The relationship between hyperuricemia and contrast-induced acute kidney injury undergoing primary percutaneous coronary intervention: secondary analysis protocol for the ATTEMPT RESCIND-1 study

Wei Guo, Feier Song, Shiqun Chen, Li Zhang, Guoli Sun, Jin Liu, Jiyan Chen, Yong Liu, Ning Tan, RESCIND group, Wei Guo, Feier Song, Shiqun Chen, Li Zhang, Guoli Sun, Jin Liu, Jiyan Chen, Yong Liu, Ning Tan, RESCIND group

Abstract

Background: Contrast-induced acute kidney injury (CI-AKI) contributes toward unfavorable clinical outcomes after primary percutaneous coronary intervention (pPCI). We will assess whether hyperuricemia is an independent predictor of CI-AKI and outcomes in patients undergoing pPCI.

Methods/design: Our study is a secondary analysis for the database from ATTEMPT study, enrolling 560 ST-segment elevation myocardial infarction (STEMI) patients undergoing pPCI. Patients will be divided into 2 groups according to the admission serum uric acid (SUA) level. Hyperuricemia will be defined as a SUA level > 7 mg/dL (417 mmol/L) in males and > 6 mg/dL (357 mmol/L) in females. The primary endpoint was CI-AKI, defined as > 25% or 0.5 mg/dL increase in serum creatinine from baseline during the first 48-72 h post-procedurally. Multivariate analyses for CI-AKI and long-term mortality will be performed using the logistic regression and Cox regression analyses, respectively.

Discussion: This study will determine the predictive value of hyperuricemia for the development of CI-AKI and outcomes in patients with STEMI undergoing pPCI. We predict that hyperuricemia will be associated with a risk of CI-AKI in patients with pPCI. Furthermore, after adjusting for other variables, long-term mortality after pPCI may be higher in those with hyperuricemia than in those with normouricemia. Results of this study may provide scientific evidence for the effect of hyperuricemia on CI-AKI and long-term outcomes, thereby offering the potential possibility of lowering SUA on the development of CI-AKI and outcomes.

Trial registration: ClinicalTrials.gov NCT02067195, Registered on 20 February 2014.

Keywords: Contrast-induced acute kidney; Hyperuricemia; Primary percutaneous coronary intervention; ST-segment elevation myocardial infarction.

Conflict of interest statement

The authors declare that they have no competing interests.

