The presence of monosodium urate deposits in the joints of patients with asymptomatic hyperuricemia is associated with a higher cardiovascular risk, but not with more advanced kidney damage
DOI:
https://doi.org/10.2478/amb-2024-0036Keywords:
articular MSU deposits, asymptomatic hyperuricemia, kidney damageAbstract
Aim: To evaluate the association between asymptomatic hyperuricemia, renal damage and cardiovascular events and to investigate whether the presence of monosodium urate (MSU) deposits in the joints is related to more advanced renal changes and increased
cardiovascular risk. Methods: This was a study on 73 consecutive patients divided into 34 patients with osteoarthritis, 25 subjects with asymptomatic hyperuricemia and no ultrasound (US) evidence of MSU crystals in the joints and 14 individuals with asymptomatic hyperuricemia and MSU deposits in the joints. Patients underwent bilateral US examination of the joints of the hands, elbows, knees, ankles, feet and the kidneys. Routine abdominal ultrasound with evaluation of kidney and parenchymal size and echogenicity and renal vascular indices was performed. The presence of cardiovascular complications in the past was evaluated from the patients‘ history. The study protocol was a continuation of another project from 2013 (14-D2013, approved by the ethics committee of the Medical University – Sofia). Informed consent was obtained from all patients prior to the inclusion in the study. The study was conducted in accordance with the Declaration of Helsinki. Results: The highest proportion of patients with cardiovascular events was detected in the group of asymptomatic hyperuricemia with MSU deposits in the joints. The patients with osteoarthritis had the lowest prevalence of eGFR < 90 ml/min. Renal parenchymal echogenicity and the prevalence of nephrolithiasis were compatible for all groups. Patients with hyperuricemia and MSU deposits in the joints had higher BMI (p = 0.018) and smaller kidney size (p = 0.015) compared to those with osteoarthritis. The comparison of hyperuricemia without MSU deposits in the joints to osteoarthritis group
demonstrated a significant difference only in the age (p = 0.001). Finally, the comparison of the two groups with hyperuricemia showed that subjects with MSU deposits in the joints had higher BMI (p = 0.041) with no difference in the age, kidney size, RRI, eGFR and thickness of renal parenchyma. Conclusions: Hyperuricemia, independent of the presence of articular crystals, is associated with compatible kidney damage. Cardiovascular risk is higher when MSU crystals are detected in the joints using US.
References
Li L, Yang C, Zhao Y, et al. Is hyperuricemia an independent risk factor for new-onset chronic kidney disease? A systematic review and metaanalysis based on observational cohort studies. BMC Nephrol 2014; 15:122.
Weiner DE, Tighiouart H, Elsayed EF, et al. Uric acid and incident kidney disease in the community. J Am Soc Nephrol 2008; 19:1204–11.
Bellomo G, Venanzi S, Verdura C, et al. Association of uric acid with change in kidney function in healthy normotensive individuals. Am J Kidney Dis 2010; 56:264-72.
Bakan A, Oral A, Elcioglu OC, et al. Hyperuricemia is associated with progression of IgA nephropathy. Int Urol Nephrol 2015; 47:673-8.
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; 35:99-104.
Iseki K, Ikemiya Y, Kinjo K, et al. Prevalence of high fasting plasma glucose and risk of developing end-stage renal disease in screened subjects in Okinawa, Japan. Clin Exp Nephrol 2004; 8:250-6.
Rosolowsky ET, Ficociello LH, Maselli NJ, et al. High-normal serum uric acid is associated with impaired glomerular filtration rate in nonproteinuric patients with type 1 diabetes. Clin J Am Soc Nephrol 2008; 3:706-13.
Mazzali M, Hughes J, Kim YG, et al. Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism. Hypertension 2001; 38:1101-6.
Kohagura K, Kochi M, Miyagi T, et al. An association between uric acid levels and renal arteriolopathy in chronic kidney disease: a biopsy-based study. Hypertens Res 2013; 36:43-9.
Dimov D. New knowledge concerning hyperuricemia and gout. Rheumatology 2009; 2.
Bekyarova G, Bratoeva K, Bekyarov N. Uric acid and vascular disorders in metabolic syndrome. Cardiovascular diseases 2013;44(1):40-44.
Chizyński K, Rózycka M. “Hyperuricemia”. Pol. Merkur. Lekarski. 2005, 19 (113): 693-6.
Backhaus M, Burmester GR, Gerber T, et al. Guidelines for musculoskeletal ultrasound in rheumatology. Ann Rheum Dis
; 60:641-9.
Viazzi F, Leoncini G, Derchi LE, Pontremoli R. Ultrasound Doppler renal resistive index: a useful tool for the management of the hypertensive patient. J Hypertens 2014; 32:149-153.
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.
Khosla UM, Zharikov S, Finch JK, et al. Hyperuricemia induces endothelial dysfunction. Kidney Int. 2005; 67:1739-1742.
Anker SD, Leyva F, Poole-Wilson PA, et al. Relation between serum uric acid and lower limb blood flow in patients with chronic heart failure. Heart. 1997, 78:39-43.
Cannon PJ, Stason WB, Demartini FE, et al. Hyperuricemia in primary and renal hypertension. N Engl J Med. 1966, 275:457-464.
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; 26:269-277.
Coutinho Tde A, Turner ST, Peyser PA, et al. Associations of serum uric acid with markers of inflammation, metabolic syndrome, and subclinical coronary atherosclerosis. Am J Hypertens. 2007; 20:83-89.
McAdams MA, Maynard JW, Huizinga M, et al. Younger age at gout onset is related to obesity in a community based cohort. Arthritis Care Res (Hoboken) 2011; 63(8):1108-1114.
Roubenoff R, Klag MJ, Mead LA, et al. Incidence and risk factors for gout in white men. JAMA. 1991; 266(21):3004-3007.
Chen SY, Chen CL, Shen ML. Manifestations of metabolic syndrome associated with male gout in different age strata. Clin Rheumatol. 2007; 26(9):1453-1457.
Gancheva R, Kundurdjiev A, Ivanova M, et al. Obesity and Echocardiographic Changes in the Different Stages of Gout [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10).
Flegal KM, Carroll MD, Ogden CL, et al. Prevalence and trends in obesity among US adults, 1999-2008. JAMA. 2010; 303(3):235-241.
Fam AG. Gout, diet, and the insulin resistance syndrome. J Rheumatol. 2002; 29:1350-1355.
Yamashita S, Matsuzawa Y, Tokunaga K, et al. Studies on the impaired metabolism of uric acid in obese subjects: marked reduction of renal urate excretion and its improvement by a low-calorie diet. Int J Obes. 1986; 10(4):255-264.
Vuorinen-Markkola H, Yki-Jarvinen H. Hyperuricemia and insulin resistance. J Clin Endocrinol Metab. 1994; 78(1):25-29.
Rathmann W, Funkhouser E, Dyer AR, et al. Relations of hyperuricemia with the various components of the insulin resistance syndrome in young black and white adults: the CARDIA study. Coronary Artery Risk Development in Young Adults. Ann Epidemiol. 1998; 8(4):250-261.
Downloads
Published
Issue
Section
License
Copyright (c) 2024 R. Gancheva, A. Koundurdjiev, T. Kundurzhiev, Zl. Kolarov, P. Peteva, M. Nikolova, I. Koundurdjieva, P. Yankova, L. Marinchev (Author)
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
You are free to share, copy and redistribute the material in any medium or format under these terms.
Journal Acta Medica Bulgarica 
