For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
24
views
120
references
 Top references
cited by
16
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      512
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Uric Acid and Arterial Stiffness

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Hyperuricemia is usually associated with hypertension, diabetes mellitus, metabolic syndrome and chronic kidney disease. Accumulating data from epidemiological studies indicate an association of increased uric acid (UA) with cardiovascular diseases. Possible pathogenic mechanisms include enhancement of oxidative stress and systemic inflammation caused by hyperuricemia. Arterial stiffness may be one of the possible pathways between hyperuricemia and cardiovascular disease, but a clear relationship between increased UA and vascular alterations has not been confirmed. The review summarizes the epidemiological studies investigating the relationship between UA and arterial stiffness and highlights the results of interventional studies evaluating arterial stiffness parameters in patients treated with UA-lowering drugs.

          Most cited references120

          • Record: found
          • Abstract: found
          • Article: not found

          Prediction of cardiovascular events and all-cause mortality with arterial stiffness: a systematic review and meta-analysis.

          Charalambos Vlachopoulos, Konstantinos Aznaouridis, Christodoulos Stefanadis (2010)
          The purpose of this study was to calculate robust quantitative estimates of the predictive value of aortic pulse wave velocity (PWV) for future cardiovascular (CV) events and all-cause mortality by meta-analyses of longitudinal studies. Arterial stiffness is increasingly recognized as a surrogate end point for CV disease. We performed a meta-analysis of 17 longitudinal studies that evaluated aortic PWV and followed up 15,877 subjects for a mean of 7.7 years. The pooled relative risk (RR) of clinical events increased in a stepwise, linear-like fashion from the first to the third tertile of aortic PWV. The pooled RRs of total CV events, CV mortality, and all-cause mortality were 2.26 (95% confidence interval: 1.89 to 2.70, 14 studies), 2.02 (95% confidence interval: 1.68 to 2.42, 10 studies), and 1.90 (95% confidence interval: 1.61 to 2.24, 11 studies), respectively, for high versus low aortic PWV subjects. For total CV events and CV mortality, the RR was significantly higher in high baseline risk groups (coronary artery disease, renal disease, hypertension) compared with low-risk subjects (general population). An increase in aortic PWV by 1 m/s corresponded to an age-, sex-, and risk factor-adjusted risk increase of 14%, 15%, and 15% in total CV events, CV mortality, and all-cause mortality, respectively. An increase in aortic PWV by 1 SD was associated with respective increases of 47%, 47%, and 42%. Aortic stiffness expressed as aortic PWV is a strong predictor of future CV events and all-cause mortality. The predictive ability of arterial stiffness is higher in subjects with a higher baseline CV risk.
          Article 0 comments Cited 565 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Transforming growth factor beta in tissue fibrosis.

            W Border, N Noble (1994)
            Article 0 comments Cited 486 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A role for uric acid in the progression of renal disease.

              Duk-Hee Kang, Takahiko Nakagawa, Lili Feng … (2002)
              Hyperuricemia is associated with renal disease, but it is usually considered a marker of renal dysfunction rather than a risk factor for progression. Recent studies have reported that mild hyperuricemia in normal rats induced by the uricase inhibitor, oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury. This led to the hypothesis that uric acid may contribute to progressive renal disease. To examine the effect of hyperuricemia on renal disease progression, rats were fed 2% OA for 6 wk after 5/6 remnant kidney (RK) surgery with or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone. Renal function and histologic studies were performed at 6 wk. Given observations that uric acid induces vascular disease, the effect of uric acid on vascular smooth muscle cells in culture was also examined. RK rats developed transient hyperuricemia (2.7 mg/dl at week 2), but then levels returned to baseline by week 6 (1.4 mg/dl). In contrast, RK+OA rats developed higher and more persistent hyperuricemia (6 wk, 3.2 mg/dl). Hyperuricemic rats demonstrated higher BP, greater proteinuria, and higher serum creatinine than RK rats. Hyperuricemic RK rats had more renal hypertrophy and greater glomerulosclerosis (24.2 +/- 2.5 versus 17.5 +/- 3.4%; P < 0.05) and interstitial fibrosis (1.89 +/- 0.45 versus 1.52 +/- 0.47; P < 0.05). Hyperuricemic rats developed vascular disease consisting of thickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were significantly more severe than a historical RK group with similar BP. Allopurinol significantly reduced uric acid levels and blocked the renal functional and histologic changes. Benziodarone reduced uric acid levels less effectively and only partially improved BP and renal function, with minimal effect on the vascular changes. To better understand the mechanism for the vascular disease, the expression of COX-2 and renin were examined. Hyperuricemic rats showed increased renal renin and COX-2 expression, the latter especially in preglomerular arterial vessels. In in vitro studies, cultured vascular smooth muscle cells incubated with uric acid also generated COX-2 with time-dependent proliferation, which was prevented by either a COX-2 or TXA-2 receptor inhibitor. Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease. These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression.
              Article 0 comments Cited 278 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Ther Clin Risk Manag
                Journal ID (iso-abbrev): Ther Clin Risk Manag
                Journal ID (publisher-id): TCRM
                Journal ID (pmc): tcriskman
                Title: Therapeutics and Clinical Risk Management
                Publisher: Dove
                ISSN (Print): 1176-6336
                ISSN (Electronic): 1178-203X
                Publication date (Electronic): 28 January 2020
                Publication date Collection: 2020
                Volume: 16
                Pages: 39-54
                Affiliations
                [1 ]2nd Department of Internal Medicine
                [2 ]4th Department of Internal Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy , Cluj-Napoca, Romania
                Author notes
                Correspondence: Ioana Para 4th Department of Internal Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy , 8 Babes Street, Cluj-Napoca400012, Romania Email ioana.para@yahoo.com
                Article
                Publisher ID: 232033
                DOI: 10.2147/TCRM.S232033
                PMC ID: 6995306
                PubMed ID: 32095074
                SO-VID: 3330422a-dbc2-4170-8f63-e7b43b709661
                Copyright © © 2020 Albu et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 22 September 2019
                Date accepted : 01 December 2019
                Page count
                Figures: 1, References: 154, Pages: 16
                Categories
                Subject: Review

                ScienceOpen disciplines: Medicine
                Keywords: uric acid,arterial stiffness,cardiovascular risk
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: uric acid, arterial stiffness, cardiovascular risk

                Comments

                Comment on this article

                scite_

                Similar content512

                See all similar

                Cited by16

                See all cited by

                Most referenced authors2,079

                See all reference authors