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      Management of Chronic Kidney Disease: The Relationship Between Serum Uric Acid and Development of Nephropathy

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          Abstract

          Chronic kidney disease (CKD) is increasingly recognized as a global health problem, and new and effective strategies are needed for the management of this condition. Recently, there has been renewed interest in the relationship between serum uric acid (SUA) levels and CKD, and several recent trials have demonstrated a possible link between SUA and the development and/or progression of CKD in patients with and without diabetes. The identification of key urate transporters such as urate transporter 1 and glucose transporter 9 has provided not only insights into the pathophysiology of hyperuricemia, but also possible links to other processes, such as glucose homeostasis. The renewed interest in the role of SUA in CKD has coincided with the development of sodium glucose co-transporter 2 inhibitors for the treatment of diabetes. In addition to improving glycemic control, these agents, acting via the kidneys in an insulin-independent manner, have also been shown to reduce SUA levels and potentially improve some measures of renal function. This review will discuss the role of uric acid in CKD treatment, and how SUA-lowering therapies may prevent or delay the progression of CKD.

          Funding : Janssen Scientific Affairs.

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          The online version of this article (doi:10.1007/s12325-015-0272-7) contains supplementary material, which is available to authorized users.

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          Chronic kidney disease as a global public health problem: approaches and initiatives - a position statement from Kidney Disease Improving Global Outcomes.

          A S Levey, R. Atkins, J Coresh … (2007)
          Chronic kidney disease (CKD) is increasingly recognized as a global public health problem. There is now convincing evidence that CKD can be detected using simple laboratory tests, and that treatment can prevent or delay complications of decreased kidney function, slow the progression of kidney disease, and reduce the risk of cardiovascular disease (CVD). Translating these advances to simple and applicable public health measures must be adopted as a goal worldwide. Understanding the relationship between CKD and other chronic diseases is important to developing a public health policy to improve outcomes. The 2004 Kidney Disease Improving Global Outcomes (KDIGO) Controversies Conference on 'Definition and Classification of Chronic Kidney Disease' represented an important endorsement of the Kidney Disease Outcome Quality Initiative definition and classification of CKD by the international community. The 2006 KDIGO Controversies Conference on CKD was convened to consider six major topics: (1) CKD classification, (2) CKD screening and surveillance, (3) public policy for CKD, (4) CVD and CVD risk factors as risk factors for development and progression of CKD, (5) association of CKD with chronic infections, and (6) association of CKD with cancer. This report contains the recommendations from the meeting. It has been reviewed by the conference participants and approved as position statement by the KDIGO Board of Directors. KDIGO will work in collaboration with international and national public health organizations to facilitate implementation of these recommendations.
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            Molecular identification of a renal urate anion exchanger that regulates blood urate levels.

            Atsushi Enomoto, Hiroaki Kimura, Arthit Chairoungdua … (2002)
            Urate, a naturally occurring product of purine metabolism, is a scavenger of biological oxidants implicated in numerous disease processes, as demonstrated by its capacity of neuroprotection. It is present at higher levels in human blood (200 500 microM) than in other mammals, because humans have an effective renal urate reabsorption system, despite their evolutionary loss of hepatic uricase by mutational silencing. The molecular basis for urate handling in the human kidney remains unclear because of difficulties in understanding diverse urate transport systems and species differences. Here we identify the long-hypothesized urate transporter in the human kidney (URAT1, encoded by SLC22A12), a urate anion exchanger regulating blood urate levels and targeted by uricosuric and antiuricosuric agents (which affect excretion of uric acid). Moreover, we provide evidence that patients with idiopathic renal hypouricaemia (lack of blood uric acid) have defects in SLC22A12. Identification of URAT1 should provide insights into the nature of urate homeostasis, as well as lead to the development of better agents against hyperuricaemia, a disadvantage concomitant with human evolution.
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              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.
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                Author and article information

                Contributors
                Christian Mende: cmende4730@aol.com
                Journal
                Journal ID (nlm-ta): Adv Ther
                Journal ID (iso-abbrev): Adv Ther
                Title: Advances in Therapy
                Publisher: Springer Healthcare (Cheshire )
                ISSN (Print): 0741-238X
                ISSN (Electronic): 1865-8652
                Publication date (Electronic): 9 December 2015
                Publication date PMC-release: 9 December 2015
                Publication date (Print): 2015
                Volume: 32
                Pages: 1177-1191
                Affiliations
                University of California, La Jolla, CA USA
                Article
                Publisher ID: 272
                DOI: 10.1007/s12325-015-0272-7
                PMC ID: 4679778
                PubMed ID: 26650815
                SO-VID: 8fa03700-fc5f-4564-bed7-2ad7bf36dbde
                Copyright © © The Author(s) 2015
                History
                Date received : 9 October 2015
                Funding
                Funded by: Janssen Scientific Affairs, LLC
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Springer Healthcare 2015

                Keywords: chronic kidney disease,diabetes,diabetic nephropathy,nephrology,renoprotection,serum uric acid,sodium glucose co-transporter 2 (sglt 2) inhibitors
                Data availability:
                Keywords: chronic kidney disease, diabetes, diabetic nephropathy, nephrology, renoprotection, serum uric acid, sodium glucose co-transporter 2 (sglt 2) inhibitors

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