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REVIEW PAPER
Gout, hyperuricemia and chronic kidney disease: New treatment possibilities
1
3rd Department of Internal Medicine and Nephrology, Regional Specialist Hospital, Włocławek, Poland
2
Department of Nephrology, Hypertension and Internal Medicine, Faculty of Medical Sciences, University of Warmia and Mazury in Olsztyn, Poland
Submission date: 2016-02-18
Acceptance date: 2016-04-07
Online publication date: 2016-05-04
Publication date: 2020-03-24
Corresponding author
Tomasz Stompór
Department of Nephrology, Hypertension and Internal Medicine, Medical Faculty, University of Warmia and Mazury in Olsztyn, Żołnierska 18, 10-561 Olsztyn, Poland. Tel.: +48 89 5386219; fax: +48 89 5386550.
Department of Nephrology, Hypertension and Internal Medicine, Medical Faculty, University of Warmia and Mazury in Olsztyn, Żołnierska 18, 10-561 Olsztyn, Poland. Tel.: +48 89 5386219; fax: +48 89 5386550.
Pol. Ann. Med. 2016;23(2):195-201
KEYWORDS
ABSTRACT
Introduction:
Gout remains one of the most frequent diseases of joints and soft tissues. Apart from symptomatic gout, uric acid is also involved in pathogenesis and progression of several other diseases such as chronic kidney disease, hypertension, metabolic syndrome and cardiovascular disease.
Aim:
To describe the role of uric acid in the development of chronic diseases such as chronic kidney disease, hypertension, metabolic syndrome and cardiovascular disease. We also aimed to discuss the role of uric acid in the development of gout, considered the most typical manifestation of hyperuricemia. The important task of our work was also identification of 'classical' and newest therapeutic strategies aimed to lower uric acid level and to improve the diseases that might be triggered with hyperuricemia.
Material and methods:
We searched the latest literature in the field identifying studies describing the different roles of uric acid in the development of several diseases. We also found and described latest clinical trials focused on therapeutic lowering of hyperuricemia.
Results and discussion:
Increasing evidence suggests contribution of uric acid in the development of chronic diseases, including chronic kidney disease, cardiovascular disease, hypertension and metabolic syndrome. The development of these pathologies may be controlled by effective lowering of hyperuricemia using both 'classical' drugs (i.e. allopurinol) and the newer agents (i.e. febuxostat).
Conclusions:
Uric acid contributes to the development of several chronic, potentially lifethreatening diseases. Hyperuricemia control should be considered as one of the strategies in their treatment.
Gout remains one of the most frequent diseases of joints and soft tissues. Apart from symptomatic gout, uric acid is also involved in pathogenesis and progression of several other diseases such as chronic kidney disease, hypertension, metabolic syndrome and cardiovascular disease.
Aim:
To describe the role of uric acid in the development of chronic diseases such as chronic kidney disease, hypertension, metabolic syndrome and cardiovascular disease. We also aimed to discuss the role of uric acid in the development of gout, considered the most typical manifestation of hyperuricemia. The important task of our work was also identification of 'classical' and newest therapeutic strategies aimed to lower uric acid level and to improve the diseases that might be triggered with hyperuricemia.
Material and methods:
We searched the latest literature in the field identifying studies describing the different roles of uric acid in the development of several diseases. We also found and described latest clinical trials focused on therapeutic lowering of hyperuricemia.
Results and discussion:
Increasing evidence suggests contribution of uric acid in the development of chronic diseases, including chronic kidney disease, cardiovascular disease, hypertension and metabolic syndrome. The development of these pathologies may be controlled by effective lowering of hyperuricemia using both 'classical' drugs (i.e. allopurinol) and the newer agents (i.e. febuxostat).
Conclusions:
Uric acid contributes to the development of several chronic, potentially lifethreatening diseases. Hyperuricemia control should be considered as one of the strategies in their treatment.
CONFLICT OF INTEREST
None declared.
REFERENCES (47)
1.
Zimmermann-Górska I. Present possibilities of therapies for gout. Reumatologia. 2009;47(2):75–81 [in Polish].
2.
Gińdzieńska-Sieśkiewicz E, Sierakowski S, Domysławska I, Sulik A. Gout: the current look at diagnostics and treatment. Reumatologia. 2010;48(6):425–428 [in Polish].
