin anaphylaxis. Conclusions. The pattern of nephrotic syndrome in black Namibian children d iffered greatly from the non-African pattern elsewhere in that MCD was unco mmon and HBV-associated GN was the most common single group. The most frequ ent pattern of HBV-associated GN was MGN with some mesangiocapillary featur es showing marked male predominance. MCD and DMP were potentially treatable and could only be identified by biopsy. HBV carrier rates exert a major in fluence on the proportions of morphological subgroups of nephrotic syndrome in children. As these HBV carrier rates alter in future due to the influen ce of vaccination and urbanisation, the relative size of nephrotic subgroup s seems likely to alter.