PREVALENCE OF HYPERURICAEMIA AND OTHER CORRELATES OF KIDNEY IMPAIRMENT IN CARIBBEAN PATIENTS WITH CHRONIC NONCOMMUNICABLE DISEASES

Main Article Content

SALEH IDRIS TUDUN WADA

Abstract

Background: Hyperuricaemia is an independent risk factor for the decline in kidney function, and its incidence increases with the progression of estimated glomerular filtration rate (eGFR) staging.

Aims: The aim is to study hyperuricaemia and its correlates in patients with chronic noncommunicable diseases in a developing economy.

Methods: This is a retrospective study conducted between January 2014 and December 2014 comprising of a total of 968 patients with diabetes, hypertension, cardiovascular diseases and chronic kidney disease. Blood sample collected from each subject was analysed for glucose, serum uric acid, blood urea nitrogen, serum creatinine, lipid profile, liver enzymes and albumin. Anthropometric indices such as height, weight, waist circumference, age, gender, education, occupation, and medical history including medications were obtained from each subject.

Results: Compared to patients with normal serum uric acid (SUA) levels, patients with raised SUA levels have higher mean age, systolic blood pressure (SBP), SUA, blood urea nitogen (BUN), triglycerides, albumin, and very low density lipoprotein cholesterol (VLDL) and lower mean value of estimated glomerular filtration rate (e-GFR) (P = 0.05). Correlation studies between SUA, e-GFR, BUN, serum creatinine, body mass index, (BMI), waist circumsference (WC) and albumin shows strong association between SUA and these parameters (p <.0001). About 223 (23.34%) of the chronic kidney disease (CKD) patients have raised uric acid levels and 745 (76.96%) have normal uric acid levels.

Conclusion: This study further emphasizes the well established association between hyperuricaemia and chronic kidney disease. However, the measures already put in place in the lifestyle clinics need to be sustained to check any trend towards increase in serum uric acid levels in the patients.

Keywords:
Chronic noncommunicable diseases, chronic kidney disease, diabetes, glomerular filtration rate, nucleotide, purine, uric acid.

Article Details

How to Cite
WADA, S. I. T. (2021). PREVALENCE OF HYPERURICAEMIA AND OTHER CORRELATES OF KIDNEY IMPAIRMENT IN CARIBBEAN PATIENTS WITH CHRONIC NONCOMMUNICABLE DISEASES. Journal of International Research in Medical and Pharmaceutical Sciences, 16(1), 10-18. Retrieved from https://ikpresse.com/index.php/JIRMEPS/article/view/5921
Section
Original Research Article

References

Fraser S, Blakeman T. Chronic kidney disease: identification and management in primary care. Pragmat Obs Res. 2016;7:21–32.

Jha V, Garcia-Garcia G, Iseki K, Li Z, Naicker S, Plattner B, et al. Chronic kidney disease: Global dimension and perspectives. Lancet. 2013;382(9888):260–272.

Foreman KJ, Marquez N, Dolgert A, Fukutaki K, Fullman N, McGaughey M, et al. Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: reference and alternative scenarios for 2016–40 for 195 countries and territories. Lancet. 2018;392(10159):2052–2090.

Stanifer JW, Jing B, Tolan S, Helmke N, Mukerjee R, Naicker S, et al. The epidemiology of chronic kidney disease in sub-Saharan Africa: a systematic review and meta-analysis. Lancet Glob Health. 2014;15:205.

Stanifer JW, Maro V, Egger J, Karia F, Thielman N, Turner N, et al. The epidemiology of chronic kidney disease in Northern Tanzania: a population-based survey. PLoS One. 2015;10:e0124506.

Seck SM, Doupa D, Gueye L, Charles Dia. Epidemiology of chronic kidney disease in northern region of Senegal: a community-based study in 2012. Pan Afr Med. J. 2014;18:307.

Kumagai T, Ota T, Tamura Y, Chang WX, Shibata S, Uchida S. Time to target uric acid to retard CKD progression. Clin Exp Nephrol. 2017;21:182–192.

Srivastava A, Kaze AD, McMullan CJ, Isakova T, Waikar SS. Uric acid and the risks of kidney failure and death in individuals with CKD. Am J Kidney Dis. 2018;71:362–370.

Miyaoka T, Mochizuki T, Takei T, Tsuchiya K, Nitta K. Serum uric acid levels and long-term outcomes in chronic kidney disease. Heart Vessel. 2014;29:504–12.

