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Abstract Number: 1995

Serum Homocysteine Related To Decreased Renal Function In Chronic Gouty Patients

Jung-Soo Song1, Jin Su Kim2 and Sang Tae Choi1, 1Rheumatology, Chung-Ang University College of Medicine, Seoul, South Korea, 2Chung-Ang University College of Medicine, Seoul, South Korea

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Kidney and gout

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Session Information

Title: Metabolic and Crystal Arthropathies II

Session Type: Abstract Submissions (ACR)

Background/Purpose: Homocysteine is a non-essential amino acid formed by the conversion of methionine to cysteine. Hyperhomocysteinemia is a risk factor for cardiovascular events by inducing reactive oxygen species and impairing endothelial function. Gout is also associated with several comorbidities including cardiovascular disease (CVD). Hyperhomocysteinemia and gout are both related to CVD, however, there are few reports about serum homocysteine levels in gout patients and the results reveal discrepancies. In this study, we investigated whether or not homocysteine levels are elevated in patients with chronic gout and which factors are associated with elevated homocysteine levels.

Methods: 91 male patients with chronic gout and 97 age-matched healthy male controls were included in this study, and the averages of age were 51.19 ± 15.08 and 51.57 ± 17.01 years old, respectively. Serum homocysteine, uric acid (UA), blood urea nitrogen (BUN), creatinine (Cr) and other laboratory findings were tested for all participants. Serum homocysteine levels were measured by a competitive immunoassay using direct chemiluminescent (Siemens Centaur Immunoassay Systems, USA). The estimated glomurular filtration rate (eGFR) was calculated using modification of diet in renal disease (MDRD) formula, then the stages of chronic kidney disease (CKD) were classified according to eGFR levels.

Results: The chronic gout group were not significantly different from the control group in serum uric acid levels (6.15 ± 2.23 mg/dL vs 5.82 ± 1.22 mg/dL, p = 0.214). However, the patients with chronic gout showed much higher serum homocysteine levels than healthy controls (13.96 ± 4.05 μmol/L vs 12.67 ± 3.51 μmol/L, p = 0.022). Serum homocysteine levels were not different between the groups that are treated with allopurinol and with benzbromarone. The patients at stages 1 or 2 of CKD had significantly lower serum homocysteine levels than the patients at stage 3 of CKD (12.99 ± 4.81 μmol/L, 13.17 ± 2.97 μmol/L, and 17.45 ± 4.68 μmol/L, p < 0.001). In patients with chronic gout, serum homocysteine levels showed the positive correlations with serum BUN and Cr levels, and the negative correlation with eGFR and systolic blood pressure (r = 0.429, p < 0.001; r = 0.435, p < 0.001; r = -0.413, p < 0.001; r = -0.251, p < 0.025, respectively). However, serum homocysteine levels are uncorrelated with serum uric acid levels or cholesterol profiles. In multiple linear analyses, serum homocysteine level was affected by eGFR (β = -0.385, p < 0.001), however, was not affected by the serum uric acid level.

Conclusion: Serum homocysteine levels were higher in the male patients with chronic gout than in the healthy male controls. Hyperhomocysteinemia in gouty patients could be related not with serum uric acid levels, but with decreased renal function.


Disclosure:

J. S. Song,
None;

J. S. Kim,
None;

S. T. Choi,
None.

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