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Review ArticlePMC Full Text2008

Uric Acid and Cardiovascular Risk

Feig DI, Kang DH, Johnson RJ • N Engl J Med

Key Finding

Hyperuricemia (>6 mg/dL women, >7 mg/dL men) associated with hypertension, metabolic syndrome (59% with UA >10 vs 5.9% with UA <6), renal dysfunction; allopurinol reduced BP ~6.9 mmHg in adolescents

Key Findings

  • 1Hyperuricemia: >6 mg/dL women, >7 mg/dL men; risk at >5.2-5.5 mg/dL
  • 2Metabolic syndrome: 59% with UA >10 mg/dL vs 5.9% with UA <6 mg/dL
  • 3Allopurinol reduced BP 6.9±4.4 mmHg systolic in hypertensive adolescents
  • 4Mechanism: UA-mediated renal vasoconstriction via NO reduction and RAAS activation

Original title: “Uric acid and cardiovascular risk”

Plain English Summary

Review examining relationship between elevated uric acid and cardiovascular disease, hypertension, metabolic syndrome, and renal disease. Mechanisms involve renal vasoconstriction and renin-angiotensin activation.

In-Depth Analysis

Study Details

Authors: Daniel I Feig (Baylor), Duk-Hee Kang (Ewha Womans University), Richard J Johnson (Colorado)
Journal: NEJM, 2008 Oct 23; 359(17):1811-1821
PMCID: PMC2684330

Key Points (from original paper)

Hyperuricemia Definitions
  • •Women: >6 mg/dL (360 μmol/L)
  • •Men: >7 mg/dL (420 μmol/L)
  • •Risk associations at "normal to high" levels: >5.2-5.5 mg/dL
Historical Context

"An association of gout with hypertension, diabetes, kidney disease, and cardiovascular disease has been observed since the late 19th century."

Key Associations

Hypertension:

  • •Elevated uric acid predicts hypertension development within 5 years
  • •Allopurinol in adolescents: reduced BP by 6.9±4.4 mmHg systolic (vs 2.0±0.4 mmHg placebo)

Metabolic Syndrome:

  • •UA >10 mg/dL (normal BMI): 59% have metabolic syndrome
  • •UA <6.0 mg/dL: 5.9% have metabolic syndrome

Renal Disease:

  • •Elevated UA independently predicts microalbuminuria and renal dysfunction
Proposed Mechanism

"Uric acid–mediated renal vasoconstriction resulting from a reduction in endothelial levels of nitric oxide, with activation of the renin–angiotensin system."

Authors' Conclusion

"There are not sufficient data to recommend the treatment of asymptomatic hyperuricemia" - though evidence warrants clinical trials.

Source: PMC full text (PMC2684330)

Paradigm Relevance

How this study applies to different clinical perspectives:

Standard Medical

Relevant

Conventional clinical guidelines used by most doctors

Why it matters:

Supports monitoring uric acid as part of cardiovascular risk assessment. Treatment of asymptomatic hyperuricemia not yet evidence-based.

Research Consensus

Relevant

Current scientific understanding, often ahead of guidelines

Why it matters:

Establishes uric acid as independent risk factor, not just a marker. Target levels should be lower than traditional gout thresholds.

Metabolic Optimization

Relevant

Proactive targets for optimal health, not just disease absence

Why it matters:

Validates aggressive uric acid optimization. Target <5.5 mg/dL for cardiovascular prevention, not just <6-7 for gout prevention.

Study Details

Type
Review Article
Methodology
Review article examining epidemiological and mechanistic evidence linking uric acid to cardiovascular outcomes.

Evidence Quality

Review from PMC2684330. Authors conclude insufficient data to recommend treating asymptomatic hyperuricemia but evidence warrants clinical trials.

Topic

CardiovascularMetabolic SyndromeInflammation

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Original Source

View on PubMedView DOIFull Text (Open Access)

DOI (Digital Object Identifier) is a permanent link to this publication. Unlike website URLs that can change, a DOI always resolves to the correct source.

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