Effect of nonsteroidal anti-inflammatory drugs on the renal excretion of uric acid

Tiitinen, S.; Nissilä, M; Ruutsalo, Helka-Marjatta; Isomäki, H

doi:10.1007/bf02041396

Cited by 19 publications

(19 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Diflunisal has a uricosuric effect [193][194][195][196]. The inhibition of xanthine oxidase activity has also been proposed in some studies [194], as an additional mechanism of action.…”

Section: Diflunisalmentioning

confidence: 99%

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

Daskalopoulou

Tzovaras²,

Mikhailidis³

et al. 2005

CPD

View full text Add to dashboard Cite

Beyond allopurinol and the well-established uricosuric drugs, several other agents can decrease serum uric acid (SUA) levels, such as losartan, fenofibrate and some non-steroidal anti-inflammatory drugs (NSAIDs). Some of these drugs increase renal urate excretion. Hyperuricaemia and gout are common problems (at least 1% of Western men are affected by gout). Raised SUA levels increase the incidence of acute gout and renal calculi. Hyperuricaemia may also predict an increased risk of vascular events. Therefore, lowering SUA levels is of clinical relevance. In this review we consider the effect on SUA levels of drugs that are prescribed for indications other than treating hyperuricaemia. These drugs may obviate the need for specific treatment (e.g. allopurinol) aimed at lowering SUA levels. Furthermore, because hyperuricaemic patients may already be on several drugs (e.g. due to associated dyslipidaemia, hypertension and/or arthritis) compliance may be improved by avoiding additional medication. The potential for adverse effects associated with polypharmacy would also be decreased.

show abstract

“…Diflunisal has a uricosuric effect [193][194][195][196]. The inhibition of xanthine oxidase activity has also been proposed in some studies [194], as an additional mechanism of action.…”

Section: Diflunisalmentioning

confidence: 99%

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

Daskalopoulou

Tzovaras²,

Mikhailidis³

et al. 2005

CPD

View full text Add to dashboard Cite

show abstract

“…For example, commonly used drugs such as some non-steroidal anti-inflammatory drugs (NSAIDs) may exert a favourable effect on urate excretion 37,[40][41][42][43] .…”

Section: Brief Commentmentioning

confidence: 99%

Uric acid levels and vascular disease

Daskalopoulou

Athyros

Elisaf

et al. 2004

Current Medical Research and Opinion

View full text Add to dashboard Cite

There is evidence showing that serum uric acid (SUA) levels predict the risk for vascular events. For example, up to 29% of the reduction in the primary composite endpoint seen in the LIFE trial (favouring losartan versus atenolol) can be attributed to a fall in SUA levels. We also discuss the findings of the GREACE study (treating to target with atorvastatin versus 'usual' care) in relation to SUA levels. In this brief comment we extend this argument to consider the SUA-lowering effect of other drugs commonly prescribed in patients with vascular disease (e.g. statins, fibrates and antihypertensive agents). A judicious use of drugs (alone or in combination) will result in small reductions in SUA levels. These changes may translate into a substantial reduction in the risk of vascular events. Results retrieved from completed trials together with new prospective findings will support or refute the proposed association between lowering SUA levels and reducing vascular morbidity and mortality.

show abstract

“…Uricosuria is not usually considered a pharmacologic effect of NSAIDs, although high-dose acetylsalicylic acid (> 3 g/day), diflunisal, indomethacin, azapropazone, and phenylbutazone have mild uricosuric activity [12], In particular, diflunisal has been reported to increase uric acid excretion by 59% [12], while phenylbutazone has caused uric acid nephrolithiasis [13]. In contrast, a therapeutic dose of suprofen (200 mg) increased the FEUA 303%, indicating marked uricosuric activity and making suprofen unique among NSAIDs studied for this effect.…”

Section: Discussionmentioning

confidence: 99%

“…In general, the adverse renal effects of uricosuric agents appear to be related to the rate of onset and potency of uricosuria. Other NSAIDs are less likely to cause this nephropathy because of lesser uricosuric activity [12], However, cer tain drugs, including phenylbutazone, probenecid, sul finpyrazone, and ticrynafen, have been implicated as causes of urate nephropathy and uric acid nephrolithia sis [14][15][16][17], In this regard, the peak FEUA with suprofen (35.5 ± 9.6%) was similar to but less than that reported with 500 mg of ticrynafen (47.5 ± 5.7%) [18], another drug that was frequently associated with acute urate nephropathy [17], The contribution of this difference in uricosuric activity to the incidence and severity of the renal lesion associated with each agent is unknown. Interestingly, both of these potent uricosuric agents have identical thienylcarbonyl components in their structure [ 19,20], No participant in this study developed clinical indica tors of acute uric acid nephropathy.…”

Section: Discussionmentioning

confidence: 99%

Suprofen-Induced Uricosuria

Abraham¹,

Halstenson²,

Opsahl³

et al. 1988

Am J Nephrol

View full text Add to dashboard Cite

Suprofen, a nonsteroidal anti-inflammatory drug, has been associated with the onset of acute flank pain, hematuria, and transient renal dysfunction after the ingestion of one or two doses, particularly in young males. Potential mechanisms of this nephropathy were evaluated in normal males following ingestion of suprofen (200 mg) on two occasions: the first with ad libitum fluid intake and the second during forced water diuresis. On the first study occasion, creatinine clearance, the fractional excretions of uric acid (FEUA) and sodium (FENa), the urinary concentration of undissociated uric acid, and the urinary excretions of prostaglandins and glomerular and tubular proteins were assessed. On the second occasion, inulin and PAH clearances and FEUA and FENa were determined. Within 90 min after suprofen administration, the FEUA increased from 8.8 ± 2.6 to 35.5 ± 9.6% (p < 0.05). Urine became supersaturated for uric acid during ad libitum fluid intake. Glomerular filtration rate, renal plasma flow, and FENa decreased significantly, while prostaglandin and protein excretions did not change. The findings are consistent with acute uric acid nephropathy as a mechanism of suprofen-induced renal dysfunction.

show abstract

Effect of nonsteroidal anti-inflammatory drugs on the renal excretion of uric acid

Cited by 19 publications

References 5 publications

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

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

Uric acid levels and vascular disease

Suprofen-Induced Uricosuria

Contact Info

Product

Resources

About