3.
Jaszczyk B, Wisłowska M. Treatment of gout in patients after organ transplantation. Reumatologia. 2013;51(3):215–220 [in Polish].
4.
Enomoto A, Kimura H, Chairoungdua A, et al. Molecular identification of a renal urate–anion exchanger that regulates blood urate levels. Nature. 2002;417(6887):447–452.
5.
Majdan M, Borys O. DNA i schorzenia towarzyszące podwyższonemu stężeniu kwasu moczowego. Ann Acad Med Stetin. 2010;56(suppl 1):34–39.
6.
Asim K, Mandal DBM. The molecular physiology of uric acid homeostasis. Annu Rev Physiol. 2014;77:323–345. http://dx.doi.org/10.1146/annu....
7.
Martillo MA, Nazzal L, Crittenden DB. The crystallization of monosodium urate. Curr Rheumatol Rep. 2014;16(2):1–8.
8.
Angielski S. [The kidney morphology, biochemistry, and clinical physiology]. In: Angielski S, Rogulski J, eds. [Clinical Biochemistry]. Warszawa: PZWL; 1991:641–698 [in Polish].
9.
Majdan M. Gout – new diagnostic and therapeutic options. Reumatologia. 2013;51(1):1–8 [in Polish].
11.
Zoppini G, Targher G, Chonchol M, et al. Serum uric acid levels and incident chronic kidney disease in patients with type 2 diabetes and preserved kidney function. Diabetes Care. 2012;35(1):99–104.
12.
Zhang W, Doherty M, Pascual E, et al. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1301–1311.
13.
Roddy E, Choi HK. Epidemiology of gout. Rheum Dis Clin North Am. 2014;40(2):155–175.
14.
Sadowska J, Rygielska M. Technological and health aspects of using high fructose syrup in food production. ZNTJ. 2014;3(94):14–26 [in Polish].
15.
Zgaga L, Theodoratou E, Kyle J, et al. The association of dietary intake of purine-rich vegetables, sugar-sweetened beverages and dairy with plasma urate, in a cross-sectional study. PLoS ONE. 2012;7(6):e38123. http://dx.doi.org/10.1371/jour....
16.
Kretowicz M, Goszka G, Brymora A, Flisiński M, Odrowąż-Sypniewska G, Manitius J. [Is there a relationship between daily consumption of fructose and blood pressure and uric acid levels in patients with chronic kidney disease without diabetes?]. Nadciśnienie Tętnicze. 2011;15(6):341–346 [in Polish].
17.
Jin M, Yang F, Yang I, et al. Uric acid, hyperuricemia and vascular diseases. Front Biosci J Virtual Libra. 2012;17:656–669.
19.
Wilson FP, Berns JS. Onco-nephrology: tumor lysis syndrome. Clin J Am Soc Nephrol. 2012;7(10):1730–1739.
21.
Nijenhuis T, Vallon V, van der Kemp AW, Loffing J, Hoenderop JG, Bindels RJ. Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia. J Clin Invest. 2005;115(6):1651–1658.
22.
Januszkiewicz-Caulier J, Franek E. Uric acid in kidney and cardiovascular diseases. Chor Serca Naczyń. 2011;8(1):31–37 [in Polish].
23.
Choi H, Atkinson K, Karlson E, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow-up study. Arch Intern Med. 2005;165(7):742–748.
24.
Kostka-Jeziorny K, Tykarski A. Relationship between hyperuricemia and other cardiovascular risk factors in patients with essential, untreated arterial hypertension in the population of RISK study. Nadciśnienie Tętnicze. 2008;12(3):190–199 [in Polish].
25.
Johnson RJ, Nakagawa T, Jalal D, Sanchez-Lozada LG, Kang D-H, Ritz E. Uric acid and chronic kidney disease: which is chasing which? Nephrol Dial Transplant. 2013;28(9):2221–2228.
26.
Jalal DI, Rivard CJ, Johnson RJ, et al. Serum uric acid levels predict the development of albuminuria over 6 years in patients with type 1 diabetes: findings from the coronary artery calcification in type 1 diabetes study. Nephrol Dial Transplant. 2010;25(6):1865–1869.
27.
