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Published on: June 23, 2015
Hyperuricemia, gout, and autosomal dominant polycystic kidney disease
E Mejías1, J Navas, R Lluberes
1Department of Internal Medicine, San Juan Veterans Administration Medical Center, Puerto Rico.
Insights
Autosomal dominant polycystic kidney disease (ADPKD) is linked to higher uric acid levels and an increased risk of gout. This study suggests ADPKD should be recognized as a condition associated with hyperuricemia and gout.
Area of Science:
- Nephrology
- Rheumatology
- Medical Genetics
Background:
- The connection between hyperuricemia, gout, and autosomal dominant polycystic kidney disease (ADPKD) is not well-established.
- Hyperuricemia is a known risk factor for gout, a type of inflammatory arthritis.
Purpose of the Study:
- To investigate the relationship between ADPKD, serum uric acid levels, and the prevalence of gout.
- To determine if abnormal renal handling of uric acid or enzyme deficiencies contribute to gout in ADPKD patients.
Main Methods:
- Compared serum uric acid concentrations in 17 ADPKD patients, 9 controls, and patient groups with gout and/or chronic renal failure.
- Assessed clinical gout prevalence and measured fractional excretion of uric acid and hypoxanthine guanine phosphoribosyl transferase (HGPRT) activity.
Main Results:
- Patients with ADPKD exhibited significantly higher mean serum uric acid levels compared to controls (8.0 vs. 6.4 mg/dl).
- Clinical gout was diagnosed in 24% of ADPKD patients; gout was absent in patients with chronic renal failure from other causes.
- No significant differences were observed in fractional uric acid excretion or HGPRT activity among the studied groups.
Conclusions:
- Autosomal dominant polycystic kidney disease (ADPKD) should be recognized as a condition associated with hyperuricemia and gout.
- The increased incidence of gout in ADPKD is not attributed to partial HGPRT deficiency or altered renal uric acid handling.
Abstract:
The relationship between hyperuricemia, gout, and autosomal dominant polycystic kidney disease (ADPKD) is not widely recognized. In an attempt to further clarify this relationship, the authors have studied 17 patients with ADPKD, 9 controls, 9 patients with proven gout and chronic renal failure, 11 patients with gout and normal renal function, and 11 patients with chronic renal failure. The mean serum uric acid concentration was higher in patients with ADPKD as a group than in controls (8.0 +/- 1.7 mg/dl vs. 6.4 +/- 1.6 mg/dl, p less than .02). Clinical gout was identified in 24% of patients with ADPKD; none of the patients with chronic renal failure of other etiologies had gout. Fractional excretion of uric acid and the activity of the enzyme hypoxanthine guanine phosphoribosyl transferase (HGPRT) were not different among the groups studied. From this study the authors conclude that ADPKD should be included among those diseases associated with hyperuricemia and gout. A partial deficiency in HGPRT or abnormal renal handling of uric acid do not appear to be responsible for the increased incidence of gout in patients with ADPKD.
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