Characterization of proteinuria in asymptomatic family members and household contacts of children with hepatitis B virus-associated membranous nephropathy
R. Bhimma et al., Characterization of proteinuria in asymptomatic family members and household contacts of children with hepatitis B virus-associated membranous nephropathy, AM J KIDNEY, 37(1), 2001, pp. 125-133
The biosocial background in which the hepatitis B virus (HBV) carrier state
with membranous nephropathy (MN) develops was studied by evaluating HBV ca
rriage and proteinuria among 195 family members and household contacts of 3
1 index HBV carrier children with MN. Unrelated individuals from the commun
ities of these index cases who were negative for HBV served as controls (n
= 123), HBV was determined by using third-generation enzyme-linked immunoso
rbent assay, slot-blot hybridization, and nested polymerase chain reaction.
Patterns of proteinuria were determined by using sodium dodecyl sulfate-po
lyacrylamide gel electrophoresis; immunoglobulin G and haptoglobulin were s
uggestive of MN, Seventy-two members (36.9%) of the study group (n = 195) w
ere HBV carriers; 21 of these carriers (29.2%) had proteinuria. Twenty eigh
t members (41.2%) of the study group who were HBV negative (n = 68) and 26.
8% of the controls showed proteinuria, This lack of association between HBV
carriage and proteinuria remained when controlled for sex and family relat
ionship. HBV was not protective against the development of proteinuria. Pro
teinuria suggestive of MN was strongly associated with an abnormal protein-
creatinine ratio (P = 0.001), but was not significantly different between s
ubjects and controls (8.7% Versus 6.5%; P = 0.5). Genetic influences or env
ironmental exposures in these subjects may be responsible for the proteinur
ia, suggesting underlying glomerular basement membrane damage. Discordance
between the HBV carrier state and patterns of proteinuria in the study grou
p suggest that HBV and MN may not be causally related or may reflect except
ional interaction between specifically Vulnerable individuals and HBV, (C)
2001 by the National Kidney Foundation, Inc.