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To the Editor:Epidemiological studies report a relationship between serum uric acid concentrations (sUA) and a wide variety of cardiovascular conditions, including hypertension, metabolic syndrome, diabetes, coronary artery disease, cerebrovascular disease, pre-eclampsia, and chronic kidney disease (CKD).1 Indeed, sUA is considered by some to be an independent risk factor for both cardiovascular disease2,3 and CKD.4 Others have noted that an elevated sUA predicts the development of hypertension, obesity, diabetes, and CKD.1 Importantly, emerging clinical data show that lowering sUA has both cardiovascular and renal benefits.5–7Endothelin (ET) 1 is the most potent endogenous vasoconstrictor produced within the vasculature. It is implicated in both the development and progression of CKD.8 Its effects are mediated via 2 receptors, the ET-A (ETA) and ET-B (ETB) receptors, with the major pathological effects being ETA receptor mediated.8 We have shown recently that chronic selective ETA receptor antagonism reduces proteinuria, blood pressure, and arterial stiffness in patients with nondiabetic, hypertensive, proteinuric CKD,9 effects that are potentially renoprotective. The current data show the effects of sitaxsentan and placebo on sUA in this same cohort of CKD …

Chronic Selective Endothelin A Receptor Antagonism Reduces Serum Uric Acid in Hypertensive Chronic Kidney Disease