Conversely, renal failure with underexcretion of uric acid can also cause hyperuricemia. Joint damage in hyperuricemia causes classical attacks of gout but tophi may also develop in cartilage, tendons and other tissues. Acute gouty monoarthritis may be diagnosed clinically and confirmed by finding crystals on aspirate from the joint. Blood chemistries usually show elevated uric acid, sedimentation rate and leukocytosis. Acute attacks may respond to indomethacin or another nonsteroidal anti-inflammatory drug in adequate dosages.
Alternative therapies are colchicine or steroids.
Steroids may be injected into the affected joint or given as a short tapering course of oral medication. Diet and medication may play a role in long-term control of hyperuricemia. Alcohol intake should be reduced and foods high in purines should be avoided. Allopurinol can lower uric acid levels by inhibiting urate synthesis. Probenecid and uricosuric agents may be ineffective if renal function is compromised.