Effect on Serum Uric Acid Levels of Drugs Prescribed for Indications other than Treating Hyperuricaemia

Daskalopoulou, Stella S.; Tzovaras, Vasilios T.; Mikhailidis, DP; Elisaf, Moses

doi:10.2174/138161205774913309

Cited by 96 publications

(78 citation statements)

References 206 publications

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“…In this context, it is noteworthy that, beyond allopurinol and the well-established uricosuric drugs, several other agents can decrease the SUA level, such as losartan and fenofibrate. 88 More importantly, we have shown that administration of statins significantly reduces SUA levels 89 and preserves renal function, 90 and these actions independently protect against vascular events in high-risk patients. 59 Thus, a reduction in SUA level could also partially contribute to the beneficial effects of statins against stroke.…”

Section: Discussionmentioning

confidence: 85%

Serum Uric Acid as an Independent Predictor of Early Death After Acute Stroke

Karagiannis

Mikhailidis²,

Τζιόμαλος

et al. 2007

Circ J

115

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Section: Discussionmentioning

confidence: 85%

Serum Uric Acid as an Independent Predictor of Early Death After Acute Stroke

Karagiannis

Mikhailidis²,

Τζιόμαλος

et al. 2007

Circ J

115

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“…Importantly, previous studies have shown that losartan lowers SUA. This hypouricemic effect does not occur with other angiotensin receptor blockers 7 and appears to be largely mediated through reductions in the level of human urate transporter 1 (URAT1) and decreased net urate reabsorption in the proximal tubule. 8 -10 With respect to cardiovascular endpoints, a subanalysis from the Losartan Intervention for Endpoint Reduction in Hypertension Trial showed that the superior effect of losartan could be partly explained by its effect on SUA.…”

mentioning

confidence: 96%

Effect of a Reduction in Uric Acid on Renal Outcomes During Losartan Treatment

et al. 2011

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Abstract-Emerging data show that increased serum uric acid (SUA) concentration is an independent risk factor for end-stage renal disease. Treatment with the antihypertensive drug losartan lowers SUA. Whether reductions in SUA during losartan therapy are associated with renoprotection is unclear. We therefore tested this hypothesis. In a post hoc analysis of 1342 patients with type 2 diabetes mellitus and nephropathy participating in the Reduction of Endpoints in Non-Insulin-Dependent Diabetes Mellitus With the Angiotensin II Antagonist Losartan Trial, we determined the relationship between month 6 change in SUA and renal endpoints, defined as a doubling of serum creatinine or end-stage renal disease. Baseline SUA was 6.7 mg/dL in placebo and losartan-treated subjects. During the first 6 months, losartan lowered SUA by Ϫ0.16 mg/dL (95% CI: Ϫ0.30 to Ϫ0.01; Pϭ0.031) as compared with placebo. The risk of renal events was decreased by 6% (95% CI: 10% to 3%) per 0.5-mg/dL decrement in SUA during the first 6 months. This effect was independent of other risk markers, including estimate glomerular filtration rate and albuminuria. Adjustment of the overall treatment effects for SUA attenuated losartan's renoprotective effect from 22% (95% CI: 6% to 35%) to 17% (95% CI: 1% to 31%), suggesting that approximately one fifth of losartan's renoprotective effect could be attributed to its effect on SUA. Losartan lowers SUA levels compared with placebo treatment in patients with type 2 diabetes mellitus and nephropathy. The degree of reduction in SUA is subsequently associated with the degree in long-term renal risk reduction and explains part of losartan's renoprotective effect. These findings support the view that SUA may be a modifiable risk factor for renal disease. (Hypertension. 2011;58:2-7.)Key Words: serum uric acid Ⅲ angiotensin receptor blocker Ⅲ losartan Ⅲ diabetic nephropathy Ⅲ type 2 diabetes mellitus O ver the past decades, serum uric acid (SUA) has emerged as a cardiovascular risk marker. Increased SUA has been shown to predict the risk of hypertension, diabetes mellitus, and cardiovascular disease. [1][2][3] More recent data also point to SUA as a risk marker for progression of chronic kidney disease. 4,5 These observations raise the question as to whether interventions that lower uric acid could confer cardiovascular or renal protection. In this respect, the angiotensin receptor blocker losartan is of potential interest. The drug has been clearly demonstrated to be renoprotective in patients with diabetic nephropathy, with this effect largely attributed to its effects on blood pressure and/or proteinuria/albuminuria. 6 However, it is unclear whether other off-target effects of the drug could contribute to the ultimate improvement in renal outcome with this agent. Importantly, previous studies have shown that losartan lowers SUA. This hypouricemic effect does not occur with other angiotensin receptor blockers 7 and appears to be largely mediated through reductions in the level of human urate transporter 1 (URAT1) ...

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“…For example, telmisartan has been reported to be beneficial for glucose and lipid metabolism (13,14), and losartan to be beneficial for uric acid reduction (6)(7)(8)(9)(10). The present study demonstrated that PRT may be of benefit in cholesterol and uric acid metabolism, although we can not exclude the possibility that the reduction of uric acid and cholesterol may be affected by diet, because we did not control diet during the study period.…”

Section: Discussionmentioning

confidence: 55%