ArticleJournal of clinical pathology1993
Beta 2-glycoprotein-1 (apolipoprotein H) excretion and renal tubular malfunction in diabetic patients without clinical proteinuria.
Article in Journal of clinical pathology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Renal impairment markers in type 2 diabetes patients with different types of hyperuricemia.Journal of diabetes investigation · 2019Article
- The application of post-translational modification oriented serum proteomics to assess experimental diabetes with complications.PloS one · 2018Article
- Transcriptional Profile of Kidney from Type 2 Diabetic db/db Mice.Journal of diabetes research · 2017Article
- Etiopathology of chronic tubular, glomerular and renovascular nephropathies: clinical implications.Journal of translational medicine · 2011Review
- Identification of diagnostic urinary biomarkers for acute kidney injury.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2010Article
- Serum N-acetyl-beta-D-glucosaminidase profiles in type 1 diabetes secondary complications: causes of changes and significance of determination.Journal of clinical laboratory analysis · 2008Article
- Identification of urinary proteins potentially associated with diabetic kidney disease.Indian journal of nephrologyArticle
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Authors and funding
3 authors.
Funding
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Abstract
aimTo compare the urinary excretion of beta 2-glycoprotein-1 with that of two other markers of early tubular disorder in diabetic patients without clinical proteinuria.
methodsThe urinary excretion of retinol binding protein, beta 2-glycoprotein-1, and N-acetyl-beta-D-glucosaminidase was measured in 90 known diabetic patients who had a negative reagent strip test for proteinuria.
resultsAmong 43 patients with urinary albumin excretion within the reference range, 23 (53%) had raised urinary N-acetyl-beta-D-glucosaminidase activity, five (12%) increased excretion of beta 2-glycoprotein-1, and five (12%) increased loss of retinol binding protein. Among 47 patients with an albumin excretion of 0.9-7.9 mg/mmol creatinine, 42 (89%) had increased urinary N-acetyl-beta-D-glucosaminidase, 23 (49%) an increased output of beta 2-glycoprotein-1, and 16 (34%) a raised excretion of retinol binding protein. The excretion of these markers of tubular defects seldom exceeded two and a half times the upper reference limit and the differences between the findings in the insulin dependent and non-insulin dependent patients with similar albumin excretion were small and insignificant.
conclusionsIn diabetic patients with a negative dipstick test for proteinuria: (a) assay of urinary beta 2-glycoprotein-1 may be a more sensitive test for the detection of impaired tubular reabsorption of protein than measurement of retinol-binding protein; (b) assay of N-acetyl-beta-D-glucosaminidase can detect tubular injury at a time when protein reabsorption remains normal; and (c) impaired renal tubular function may be present in the absence of evidence of glomerular malfunction.
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