Toda A, Ishizaka Y, Tani M, Yamakado M. Hyperuricemia is a significant risk factor for the onset of chronic kidney disease. Nephron Clin Pract. 2014;126:33–8.

Ohta Y, Tsuchihashi T, Kiyohara K, Oniki H. Increased uric acid promotes decline of the renal function in hypertensive patients: a 10-year observational study. Intern Med. 2013; 52:1467–72.

Yan D, Tu Y, Jiang F, Wang J, Zhang R, Sun X, Wang T, Wang S, Bao Y, Hu C, Jia W. Uric acid is independently associated with diabetic kidney disease: a cross-sectional study in a chinese population. PLoS One. 2015;10:e129797.

Weiner DE, Tighiouart H, Elsayed EF, Griffith JL, Salem DN, Levey AS. Uric acid and incident kidney disease in the community. J Am Soc Nephrol. 2008;19:1204–11.

Goicoechea M, de Vinuesa SG, Verdalles U, et al. Effect of allopurinol in chronic kidney disease progression and cardiovascular risk. Clin J Am Soc Nephrol 2010;5:1388–1393.

Miao Y, Ottenbros SA, Laverman GD, et al. Effect of a reduction in uric acid on renal outcomes during losartan treatment: A post hoc analysis of the reduction of endpoints in non-insulin-dependent diabetes mellitus with the Angiotensin II Antagonist Losartan Trial. Hypertension. 2011;58:2–7.

Ficociello LH, Rosolowsky ET, Niewczas MA, et al. High-normal serum uric acid increases risk of early progressive renal function loss in type 1 diabetes: Results of a 6-year follow-up. Diabetes Care. 2010;33:1337–1343.

Pilemann-Lyberg S, Hansen TW, Persson F, et al. Uric acid is not associated with diabetic nephropathy and other complications in type 1 diabetes. Nephrol Dial Transplant. 2019;4:659–666.

Pilemann-Lyberg S, Lindhardt M, Persson F, Andersen S, Rossing P. Serum uric acid and progression of diabetic nephropathy in type 1 diabetes. J Diabetes Complications. 2018;32:470–473.

Liu WC, Hung CC, Chen SC, et al. Association of hyperuricemia with renal outcomes, cardiovascular disease, and mortality. Clin J Am Soc Nephrol. 2012;7:541–548.

Hovind P, Rossing P, Johnson RJ, Parving HH. Serum uric acid as a new player in the development of diabetic nephropathy. J Ren Nutr. 2011;21:124-7.

Iseki K, Ikemiya Y, Inoue T, Iseki C, Kinjo K, Takishita S. Significance of hyperuricemia as a risk factor for developing ESRD in a screened cohort. Am J Kidney Dis. 2004;44:642-50.

Siu YP, Leung KT, Tong MK, Kwan TH. Use of allopurinol in slowing the progression of renal disease through its ability to lower serum uric acid level. Am J Kidney Dis. 2006;47:51-9.

Jung DH, Lee YJ, Lee HR, Lee JH, Shim JY. Association of renal manifestations with serum uric acid in Korean adults with normal uric acid levels. J Korean Med Sci. 2010;25:1766-70.

Wheeler JG, Juzwishin KD, Eiriksdottir G, Gudnason V, Danesh J. Serum uric acid and coronary heart disease in 9,458 incident cases and 155,084 controls: prospective study and meta-analysis. PLoS Med. 2005;2:e76.

Verzola D, Ratto E, Villaggio B et al.,. Uric acid promotes apoptosis in human proximal tubule cells by oxidative stress and activation of NAPDH oxidase NOX 4. PLoS ONE. 2014;9(12):e115210.

Sánchez-Lozada LG, Tapia E, Santamaría J et al. Mild hyperuricemia induces vasoconstriction and maintains glomerular hypertension in normal and remnant kidney rats. Kidney Internationa. 2005;67(1):237–247.

Kanbay M, Yilmaz MI, Sonmez A et al. Serum uric acid level and endothelial dysfunction in patients with nondiabetic chronic kidney disease. American Journal of Nephrology. 2011;33(4):298–304.

Adeera L, Paul ES, Rudy WB, Josef C, Angel LMD, Paul EDJ, et al. Kidney disease improving global outcomes (KDIGO): KDIGO clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2013;3(Suppl 1):1-150.

Levey AS, Stevens LA, Schmidt CH, Zhang YL, Castro AF, Feldman HI, et al. Chronic kidney disease epidemiology collaboration. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604-12.

