EDITORIAL
Gout
Gout, diuretics and the kidney
1 Hospital General Universitario de Alicante, Universidad Miguel Hernandez, Alicante, Spain
2 Nephrology section, Hospital General Universitario de Alicante
Correspondence to:
Correspondence to:
Professor E Pascual
Sección de Reumatología, Hospital General Universitario de Alicante, Maestro Alonso 109, 03010 Alicante, Spain; pascual_eli@gva.es
Accepted 13 March 2006
Occurrence of gout may depend on the condition for which diuretics are prescribed rather than resulting from the drugs themselves
Keywords: gout; diuretics; case-control study; cardiovascular diseases; hypertension
| The first 150 words of the full text of this article appear below. |
Gout is a monosodium urate crystal deposition disease. Formation of the crystals requires high serum uric acid levels; the local factors responsible for their predilection for the joints are only started to be grasped.1,2 Steady serum urate levels result from the balance between its production and excretion; hyperuricaemia results when formation is increased or difficulties in (mostly) renal excretion occur. In humans, urate is the final breakdown product of purine nucleotides, constituents of cellular energy stores such as ATP, and of DNA and RNA both internal or, to a lesser extent, ingested.
Increased urate formation is the cause of hyperuricaemia and gout in some well defined enzymatic defects, and also occurs as a consequence of increased destruction of cells in some malignancies, polycythaemia vera or some haemolytic anaemias. Patients with increased production of urate are classified as overproducers, and detection of an increased amount of excreted urate is considered
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