Madero M, Sarnak MJ, Wang X, et al. Uric acid and long-term outcomes in CKD. Am J Kidney Dis. 2009;53(5):796–803.
28.
Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee For International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1312–1324.
29.
Jordan KM, Cameron JS, Snaith M, et al. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of gout. Rheumatology. 2007;46(8):1372–1374.
30.
Khanna D, Khanna PP, Fitzgerald JD, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res. 2012;64(10):1447–1461.
31.
KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Chapter 3: Management of progression and complications of CKD. Kidney Int Suppl. 2013;3(1):73–90.
32.
Khanna D, Fitzgerald JD, Khanna PP, et al. American College of Rheumatology guidelines for management of gout. Part 1: Systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res. 2012;64(10):1431–1446.
33.
Gigiel E, Hrycaj P. New drugs for gout. Reumatologia. 2009;47(6):344–347 [in Polish].
34.
Schumacher HR, Becker MA, Wortmann RL, et al. Effects of febuxostat versus allopurinol and placebo in reducing serum urate in subjects with hyperuricemia and gout: a 28-week, phase III, randomized, double-blind, parallelgroup trial. Arthritis Care Res. 2008;59(11):1540–1548.
35.
Becker MA, Schumacher HR, Wortmann RL, et al. Febuxostat, a novel nonpurine selective inhibitor of xanthine oxidase: a twenty-eight-day, multicenter, phase II, randomized, double-blind, placebo-controlled, dose–response clinical trial examining safety and efficacy in patients with gout. Arthritis Rheum. 2005;52(3):916–923.
36.
Okamoto K, Eger BT, Nishino T, Pai EF, Nishino T. Mechanism of inhibition of xanthine oxidoreductase by allopurinol: crystal structure of reduced bovine milk xanthine oxidoreductase bound with oxipurinol. Nucleosides Nucleotides Nucleic Acids. 2008;27(6–7):888–893.
37.
Becker MA, Schumacher Jr HR, Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353(23):2450–2461.
38.
Becker MA, Schumacher HR, Espinoza LR, et al. The uratelowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial. Arthritis Res Ther. 2010;12(2):R63. http://dx.doi.org/10.1186/ar29....
39.
Shibagaki Y, Ohno I, Hosoya T, Kimura K. Safety, efficacy and renal effect of febuxostat in patients with moderateto-severe kidney dysfunction. Hypertens Res. 2014;37(10):919–925.
40.
Sakai Y, Otsuka T, Ohno D, Murasawa T, Sato N, Tsuruoka S. Febuxostat for treating allopurinol-resistant hyperuricemia in patients with chronic kidney disease. Ren Fail. 2013;36(2):225–231.
41.
Naka T, Sumiyoshi A, Ando T, Shibuya M, Masuyama T. Effect of treatment of hyperuricemia with febuxostat in hypertensive patients with chronic heart failure and chronic kidney disease. Cardiology. 2015;131(Suppl. 2):147.
42.
Tojimbara T, Nakajima I, Yashima J, Fuchinoue S, Teraoka S. Efficacy and safety of febuxostat, a novel nonpurine selective inhibitor of xanthine oxidase for the treatment of hyperuricemia in kidney transplant recipients. Transplant Proc. 2014;46(2):511–513.
43.
Stamp LK, Chapman PT. Gout and its comorbidities: implications for therapy. Rheumatology. 2013;52(1):34–44.
44.
Tohkin M, Kaniwa N, Saito Y, et al. A whole-genome association study of major determinants for allopurinol-related Stevens–Johnson syndrome and toxic epidermal necrolysis in Japanese patients. Pharmacogenomics J. 2013;13(1):60–69.
45.
Becker MA, Schumacher HR, MacDonald PA, Lloyd E, Lademacher C. Clinical efficacy and safety of successful longterm urate lowering with febuxostat or allopurinol in subjects with gout. J Rheumatol. 2009;36(6):1273–1282.
46.
Schumacher H, Becker M, Lloyd E, MacDonald P, Lademacher C. Febuxostat in the treatment of gout: 5-yr findings of the FOCUS efficacy and safety study. Rheumatology. 2009;48(2):188–194.
47.
Schlesinger N, Yasothan U, Kirkpatrick P. Pegloticase. Nat Rev Drug Discov. 2011;10(1):17–18.
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