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Dysuricemia.

Akiyoshi Nakayama1, Masafumi Kurajoh2, Yu Toyoda1,3

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Elevated serum urate (SU) causes gout, but both high and low SU levels are problematic. Understanding uric acid

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Alzheimer’s disease (AD)Parkinson’s disease (PD)anti-oxidative effectsbucket-and-balls theorycardiovascular disease (CVD)chronic kidney disease (CKD)crystal formationmonosodium urate (MSU)neurodegenerative diseases (NDs)pro-oxidative effects

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Area of Science:

  • Urology
  • Nephrology
  • Biochemistry
  • Genetics

Background:

  • Gout and hyperuricemia are globally prevalent, burdensome diseases linked to elevated serum urate (SU) levels.
  • Uric acid plays a crucial physiological role, acting as both an antioxidant and pro-oxidant, influencing reactive oxygen species (ROS) generation.
  • Genetic factors, including urate transporters like URAT1, significantly impact SU levels and are implicated in conditions like hereditary renal hypouricemia (RHUC).

Purpose of the Study:

  • To review current evidence on uric acid's multifaceted roles beyond being a metabolic waste product.
  • To highlight the dual nature of uric acid in health and disease, including its involvement in chronic kidney and cardiovascular diseases.
  • To propose a novel disease concept, 'dysuricemia', encompassing the spectrum from hypouricemia to hyperuricemia/gout.

Main Methods:

  • Comprehensive review of existing scientific literature on serum urate, gout, hypouricemia, and related physiological and pathological processes.
  • Analysis of the genetic basis of urate transport and metabolism, focusing on key enzymes and transporters.
  • Synthesis of evidence regarding uric acid's role in oxidative stress and its potential as a biomarker for chronic diseases.

Main Results:

  • Serum urate levels are critical, with both excessively high (hyperuricemia) and low (hypouricemia) levels associated with adverse health outcomes.
  • Uric acid's dual role as an antioxidant and pro-oxidant is significant, impacting cellular processes and disease progression.
  • Research implicates urate transporters and xanthine oxidoreductase (XOR) in SU regulation and ROS production, linking them to kidney and cardiovascular health.

Conclusions:

  • The simplistic 'lower is better' approach to serum urate is inaccurate; optimal levels are crucial for physiological function.
  • Uric acid is a vital molecule with complex roles, not merely a waste product.
  • The proposed concept of 'dysuricemia' unifies hypouricemia and hyperuricemia/gout as a single disease spectrum, advocating for 'normouricemia' (optimal SU level) as the therapeutic goal.