Oh TR, Choi HS, Kim CS, et al. Hyperuricemia has increased the risk of progression of chronic kidney disease: propensity score matching analysis from the KNOW-CKD study. Sci Rep. 2019;9(1):1–9.

Li L-X, Dong X-H, Li M-F, et al. Serum uric acid levels are associated with hypertension and metabolic syndrome but not atherosclerosis in Chinese inpatients with type 2 diabetes. J Hypertens. 2015;33(3):482.

Lytvyn Y, Skrtic M, Yang GK, Yip PM, Perkins BA, Cherney DZ. Glycosuria-mediated urinary uric acid excretion in patients with uncomplicated type 1 diabetes mellitus. Am J Physiol Renal Physiol. 2015;308:F77–83.

Li F, Guo H, Zou J, Chen W, Lu Y, Zhang X, Fu C, Xiao J, Ye Z. The association of urinary sodium and potassium with renal uric acid excretion in patients with chronic kidney disease. Kidney Blood Press Res. 2018;43:1310–21.

Kuo C-F., Grainge MJ, Zhang W, Doherty M. Global epidemiology of gout: prevalence, incidence and risk factors. Nature Reviews Rheumatology. 2015;11:649–662 (2015).

Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007–2008. Arthritis & Rheumatology 2011;63:3136–3141.

Liu H, Zhang XM, Wang YL, Liu BC. Prevalence of hyperuricemia among Chinese adults: a national cross-sectional survey using multistage, stratified sampling. Journal of Nephrology. 2014;27:653–658.

Palmer TM, Nordestgaard BG, Benn M et al., Association of plasma uric acid with ischaemic heart disease and blood pressure: Mendelian randomisation analysis of two large cohorts. BMJ. 2013;347:(1) f4262.

Borgi L, McMullan C, Wohlhueter A, Curhan GC, Fisher ND, Forman JP. Effect of uric acid-lowering agents on endothelial function: a randomized, double-blind, placebo-controlled trial. Hypertension. 2017;69(2):243–248.

McMullan CJ, Borgi L, Fisher N, Curhan G, Forman J. Effect of uric acid lowering on renin-angiotensin-system activation and ambulatory BP: a randomized controlled trial. Clinical Journal of the American Society of Nephrology. 2017;12 (5):807–816.

Sturm G, Kollerits B, Neyer U, Ritz E, Kronenberg F, MMKD Study Group. Uric acid as a risk factor for progression of non-diabetic chronic kidney disease? The Mild to Moderate Kidney Disease (MMKD) Study. Exp Gerontol. 2008; 43(4): 347-352.

Kodama S, Saito K, Yachi Y, et al. Association between serum uric acid and development of type 2 diabetes. Diabetes Care. 2009; 32(9):1737-1742.

Naseer MA, Omar SA. Kaiser AW, Majid SA. Serum uric acid to creatinine ratio and risk of metabolic syndrome in saudi Type 2 Diabetic Patients. Nature Scientific Report 2017;7(1).

Fox IH. Adenosine triphosphate degradation in specific disease. J Clin Med. 1985;106:101-10.

Fox IH. Metabolic basis for disorders of purine nucleotide degradation. Metabolism. 1981; 30:616-34.

Fox IH, Kelley WN. Studies on the mechanism of fructose induced hyperuricaemai in man. Matabolism. 1972;21:713-21.

Faller J, Fox IH. Ethanol induced hyperuricaemia. Evidence for increasd urate production by activation of adenine nucleotide turnover. N Engl J Med. 1982;307:1598-602.

Jalal DI, Chonchol M, Chen W, et al. Uric acid as a target of therapy in CKD. Am J Kidney Dis. 2013;61:134–146.

Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007–2008. Arthritis & Rheumatology. 2011;63:3136–3141.

Marie D, Marie P, Jude M, et al. Determinants of hyperuricemia in nondialysed chronic kidkney disease patients in three hospitals in Cameroon. BMC Nephrology. 2018;19:169.

Adejumo OA, Okaka EI, Madumezia G, et al. Assessment of some cardiovascular risk factors in predialysis chronic kidney disease patients in Southern Nigeria. Niger Med J. 2015;56:394–399.

Kim Y, Kang J and Kim GT. Prevalence of hyperuricemia and its associated factors in the general Korean population: an analysis of a population-based nationally representative sample. Clin Rheumatol. 2018;37:2529–2538.

Hediger MA, Johnson RJ, Miyazaki H, et al. Molecular physiology of urate transport. Physiology. 2005;20:125–133.