Kidney Week Educational Symposia-Principles of Gout Management in Patients with Kidney Diseases

Video Transcription

Video Summary

This recorded symposium on gout management in patients with kidney disease opened by highlighting gout’s long history and its high relevance to nephrology: gout is far more common in CKD (about 1 in 4) and is associated with higher rates of cardiovascular and metabolic comorbidities.  <br /><br />Dr. Richard Johnson reviewed the evolutionary loss of uricase 12–15 million years ago, likely providing a survival advantage by promoting fat storage during periods of starvation, especially through fructose-driven uric acid generation. Modern “Western” diets (sugar/fructose, alcohol, purines) raise urate far beyond ancestral levels, increasing crystal formation and gout. He described evidence that uric acid is pro-inflammatory in tissues, that urate crystals can persist between flares, and that crystals may deposit in atherosclerotic plaques (often detectable by dual-energy CT). Observational data suggest improved cardiovascular and renal outcomes when serum urate is reduced below 6 mg/dL with sustained adherence, while several negative CKD trials may have failed due to excluding gout, including patients with normal urate, lack of treat-to-target design, short duration, and poor adherence.<br /><br />Dr. Angelo Gaffo emphasized “treat-to-target” urate lowering (generally <6 mg/dL, lower for severe tophaceous disease) and showed trial evidence that structured care improves urate control, flares, and tophi. He argued against “renal dosing” allopurinol that prevents reaching target; instead start low (especially in CKD), titrate gradually, and use prophylaxis. He reviewed allopurinol hypersensitivity risk factors (high starting dose, CKD, certain ancestries; optional HLA-B*58:01 testing). Febuxostat cardiovascular risk concerns from CARES were tempered by FAST. Prophylaxis in CKD is difficult (avoid NSAIDs; adjust colchicine; low-dose prednisone or off-label IL-1 inhibitors). For refractory gout, pegloticase effectiveness can be improved with immunosuppression (e.g., mycophenolate). Dialysis lowers urate but may cause fluctuations; ULT can be reassessed over time. A final discussion addressed the controversy of treating asymptomatic hyperuricemia (guidelines: generally no; some advocate treatment at very high levels).

Asset Subtitle

Moderator(s): Paul Palevsky

Presentation(s):

Introduction - Paul Palevsky
Pathophysiology of Hyperuricemia and Gout - Richard Johnson
Management of Complex Patients with Gout: Special Considerations in CKD and ESKD - Angelo Gaffo

Support is provided by an educational grant from Horizon Therapeutics USA, Inc.

Meta Tag

Date 11/4/2023

Pathway 1 CKD Non-Dialysis

Pathway 2 Diabetic Kidney Disease

Session ID 468534

Session Type ES - Educational Symposium

Keywords

gout management

chronic kidney disease (CKD)

hyperuricemia

serum urate treat-to-target

allopurinol titration

HLA-B*58:01 testing

febuxostat cardiovascular safety

gout flare prophylaxis in CKD

dual-energy CT urate crystals

pegloticase with immunosuppression

asymptomatic hyperuricemia controversy