title: Decreased excretion of glycosaminoglycans in patients with primary glomerular diseases.
abstract: Urine glycosaminoglycans (GAG) concentrations were measured in 150 patients with primary glomerulonephritides: endocapillary glomerulonephritis, mesangial proliferative glomerulonephritis, IgA nephropathy, membranous glomerulonephritis and minimal change nephropathy, and in 63 healthy controls and 19 patients with diabetes nephropathy. The urine GAG to creatinine ratios (GCR) were significantly reduced (p < 0.01) in all the glomerulonephritides investigated (0.20 mg/mmol in endocapillary glomerulonephritis, 1.60 mg/mmol in mesangial proliferative glomerulonephritis, 1.74 mg/mmol in IgA nephropathy, 1.09 mg/mmol in membranous nephropathy, and 1.16 mg/mmol in minimal change nephropathy) compared to healthy controls (2.87 mg/mmol) but not compared to diabetes patients (1.17 mg/mmol). Also, the GCR in a group of 23 non-albuminuric glomerulonephritis patients (1.98 mg/mmol) was shown to be significantly decreased (p < 0.01) compared to healthy controls. Moreover, the GCR was significantly lower (p < 0.01) in endocapillary glomerulonephritis than in any of the other diseases studied. The GAG excretion per functioning 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 excretion in glomerulonephritides, obtained in the present study, might be a consequence of decreased synthesis or turnover of GAG in the functioning nephrons whereas the mechanisms for the reduced GAG excretion in diabetes nephropathy might be of a different nature. Urinary GAG excretion in this group of glomerular disorders and particularly in endocapillary glomerulonephritis, may lead to new approaches in non-invasive renal diagnostics and, particularly with regard to the differentiation of acute and chronic forms of glomerulonephritides.
authors.affiliation: Department of Nephrology, Lund University Hospital, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Tencer
authors.forename: O
authors.initials: O
authors.lastname: Torffvit
authors.forename: S
authors.initials: S
authors.lastname: Björnsson
authors.forename: H
authors.initials: H
authors.lastname: Thysell
authors.forename: A
authors.initials: A
authors.lastname: Grubb
authors.forename: B
authors.initials: B
authors.lastname: Rippe
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D000510:Alpha-Globulins / Q000652:urine; D003404:Creatinine / Q000097:blood; D003928:Diabetic Nephropathies / Q000652:urine*; D005260:Female; D005921:Glomerulonephritis / Q000652:urine*; D005922:Glomerulonephritis, IGA / Q000652:urine*; D006025:Glycosaminoglycans / Q000652:urine*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009402:Nephrosis, Lipoid / Q000652:urine*; D011480:Protease Inhibitors / Q000652:urine; D012709:Serum Albumin / Q000032:analysis; D012737:Sex Factors
chemical_list: D000510:Alpha-Globulins; D006025:Glycosaminoglycans; D011480:Protease Inhibitors; D012709:Serum Albumin; C016001:alpha-1-microglobulin; D003404:Creatinine