ArticleDiabetes2013
ADAMTS13 predicts renal and cardiovascular events in type 2 diabetic patients and response to therapy.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
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- Association of a disintegrin and metalloproteinase with a thrombospondin type 1 motif member 13 polymorphisms with severity of coronary stenosis in type 2 diabetes mellitus.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2018Article
- ADAMTS13 Retards Progression of Diabetic Nephropathy by Inhibiting Intrarenal Thrombosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- ADAMTS13 activity as a novel risk factor for incident type 2 diabetes mellitus: a population-based cohort study.Diabetologia · 2017Article
- The Role of von Willebrand Factor in Vascular Inflammation: From Pathogenesis to Targeted Therapy.Mediators of inflammation · 2017Review
- Regulation of VWF expression, and secretion in health and disease.Current opinion in hematology · 2016Review
- Von Willebrand Factor, ADAMTS13 and D-Dimer Are Correlated with Different Levels of Nephropathy in Type 1 Diabetes Mellitus.PloS one · 2015Article
- Genetics of diabetes complications.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Review
- Article
- Plasma von Willebrand Factor and a Disintegrin and Metalloproteinase with Eight Thrombospondin-type 1 Motif Levels in Hemodialysis Patients: Relation to Vascular Access Thrombosis.Indian journal of nephrologyArticle
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16 authors at 5 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
In patients with diabetes, impaired ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13) proteolysis of highly thrombogenic von Willebrand factor (VWF) multimers may accelerate renal and cardiovascular complications. Restoring physiological VWF handling might contribute to ACE inhibitors' (ACEi) reno- and cardioprotective effects. To assess how Pro618Ala ADAMTS13 variants and related proteolytic activity interact with ACEi therapy in predicting renal and cardiovascular complications, we genotyped 1,163 normoalbuminuric type 2 diabetic patients from BErgamo NEphrologic DIabetes Complications Trial (BENEDICT). Interaction between Pro618Ala and ACEi was significant in predicting both renal and combined renal and cardiovascular events. The risk for renal or combined events versus reference Ala carriers on ACEi progressively increased from Pro/Pro homozygotes on ACEi (hazard ratio 2.80 [95% CI 0.849-9.216] and 1.58 [0.737-3.379], respectively) to Pro/Pro homozygotes on non-ACEi (4.77 [1.484-15.357] and 1.99 [0.944-4.187]) to Ala carriers on non-ACEi (8.50 [2.416-29.962] and 4.00 [1.739-9.207]). In a substudy, serum ADAMTS13 activity was significantly lower in Ala carriers than in Pro/Pro homozygotes and in case subjects with renal, cardiovascular, or combined events than in diabetic control subjects without events. ADAMTS13 activity significantly and negatively correlated with all outcomes. In patients with diabetes, ADAMTS13 618Ala variant associated with less proteolytic activity, higher risk of chronic complications, and better response to ACEi therapy. Screening for Pro618Ala polymorphism may help identify patients with diabetes at highest risk who may benefit the most from early reno- and cardioprotective therapy.
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