[Pathophysiology of gout]

Abstract

Hyperuricemia is rather often metabolic disorder in general population. It is multifactorial disorder influenced by purine rich diet, alcohol consumption, diuretics use and renal deterioration. In the presence of local urate superasturation and lower solubility, monosodium crystals are deposited in joints, kidneys and soft tissue leading to clinical manifestations, such as gout, tophaceus deposits, nephrolithiasis and uric nephropathy. Major advances in understanding the pathogenesis of hyperuricemia and gout have been made recently, including genetic studies of urate transporters in kidneys as well as innate immune inflammatory responses and cytokine production which will be discussed thoroughly in this paper.