Hyperhomocyst(e)inemia is an independent risk factor for atherothrombosis i
n several clinical settings in which renal function is impaired, but its pr
evalence in the nephrotic syndrome has not been investigated in detail, eve
n though this syndrome provides an excellent model in which to study a poss
ible link between albuminuria, proteinuria, and hyperhomocyst(e)inemia. We
obtained plasma and urine from 27 patients with biopsy-confirmed membranous
glomerulonephritis presenting nephrotic syndrome and 27 matched controls a
nd determined the concentrations of homocyst(e)ine and proteins considered
putative markers of glomerular and tubular function. Hyperhomocyst(e)inemia
, defined as the mean +SD of the plasma homocyst(e)ine concentration of the
controls [plasma homocyst(e)ine concentration >10.8 mu mol/l] was present
in 26% of the patients with nephrotic syndrome but in only 7.4% of the cont
rols. Furthermore, the degree of hyperhomocyst(e)inemia was more severe in
the nephrotic patients than in the controls, The existence of renal failure
, tubular damage, and, interestingly, relatively well conserved glomerular
function barrier were the main predictors of increased levels of plasma hom
ocyst(e)ine. In conclusion, hyper homocyst(e)inemia is a frequent cardiovas
cular risk factor present in patients with nephrotic syndrome and renal fai
lure, but it is not directly associated with proteinuria.