Purpose of review: Gout is increasing worldwide. An appreciation that hyperuricaemia and gout are associated with hypertension and chronic kidney disease is well established, but the cause and effect relationships are controversial. Studies which address this conundrum have been reviewed.
Recent findings: Epidemiological surveys have confirmed the strong relationship of gout and hyperuricaemia with hypertension and diuretic treatment. There are multiple confounders such as obesity and alcohol consumption which despite adjustments make interpretation of the epidemiology difficult. There are data to suggest that hyperuricaemia itself causes hypertension and renovascular disease, and that lowering of serum urate may assist in control of hypertension. The mechanism for diuretic-induced hyperuricaemia may operate through volume depletion and reduced secretion of uric acid. The latter effect may be genetically influenced.
Summary: Recent population surveys have strongly supported the association of gout and hyperuricaemia with hypertension. The prevailing explanation that renal dysfunction causes both phenomena or that they are caused by shared factors is challenged by the evidence that hyperuricaemia drives hypertension. A confounder of epidemiology studies is the use of diuretics for treating hypertension. A closer understanding of the mechanisms of diuretic-induced hyperuricaemia may lead to the creation of uricosuric diuretics. Losartan is exceptional amongst antihypertensive drugs in possessing mild uricosuric properties and therefore has a role in treating hypertensive patients with gout. Overcoming diuretic-induced hyperuricaemia is difficult and there is need for a uricosuric diuretic.