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Decreased excretion of urine glycosaminoglycans as marker in renal amyloidosis

Tencer, Jan LU ; Torffvit, O LU ; Grubb, Anders LU orcid ; Björnsson, S LU ; Thysell, H LU and Rippe, B LU (1997) In Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 12(6). p.1161-1166
Abstract

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... (More)

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.

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author
; ; ; ; and
publishing date
type
Contribution to journal
publication status
published
keywords
Adult, Aged, Aged, 80 and over, Albuminuria/complications, Amyloidosis/diagnosis, Biomarkers/urine, Creatinine/urine, Female, Glycosaminoglycans/urine, Humans, Kidney Diseases/diagnosis, Kidney Glomerulus, Male, Middle Aged
in
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
volume
12
issue
6
pages
6 pages
publisher
Oxford University Press
external identifiers
  • pmid:9198045
  • scopus:0030982032
ISSN
0931-0509
DOI
10.1093/ndt/12.6.1161
language
English
LU publication?
no
id
892d1221-848f-4a61-86b7-b2217f92278e
date added to LUP
2021-10-29 11:19:11
date last changed
2024-06-01 19:51:55
@article{892d1221-848f-4a61-86b7-b2217f92278e,
  abstract     = {{<p>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.</p><p>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.</p><p>RESULTS: The median urine GAG to creatinine ratio and the median fractional GAG excretion were significantly decreased (P &lt; 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.</p><p>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.</p>}},
  author       = {{Tencer, Jan and Torffvit, O and Grubb, Anders and Björnsson, S and Thysell, H and Rippe, B}},
  issn         = {{0931-0509}},
  keywords     = {{Adult; Aged; Aged, 80 and over; Albuminuria/complications; Amyloidosis/diagnosis; Biomarkers/urine; Creatinine/urine; Female; Glycosaminoglycans/urine; Humans; Kidney Diseases/diagnosis; Kidney Glomerulus; Male; Middle Aged}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{1161--1166}},
  publisher    = {{Oxford University Press}},
  series       = {{Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association}},
  title        = {{Decreased excretion of urine glycosaminoglycans as marker in renal amyloidosis}},
  url          = {{http://dx.doi.org/10.1093/ndt/12.6.1161}},
  doi          = {{10.1093/ndt/12.6.1161}},
  volume       = {{12}},
  year         = {{1997}},
}