Diagnosis and Management of Gout Nephropathy

Abstract

Introduction: Gout is a crystal-induced arthritis caused by the deposition of monosodium urate (MSU) and is frequently linked to chronic kidney disease (CKD). The bidirectional relationship between gout and CKD increases morbidity, complicates diagnosis, and necessitates integrated management strategies.

Methods: This is a narrative review of recent literature, synthesized into a practical framework for internists, emphasizing the ACR/EULAR criteria, the roles of musculoskeletal ultrasonography and dual-energy CT (DECT), and the implications of renal comorbidity for therapeutic choices

Results: Gouty nephropathy involves both crystal-dependent mechanisms, such as tubular obstruction by urate crystals, and crystal-independent mechanisms, including endothelial dysfunction and the activation of inflammatory, oxidative, and RAAS pathways. In practice, the confirmation of MSU through synovial fluid analysis remains the gold standard. When aspiration is not feasible, musculoskeletal ultrasonography (showing the "double-contour sign") and DECT are used to detect urate deposition and map the disease burden. For acute flares, first-line therapy includes NSAIDs, low-dose colchicine, or glucocorticoids, which should be initiated as early as possible. For long-term prevention, a treat-to-target strategy is employed to lower serum urate levels to <6 mg/dL (or ≤5 mg/dL in severe cases) using xanthine oxidase inhibitors or uricosurics, accompanied by flare prophylaxis for 3–6 months. For renal assessment, biomarkers such as cystatin C and NGAL offer early detection of tubulointerstitial injury beyond conventional markers

Conclusions: A multimodal approach that integrates crystal confirmation, urate-specific imaging, flare control, and target-based urate lowering, alongside the screening and optimization of kidney function, is essential to slow progression and improve outcomes in gout nephropathy.