Asymptomatic hyperuricemia: is it really asymptomatic?

Abstract

Purpose of review Hyperuricemia is highly prevalent, affecting approximately 38 million individuals in the United States. However, the significance of asymptomatic hyperuricemia – hyperuricemia in the absence of gout – continues to be debated. Recent findings Asymptomatic hyperuricemia results in monosodium urate crystal deposition in tissues, which may promote chronic inflammation. Intracellularly, hyperuricemia inhibits the master regulator adenosine monophosphate (AMP)-associated protein kinase and may condition innate immune responses through durable epigenetic modifications. At the population level, asymptomatic hyperuricemia is associated with multiple comorbidities, including hypertension, chronic kidney disease, coronary artery disease, and diabetes; limitations of these studies include that most are retrospective and some do not rigorously distinguish between asymptomatic hyperuricemia and gout. Treatment studies suggest that urate lowering may reduce the risk of incidence or progression of some of these comorbidities; unfortunately, many of these treatment studies are small or flawed, and not all study results are consistent. Summary Accumulating evidence suggests that asymptomatic hyperuricemia contributes to the comorbidities with which it associates and that proper asymptomatic hyperuricemia treatment may reduce future risk. Additional prospective trials are needed to definitely establish causality and support decision-making as to whether, and which patients with asymptomatic hyperuricemia would warrant urate-lowering treatment.

Prevalence of asymptomatic hyperuricemia and its association with prediabetes, dyslipidemia and subclinical inflammation markers among young healthy adults in Qatar

“…However, this finding may possibly be contradictory with previous studies, which suggest that uric acid may hinder the production of insulin via inhibiting the proliferation of beta-cells in the pancreas, as well as decreasing gene expression of insulin [ 30 , 31 ]. Therefore, the positive association between glucose and asymptomatic hyperuricemia may be scientifically plausible since several studies have stated that uric acid levels may contribute to elevated serum glucose by increasing hepatic gluconeogenesis and inhibiting insulin-mediated entry of glucose into cells [ 10 , 32 ].…”

“…Asymptomatic hyperuricemia, hyperuricemia in individuals who have not experienced gout nor nephrolithiasis, is viewed as a non-pathological condition whilst its prevalence is estimated to range between 10 and 20% worldwide [ 10 ]. Until recently, it was thought that uric acid in the soluble form is inert and does not initiate an inflammatory response.…”

The Role of Soluble Uric Acid in Modulating Autophagy Flux and Inflammasome Activation during Bacterial Infection in Macrophages

“…Hyperuricemia does not always lead to the development of gout and could be asymptomatic. However, asymptomatic hyperuricemia has been linked to a condition, such as chronic inflammatory states, kidney disease, cardiovascular disease, and metabolic syndrome [13].…”

A systematic review and meta-analysis of the association between uric acid levels and chronic kidney disease

“…The definition of the role of UA is still complex, especially due to the coexistence of risk factors such as hypertension, chronic inflammation and pathophysiological peculiarities of CKD. Recent studies have shown that soluble UA exhibits a behavioral duality acting as pro-oxidant within the cell and antioxidant in the extracellular environment 10 , 51 , 52 .…”