Abstract
Background Gout is commonly associated with metabolic syndrome. Strong association between the serum uric acid level and microalbuminuria has also been observed in various studies. Aim To observe the change in urinary microalbumin after urate-lowering treatment in patients with gout and microalbuminuria. Methodology. A prospective, observational study was conducted at a tertiary-level rheumatic center (NCRD) in Kathmandu, Nepal. Adults diagnosed with gout using the 2015 ACR/EULAR criteria and microalbuminuria were enrolled in the study after obtaining informed consent. Sociodemographic profile and clinical history were recorded at baseline. Serum uric acid levels, spot urinary microalbumin (MAU) excretion, blood sugar, lipid profile, and blood pressure were measured at baseline, 3-month follow-up, and 6-month follow-up. A paired t-test was used to compare the change in mean MAU after treatment. Results A total of 778 patients diagnosed with gout were screened for microalbuminuria. Among them, 114 (14.6%) had urinary microalbumin levels of >30.0 mg/L during presentation. Mean MAU level among those with microalbuminuria was 132.4 ± 124.6 mg/L. Thirty-five patients had concomitant HTN and were put on ARBs (20 mg of telmisartan). All received 40 mg of febuxostat. In patients with ARBs, MAU reduced significantly after 3 months of treatment with ARBs. Reduction in MAU in those without ARBs was seen after the 6-month follow-up, and the change was statistically significant. Conclusions There is significant reduction in MAU after the use of urate-lowering drugs in patients with gout.
Highlights
Gout is increasingly recognized as one of the major health problems in recent decades [1]
Gout can be considered as a risk factor for hypertension (HTN), cardiovascular disease, chronic kidney disease (CKD), and diabetes [8]
While hyperuricemia can cause the progression of renal disease, kidney dysfunction itself can increase serum urate levels due to glomerular damage leading to reduced excretion of serum uric acid [6, 7]
Summary
Gout is increasingly recognized as one of the major health problems in recent decades [1] It is usually associated with an elevated serum uric acid (SUA) level. Few studies suggest that uric acid contributes to increased inflammation leading to CKD progression, demonstrating the relationship between serum urate levels and kidney function. While hyperuricemia can cause the progression of renal disease, kidney dysfunction itself can increase serum urate levels due to glomerular damage leading to reduced excretion of serum uric acid [6, 7]. Strong association between the serum uric acid level and microalbuminuria has been observed in various studies. Spot urinary microalbumin (MAU) excretion, blood sugar, lipid profile, and blood pressure were measured at baseline, 3-month follow-up, and 6-month follow-up. There is significant reduction in MAU after the use of urate-lowering drugs in patients with gout
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