Nephrology Dialysis Transplantation, Vol 12, Issue 6 1161-1166, Copyright © 1997 by Oxford University Press
J Tencer, O Torffvit, A Grubb, S Bjornsson, H Thysell and B Rippe
Background. The diagnosis of renal amyloidosis is
normally established by kidney biopsy. In order to advance the
determination of the diagnosis and the initiation of the therapy, fast and
cheap, non-invasive diagnostic techniques are required.
Methods. Urine excretion of glycosaminoglycans (GAG)
was measured in 10 patients with AA amyloidosis and 5 patients with AL
amyloidosis and compared to 25 controls with primary glomerular diseases
and 22 healthy controls. The subjects with primary glomerular disease were
matched with regard to their renal function and the degree of albuminuria.
Results. The median urine GAG to creatinine ratio and
the median fractional GAG excretion were significantly decreased
(P<0.05) in both AA amyloidosis (0.21 mg/mmol
and 0.053 respectively) and AL amyloidosis (0.33 mg/mmol and 0.077
respectively) compared to control patients with primary glomerular disease
(1.73 mg/mmol and 0.336 respectively) and healthy controls (2.67 mg/mmol
and 0.226 respectively). The urine GAG to creatinine ratio did not
correlate to age, sex, serum creatinine, urine albumin, or to the plasma
levels of acute phase proteins. Conclusions. The
decreased GAG excretion in renal amyloidosis is probably caused both by
diminished number of functioning nephrons, decreased GAG synthesis in
functioning glomeruli, and the trapping of GAG by amyloid fibrils. Urinary
GAG excretion may serve as an independent marker of renal amyloidosis. It
may be used in diagnostic work-up of renal amyloidosis in patients with
glomerular diseases and in screening of amyloidosis in patients with
chronic inflammatory disorders, with or without signs of renal disease.
Keywords: AA amyloidosis; AL amyloidosis, glomerular
disease; glycosaminoglycans
ORIGINAL ARTICLES
Decreased excretion of urine glycosaminoglycans as marker in renal amyloidosis
Department of Nephrology, Division of Diabetology and Endocrinology, Department of Clinical Chemistry, Division of Clinical Chemistry, Lund University Hospital, S-221 85 Lund, Sweden; Vaxjo Central Hospital, S-351 85 Vaxjo, Sweden; Corresponding author
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