Pathophysiology of hyperuricemia and its clinical significance - a narrative review

Abstract

Hyperuricemia, i.e. increased serum uric acid (UA) concentration, is a common problem in clinical practice. While there are clear guidelines concerning management of symptomatic hyperuricemia in acute conditions such as gout, urolithiasis or acute urate nephropathy, less is known about their secondary prevention. Moreover, despite the ongoing debate on the role of UA in the pathogenesis of chronic kidney disease, hypertension, cardiovascular disease and heart failure, the management of asymptomatic hyperuricemia in patients with these chronic conditions is still mainly up to physicians' judgement. Individual considerations should always be taken into account when prescribing urate-lowering therapy. In this narrative review study, we attempt to present current trends concerning treatment of patients with either symptomatic or asymptomatic hyperuricemia in the light of the available knowledge on the role of hyperuricemia in the development of gout, renal, cardiovascular and other diseases.

Keywords: comorbidity; hyperuricemia; urate-lowering therapy; uric acid.

Fig. 1

Causes of hyperuricemia.

Fig. 2

Mechanism of action of urate-lowering drugs. OAT4 – organic anion transporter 4, OAT10 – organic anion transporter 10, URAT1 – urate transporter 1.

Fig. 3

Tumor lysis syndrome prophylaxis [60]. ARF – additional risk factors, LDH – lactate dehydrogenase, UNL – upper norm limit, WBC – white blood cells.

Fig. 4

Algorithm for management of asymptomatic hyperuricemia. UA – uric acid, ULT – urate-lowering therapy.