| Autor: |
Perez-Ruiz F; Rheumatology Division, Hospital Universitario Cruces and BioCruces Health Research Institute, Pza. Cruces sn, 48903, Baracaldo, Spain, fperezruiz@telefonica.net., Aniel-Quiroga MA, Herrero-Beites AM, Chinchilla SP, Erauskin GG, Merriman T |
| Jazyk: |
angličtina |
| Zdroj: |
Rheumatology international [Rheumatol Int] 2015 Sep; Vol. 35 (9), pp. 1519-24. Date of Electronic Publication: 2015 Mar 13. |
| DOI: |
10.1007/s00296-015-3242-0 |
| Abstrakt: |
Inefficient renal excretion of uric acid is the main pathophysiological mechanism for hyperuricemia in gout patients. Polymorphisms of renal tubular transporters linked with sodium and monosaccharide transport have yet to be demonstrated. We intended to evaluate the impact of insulin resistance, evaluated with the homeostasis model assessment (HOMA), through a transversal study of non-diabetic patients with gout, with normal renal function, not treated with any medication but colchicine as prophylaxis. One hundred and thirty-three patients were evaluated. Clearance of uric acid was inversely correlated with insulin resistance and directly correlated with fractional excretion of sodium. In multivariate analysis, hypertension and hyperlipidemia, in addition to insulin resistance and fractional excretion of sodium, were associated with renal clearance of uric acid. HOMA cutoff for efficient versus inefficient renal handling of uric acid was 2.72, close to that observed in studies of reference population. The impact of insulin resistance and renal handling of sodium on renal clearance of uric acid may help to explain why hyperuricemia is more commonly associated with diabetes and hypertension. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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