Abstract
Gout and chronic kidney disease (CKD) frequently coexist, but quality evidence to guide gout management in people with CKD is lacking. Use of urate-lowering therapy (ULT) in the context of advanced CKD varies greatly, and professional bodies have issued conflicting recommendations regarding the treatment of gout in people with concomitant CKD. As a result, confusion exists among medical professionals about the appropriate management of people with gout and CKD. This Consensus Statement from the Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN) discusses the evidence and/or lack thereof for the management of gout in people with CKD and identifies key areas for research to address the challenges faced in the management of gout and CKD. These discussions, which address areas for research both in general as well as related to specific medications used to treat gout flares or as ULT, are supported by separately published G-CAN systematic literature reviews. This Consensus Statement is not intended as a guideline for the management of gout in CKD; rather, it analyses the available literature on the safety and efficacy of drugs used in gout management to identify important gaps in knowledge and associated areas for research.
Highlights
Kidney impairment is common in people with gout: as many as ~70% of adults with gout have an estimated glomerular filtration rate of
Monosodium urate (MSU) crystals, which form in the presence of hyperuricaemia, cause gout flares in large part by activating monocytes and macrophages, with resultant NLRP3 inflammasome-mediated IL-1β release, many other local and systemic high-grade pro-inflammatory responses, and articular neutrophil influx and activation[8]
We focused on medications currently approved for or commonly used for gout, including those used in the management of gout flares and flare prophylaxis when starting urate-lowering therapy (ULT) and those used as ULT
Summary
CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate. and metformin and ω-3 fatty acids (which inhibit MSU crystal-induced inflammation)[11–13]. Ultra sonography studies have demonstrated renal medullary echogenicity in patients with severe gout[14], potentially attributable to MSU crystalluria and the development of tophi within the renal medulla[15]. MSU crystal-driven inflammation might directly affect renal structure and function in patients with gout. Gout is generally consid ered a chronic disease, with episodic highly symptomatic flares. Controlled gout can have a substantial impact on an affected individual and the individual’s family. Treated gout leads to recurrent gout flares, the formation of tophi (which contain aggregated masses of MSU crystals in joints and certain soft tissues), chronic gouty arthritis and joint erosion. Substantial time off work, poor health-related quality of life and disability are common in those with poorly controlled gout[18–20]. Not all individuals with gout develop severe disease, and whether everyone
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