Gout is caused by body fluid urate saturation complicated by deposition of monosodium urate crystals in tissues. Elevated uric acid levels can be caused by overproduction of uric acid from purine catabolism or insufficient excretion by the kidneys and are necessary but not sufficient for the development of gout. The deposition of urate crystals in tissues leads to inflammation and subsequent tissue damage. The most common sites involved are the skin and joints. Gout can present as acute gouty arthritis or chronic tophaceous gout. Patients may also develop uric acid nephrolithiasis.

The acute form of gout presents as a painful, swollen, warm, and erythematous joint, usually monoarticular. The most common joints affected are the first metatarsophalangeal joints (great toe, also known as podagra or foot gout), ankles, feet, and knees. The pain can be debilitating. Flares can last days to weeks if untreated and can become more severe and more frequent over time.

Chronic tophaceous gout presents most commonly involving the ear but can also affect other soft tissues, articular structures, bursas, and tendons. Smooth or multilobulated nodules can ulcerate, leading to extrusion of a chalk-like substance. Rarely, urate bullae may develop. In uncontrolled chronic gout, there may be frequent acute attacks that lead to destructive arthritis and joint deformity.

Men aged 40-50 years are most commonly affected. Other risk factors include renal insufficiency, obesity, increased alcohol consumption, medications (eg, diuretics), lymphomas, leukemias, tumor lysis syndrome, and hemolysis, as well as lead exposure (eg, from illegally distilled liquor, or "moonshine"; known colloquially as "saturnine gout").

Individuals who are immunocompromised (such as from chronic kidney disease, diabetes mellitus, autoimmune disorders, and malignancies, including leukemia or lymphoma) may have an altered presentation of gout and an increased risk of complications, including infections complicating ulcerated tophaceous gout.