Gout, a prevalent inflammatory arthritis, is triggered by monosodium urate (MSU) crystal deposits in joints due to elevated serum urate (SU) levels. This causes intense pain and swelling, and chronic gout can lead to joint damage and visible MSU deposits (tophi). The inflammatory response involves the NLRP3 inflammasome in macrophages and monocytes. Gout significantly impacts quality of life and healthcare systems worldwide, with a global prevalence ranging from 0.1% to 10%. In the United States., the prevalence is 3% to 4%.

Patients with gout and chronic kidney disease (CKD) struggle to maintain optimal SU levels due to reduced renal urate excretion. Hyperuricemia is common in CKD stages 3 to 5 and can worsen kidney function. Gout prevalence increases fivefold in patients with an eGFR ≤60 ml/min/1.73 m². Treating gout in patients with CKD is challenging due to limited data and safety concerns. The 2020 American College of Rheumatology guidelines recommend urate-lowering therapy (ULT) to achieve SU levels <6 mg/dL. However, initiating ULT can trigger flares, necessitating prophylactic agents. Treatment options include NSAIDs, colchicine, glucocorticoids, and IL-1 inhibitors, each with varying efficacy and safety in patients with CKD.

Reference: Kannuthurai V, Gaffo A. Management of Patients with Gout and Kidney Disease: A Review of Available Therapies and Common Missteps. Kidney360. 2023;4(9):e1332-e1340. doi: 10.34067/KID.0000000000000221.