Uric acid\u00a0levels are raised in chronic renal failure, and in view of that, gout sometimes seems less common than expected.<\/p>\n
Is more likely to cause toxicity in renal impairment and initial dose should be 100mg.\u00a0 It may rarely cause interstitial nephritis.\u00a0 Its introduction may precipitate acute gout and this needs to be protected against with nonsteroidals or colchicine.<\/p>\n
Allopurinol inhibits metabolism of azathioprine.\u00a0 Although some advice suggests reducing azathioprine dose by two thirds, consideration should be given to alternatives, or cessation of azathioprine, if allopurinol is clinically necessary.<\/p>\n
Are not necessarily completely contraindicated in moderate renal failure, if used with monitoring and for a limited period.<\/p>\n
Is the first choice for treatment of acute gout in patients with significant renal impairment.\u00a0 It has a narrow therapeutic ratio, toxicity manifesting as diarrhoea, nausea and vomiting.\u00a0 Reduced dosing is recommended at GFR 10-50, and extreme caution if GFR is less than 10. The BNF recommendations (2mg then 500mcg every 2-3h) will often cause severe side-efffects; safer to start with 500mcg tds and increase as necessary (reduce if necessary). Start with less in very small people or with severe renal impairment.<\/p>\n
Lower doses (e.g. 500mcg 1-3 times daily) are useful prophylactically.<\/p>\n
Ref: Morris et al 2003. Colchicine in acute gout. Br Med J 327:1275-6<\/p>\n
Are of little value in the presence of significant renal impairment.\u00a0 In addition to the conventional uricosurics probenecid and benzbromarone, losartan and fenofibrate have some uricosuric activity.<\/p>\n
Occurs particularly in tumour lysis syndromes (though prophylactic allopurinol usually prevents it), or in high turnover haematological malignancies such as AML.\u00a0 Causes acute renal failure through crystalluria.\u00a0 Treatment has three elements:<\/p>\n
<\/p>\n
Acknowledgements:\u00a0\u00a0<\/strong> Neil Turner was the main author for this page. The page was created in November 2006 and the last modified date is shown in the footer.<\/span><\/p>\n <\/p>\n <\/p>\n","protected":false},"excerpt":{"rendered":" Uric acid\u00a0levels are raised in chronic renal failure, and in view of that, gout sometimes seems less common than expected. Asymptomatic hyperuricaemia\u00a0should usually not be treated. Patients with very early onset gout should be screened for predisposing genetic abnormalities. Lead poisoning should be remembered as a cause, but is rarely\u2026<\/p>\n