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Resurrection of uric acid as a causal risk factor in essential hypertension.

In his landmark paper describing the entity of essential hypertension, Frederick Akbar Mahomed observed that many hypertensive subjects came from gouty families, leading him to suggest uric acid as a causal factor in the blood pressure response.1 Ten years later this hypothesis was championed by Haig, who proposed low purine diets as a means to prevent hypertension and vascular disease.2 During the same period the French academician, Henri Huchard, noted that renal arteriolosclerosis (the histological lesion of hypertension) was primarily observed in 3 groups: those with gout or lead poisoning or those with a diet enriched in fatty meat, all conditions associated with hyperuricemia.3

During the early 1900s there continued to be reports linking uric acid with hypertension.4 In the 1960s and 1970s, at a time when hyperuricemia was present in ≈5% of the US population,5 an elevated uric acid level was observed in 40% to 60% of hypertensive subjects6; similarly, hypertension was observed in 50% to 65% of subjects with gout.7 Cannon et al reported that hyperuricemia was observed in 25% of untreated hypertensive subjects, 50% of those on treatment, and 75% to 100% of those with malignant hypertension or renal dysfunction.8 Population-based studies also found an increased frequency of hypertension with stepwise increases in serum uric acid levels in both blacks and whites.9

Whereas these studies …