Elevation of serum uric acid level without clinically visible arthritis (known as asymptomatic hyperuricemia) is not traditionally considered to be gout disease, but only a possible cause of it, even though it may be accompanied by tissue uric acid crystal deposition. On the other hand, gout is traditionally recognized as recurrent, overt arthritis, visible only after a long period of time due to uric acid accumulation in joints. Advanced imaging techniques have substantially changed the perception of this problem, identifying gout as a low-grade chronic inflammatory disease from the very beginning, visible only by phases of acute arthritis attacks. According to ultrasonography, uric acid crystal hyperechoic aggregates (tophi) are seen not only in the symptomatic gout disease phase, but also in the preceding ? asymptomatic (latent) ? gout phase. New perception of the problem was approved by the recently described NETs (neutrophil extracellular traps) phenomenon. Also, hyperuricemia has recently been identified as a systemic disorder, responsible not only for the apparent gout arthritis, but also for the renal and cardiovascular disease occurrence and progression. Positive effect of urate-lowering therapy (xanthine oxidase inhibitors and uricosurics) on hypertension and chronic kidney disease indicates a possibility of its utility in asymptomatic hyperuricemia and asymptomatic gout therapy, apart from the use in clinically manifested gout treatment and for certain conditions, such as tumor lysis syndrome.
Folic acid reverses uric acid crystal-induced surface OAT1 internalization by inhibiting RhoA activity in uric acid nephropathy
