Is Thiazide-Produced Uric Acid Elevation Harmful? Analysis of Data From the Hypertension Detection and Follow-up Program

doi:10.1001/archinte.1987.00370040027005

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Vol. 147 No. 4, April 1987

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Is Thiazide-Produced Uric Acid Elevation Harmful?

Analysis of Data From the Hypertension Detection and Follow-up Program

Herbert G. Langford, MD; M. Donald Blaufox, MD; Nemat O. Borhani, MD; J. David Curb, MD; Agostino Molteni, MD, PhD; Kenneth A. Schneider, MD; Sara Pressel, MS

Arch Intern Med. 1987;147(4):645-649.

Abstract

• Interaction of thiazide diuretics and the serum uricacid and creatinine levels was studied in 3693 stepped careparticipants in the Hypertension Detection and Follow-up Programnot receiving treatment at baseline. Among men grouped intoquartiles by their level of uric acid at baseline, the upperquartile (average uric acid, 7.7 mg/dL [458 µmol/L]) hadan average serum creatinine level of 1.2 mg/dL (106 µmol/L)and the lowest quartile (uric acid, 4.9 mg/dL [291 µmol/L])had an average serum creatinine level of 1.1 mg/dL (97 µmol/L). Similar findings were present in women. Therapy with chlorthalidoneor other thiazide-type diuretics tended to increase levels ofuric acid and creatinine, but the increase in both was lessin the upper quartile than in the lower quartile. Among individualswho were prescribed uric acid—lowering drugs, the levelof serum creatinine increased just as much as in those whoseuric acid level was not pharmacologically lowered. Baselineuric acid level was a weak predictor of mortality in men; theintroduction of an interaction term for creatinine suggestedthat this effect was primarily restricted to those with elevatedlevels of both uric acid and creatinine at baseline. Changein uric acid level at one year after therapy was inversely correlatedwith mortality in men. There were few episodes of gout (only15 recorded in five years among 3693 participants at risk).These results suggest that neither the baseline uric acid levelnor the change in uric acid level produced by therapy injuresthe kidney. These results suggest no reason to lower uric acidlevels pharmacologically in the treated hypertensive patientwho is not gouty. They leave unanswered whether there is a predictivevalue to baseline uric acid level not explainable by other correlatedcardiovascular risk factors.

(Arch Intern Med 1987;147:645-649)

Footnotes

Accepted for publication July 7, 1986.

A complete list of members who participated in this researchstudy appears at the end of this article.

Reprint requests to Hypertension Detection and Follow-up Program,DHVD, National Heart, Lung, and Blood Institute, National Institutesof Health, Room 6A-14, Federal Bldg, 7550 Wisconsin Ave, Bethesda,MD 20892 (Scientific Project Officer).

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