M. Praga et al., Absence of hypoalbuminemia despite massive proteinuria in focal segmental glomerulosclerosis secondary to hyperfiltration, AM J KIDNEY, 33(1), 1999, pp. 52-58
We observed that some patients do not develop hypoalbuminemia despite the p
resence of massive proteinuria. To investigate whether the absence or prese
nce of hypoalbuminemia could be a marker in the distinction between idiopat
hic focal segmental glomerulosclerosis (FSG) and FSG secondary to hyperfilt
ration, we reviewed all our patients with biopsy-proven FSG and persistent
nephrotic-range proteinuria (>3.5 g/24 h), Patients who met these condition
s were then separated into those with hypoalbuminemia (serum albumin level
<3 g/dL; group I; n = 19) and those with normoalbuminemia (>3.5 g/24 h; gro
up II; n = 18). All group I patients had nephrotic edema in contrast with t
he absence of edema in all group II patients. Serum cholesterol and triglyc
eride levels were significantly greater in group I. All group I patients ha
d been diagnosed with idiopathic FSG, The diagnoses of group II patients we
re FSG secondary to massive obesity in eight patients (44%), vesicoureteral
reflux in five patients (27%), and renal mass reduction in three patients
(16%); only two patients (11%) in this group had idiopathic FSG, The case h
istories of 19 other patients with nephrotic-range proteinuria associated w
ith hyperfiltering disorders (reflux nephropathy, massive obesity, renal ma
ss reduction), but without renal biopsy, were also reviewed; despite massiv
e proteinuria (5.8 +/- 3.1 g/24 h), serum albumin and total protein levels
were always within normal values. In conclusion, patients with FSG secondar
y to hyperfiltration do not develop hypoalbuminemia or the other characteri
stic complications of nephrotic syndrome, despite the presence of massive p
roteinuria values. (C) 1999 by the National Kidney Foundation, Inc.