References

    1. Marenzi G, Lauri G, Assanelli E, et al. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction. J Am Coll Cardiol. 2004;44:1780–1785. doi: 10.1016/j.jacc.2004.07.043.
    1. Goldberg A, Hammerman H, Petcherski S, et al. Inhospital and 1-year mortality of patients who develop worsening renal function following acute ST-elevation myocardial infarction. Am Heart J. 2005;150:330–337. doi: 10.1016/j.ahj.2004.09.055.
    1. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004;44:1393–1399.
    1. Kanbay M, Segal M, Afsar B, et al. The role of uric acid in the pathogenesis of human cardiovascular disease. Heart. 2013;99:759–766. doi: 10.1136/heartjnl-2012-302535.
    1. Borghi C, Rosei EA, Bardin T, et al. Serum uric acid and the risk of cardiovascular and renal disease. J Hypertens. 2015;33:1729–1741. doi: 10.1097/HJH.0000000000000701.
    1. Guo W, Liu Y, Chen J-Y, et al. Hyperuricemia is an independent predictor of contrast-induced acute kidney injury and mortality in patients undergoing percutaneous coronary intervention. Angiology. 2015;66:721–726. doi: 10.1177/0003319714568516.
    1. Liu Y, Tan N, Chen J, et al. The relationship between hyperuricemia and the risk of contrast-induced acute kidney injury after percutaneous coronary intervention in patients with relatively normal serum creatinine. Clinics (Sao Paulo) 2013;68:19–25. doi: 10.6061/clinics/2013(01)OA04.
    1. Barbieri L, Verdoia M, Schaffer A, et al. Uric acid levels and the risk of contrast induced nephropathy in patients undergoing coronary angiography or PCI. Nutr Metab Cardiovasc Dis. 2015;25:181–186. doi: 10.1016/j.numecd.2014.08.008.
    1. Kanbay M, Solak Y, Afsar B, et al. Serum uric acid and risk for acute kidney injury following contrast. Angiology. 2017;68:132–144. doi: 10.1177/0003319716644395.
    1. Park S-H, Shin W-Y, Lee E-Y, et al. The impact of hyperuricemia on in-hospital mortality and incidence of acute kidney injury in patients undergoing percutaneous coronary intervention. Circ J. 2011;75:692–697. doi: 10.1253/circj.CJ-10-0631.
    1. Toprak O, Cirit M, Esi E, et al. Hyperuricemia as a risk factor for contrast-induced nephropathy in patients with chronic kidney disease. Catheter Cardiovasc Interv. 2006;67:227–235. doi: 10.1002/ccd.20598.
    1. Toprak O, Cirit M, Yesil M, et al. Impact of diabetic and pre-diabetic state on development of contrast-induced nephropathy in patients with chronic kidney disease. Nephrol Dial Transplant. 2007;22:819–826. doi: 10.1093/ndt/gfl636.
    1. Zuo T, Jiang L, Mao S, et al. Hyperuricemia and contrast-induced acute kidney injury: a systematic review and meta-analysis. Int J Cardiol. 2016;224:286–294. doi: 10.1016/j.ijcard.2016.09.033.
    1. Karabulut A, Sahin I, Ilker Avci I, et al. Impact of serum alkaline phosphatase level on the pathophysiologic mechanism of contrast-induced nephropathy. Kardiol Pol. 2014;72:977–982. doi: 10.5603/KP.a2014.0072.
    1. Kowalczyk J, Francuz P, Swoboda R, et al. Prognostic significance of hyperuricemia in patients with different types of renal dysfunction and acute myocardial infarction treated with percutaneous coronary intervention. Nephron Clin Pract. 2010;116:c114–c122. doi: 10.1159/000314660.
    1. Elbasan Z, Sahin DY, Gur M, et al. Contrast-induced nephropathy in patients with ST elevation myocardial infarction treated with primary percutaneous coronary intervention. Angiology. 2014;65:37–42. doi: 10.1177/0003319712463816.
    1. Mendi MA, Afsar B, Oksuz F, et al. Uric acid is a useful tool to predict contrast-induced nephropathy. Angiology. 2016;68:627–632. doi: 10.1177/0003319716639187.
    1. Saritemur M, Turkeli M, Kalkan K, et al. Relation of uric acid and contrast-induced nephropathy in patients undergoing primary percutaneous coronary intervention in the ED. Am J Emerg Med. 2014;32:119–123. doi: 10.1016/j.ajem.2013.10.011.
    1. Liu Y, Chen JY, Huo Y, et al. Aggressive hydraTion in patients with ST-Elevation Myocardial infarction undergoing Primary percutaneous coronary intervention to prevenT contrast-induced nephropathy (ATTEMPT): Study design and protocol for the randomized, controlled trial, the ATTEMPT, RESCIND 1 (First study for REduction of contraSt-induCed nephropathy followINg carDiac catheterization) trial. Am Heart J. 2016;172:88–95. doi: 10.1016/j.ahj.2015.10.007.
    1. Tan N, Liu Y, Chen JY, et al. Use of the contrast volume or grams of iodine-to-creatinine clearance ratio to predict mortality after percutaneous coronary intervention. Am Heart J. 2013;165:600–608. doi: 10.1016/j.ahj.2012.12.017.
    1. Narula A, Mehran R, Weisz G, et al. Contrast-induced acute kidney injury after primary percutaneous coronary intervention: results from the HORIZONS-AMI substudy. Eur Heart J. 2014;35:1533–1540. doi: 10.1093/eurheartj/ehu063.
    1. Zoungas S, Ninomiya T, Huxley R, et al. Systematic review: sodium bicarbonate treatment regimens for the prevention of contrast-induced nephropathy. Ann Intern Med. 2009;151:631–638. doi: 10.7326/0003-4819-151-9-200911030-00008.
    1. Bhatt H, Turkistani A, Sanghani D, Julliard K, Fernaine G. Do cardiovascular risk factors and coronary SYNTAX score predict contrast volume use during cardiac catheterization? Angiology. 2015;66:933–940. doi: 10.1177/0003319715573909.
    1. Krishnan E, Svendsen K, Neaton JD, et al. Long-term cardiovascular mortality among middle-aged men with gout. Arch Intern Med. 2008;168:1104–1110. doi: 10.1001/archinte.168.10.1104.
    1. Kuo CF, See LC, Luo SF, et al. Gout: an independent risk factor for all-cause and cardiovascular mortality. Rheumatology (Oxford) 2010;49:141–146. doi: 10.1093/rheumatology/kep364.
    1. Pagidipati NJ, Hess CN, Clare RM, et al. An examination of the relationship between serum uric acid level, a clinical history of gout, and cardiovascular outcomes among patients with acute coronary syndrome. Am Heart J. 2017;187:53–61. doi: 10.1016/j.ahj.2017.02.023.
    1. Tscharre M, Herman R, Rohla M, et al. Uric acid is associated with long-term adverse cardiovascular outcomes in patients with acute coronary syndrome undergoing percutaneous coronary intervention. Atherosclerosis. 2018;270:173–179. doi: 10.1016/j.atherosclerosis.2018.02.003.
    1. Sautin YY, Nakagawa T, Zharikov S, et al. Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress. Am J Physiol Cell Physiol. 2007;293:C584–C596. doi: 10.1152/ajpcell.00600.2006.
    1. Corry DB, Eslami P, Yamamoto K, et al. Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin-angiotensin system. J Hypertens. 2008;26:269–275. doi: 10.1097/HJH.0b013e3282f240bf.
    1. Kang DH, Park SK, Lee IK, et al. Uric acid-induced C-reactive protein expression: implication on cell proliferation and nitric oxide production of human vascular cells. J Am Soc Nephrol. 2005;16:3553–3562. doi: 10.1681/ASN.2005050572.
    1. Kanbay M, Yilmaz MI, Sonmez A, et al. Serum uric acid level and endothelial dysfunction in patients with nondiabetic chronic kidney disease. Am J Nephrol. 2011;33:298–304. doi: 10.1159/000324847.

Source: PubMed

3
订阅