Abstract
Background: Although gout is accompanied by the substantial burden of kidney disease, there are limited data to assess renal function as a therapeutic target. This study evaluated the importance of implementing a “treat-to-target” approach in relation to renal outcomes. Methods: Patients with gout who underwent continuous urate-lowering therapy (ULT) for at least 12 months were included. The effect of ULT on renal function was investigated by means of a sequential comparison of the estimated glomerular filtration rate (eGFR). Results: Improvement in renal function was only demonstrated in subjects in whom the serum urate target of <6 mg/dL was achieved (76.40 ± 18.81 mL/min/1.73 m2 vs. 80.30 ± 20.41 mL/min/1.73 m2, p < 0.001). A significant difference in the mean change in eGFR with respect to serum urate target achievement was shown in individuals with chronic kidney disease stage 3 (−0.35 ± 3.87 mL/min/1.73 m2 vs. 5.33 ± 11.64 mL/min/1.73 m2, p = 0.019). Multivariable analysis predicted that patients ≥65 years old had a decreased likelihood of improvement (OR 0.31, 95% CI 0.13–0.75, p = 0.009). Conclusions: The “treat-to-target” approach in the long-term management of gout is associated with better renal outcomes, with a greater impact on those with impaired renal function.
Highlights
Gout is one of the most common forms of inflammatory arthritis, which is caused by the deposition of monosodium urate crystals in and around the joints
We aimed to demonstrate the clinical importance of the “treat-to-target” approach in the long-term management of gout by evaluating the changes in renal function and the factors influencing the renal outcomes
We identified individuals who were newly prescribed with urate-lowering agents, namely, allopurinol, febuxostat, or benzbromarone, after a working diagnosis of gout had been established by a board-certified rheumatologist in a single tertiary hospital between 1 March 2007, and 28 February 2017
Summary
Gout is one of the most common forms of inflammatory arthritis, which is caused by the deposition of monosodium urate crystals in and around the joints. Comorbidities are common, with renal problems being top tiered This generally leads to a substantial healthcare burden [2]. 25% of patients with gout evidenced chronic kidney disease (CKD) stage 3 or greater (defined as an estimated glomerular filtration rate (eGFR) of
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