J. Tencer et al., DECREASED EXCRETION OF GLYCOSAMINOGLYCANS IN PATIENTS WITH PRIMARY GLOMERULAR-DISEASES, Clinical nephrology, 48(4), 1997, pp. 212-219
Urine glycosaminoglycans (GAG) concentrations were measured in 150 pat
ients with primary glomerulonephritides: endocapillary glomerulonephri
tis, mesangial proliferative glomerulonephritis, IgA nephropathy, memb
ranous glomerulonephritis and minimal change nephropathy, and in 63 he
althy controls and 19 patients with diabetes nephropathy. The urine GA
G to creatinine ratios (GCR) were significantly reduced (p < 0.01) in
all the glomerulonephritides investigated (0.20 mg/mmol in endocapilla
ry glomerulonephritis, 1.60 mg/mmol in mesangial proliferative glomeru
lonephritis, 1.74 mg/mmol in IgA nephropathy, 1.09 mg/mmol in membrano
us nephropathy and 1.16 mg/mmol in minimal change nephropathy compared
to healthy controls (2.87 mg/mmol) but not compared to diabetes patie
nts (1.17 mg/mmol). Also, the GCR in a group of 23 non-albuminuric glo
merulonephritis patients (1.98 mg/mmol) was shown to be significantly
decreased (p < 0.01) compared to healthy controls. Moreover, the GCR w
as significantly lower (p < 0.01) in endocapillary glomerulonephritis
than in any of the other diseases studied. The GAG excretion per funct
ioning glomerular area, calculated as fractional GAG excretion (FGE),
was decreased in all the glomerulonephritides investigated compared to
both healthy controls and diabetes nephropathy. The decreased GAG exc
retion in glomerulonephritides, obtained in the present study, might b
e a consequence of decreased synthesis or turnover of GAG in the funct
ioning nephrons whereas the mechanisms for the reduced GAG excretion i
n diabetes nephropathy might be of a different nature. Urinary GAG exc
retion in this group of glomerular disorders and particularly in endoc
apillary glomerulonephritis, may lead to new approaches in non-invasiv
e renal diagnostics and, particularly with regard to the differentiati
on of acute and chronic forms of glomerulonephritides.