Treatment of ADTKD Caused by UMOD Mutation with Hyperuricemia in Patients on ACE Inhibitor or ARB Therapy

This protocol addresses patients with autosomal dominant tubulointerstitial kidney disease (ADTKD) caused by a uromodulin (UMOD) gene mutation who have hyperuricemia and are currently receiving an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB).

ADTKD-UMOD is typically characterised by inappropriately decreased fractional urate excretion, which leads to hyperuricemia and often gout. When patients with this condition require renin-angiotensin system therapy, the concurrent presence of hyperuricemia makes agent selection clinically important.

Where renin-angiotensin system therapy is in use, one specific agent within this class is preferred in the setting of hyperuricemia because of its distinct capacity to lower serum urate through enhanced urinary urate excretion — a property not shared by other agents in the class.