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Is thiazide-produced uric acid elevation harmful? Analysis of data from the Hypertension Detection and Follow-up
Insights
Thiazide diuretics can increase uric acid and creatinine levels, but this does not appear to harm the kidneys. Lowering uric acid pharmacologically is not recommended for non-gouty hypertensive patients.
Area of Science:
- Nephrology
- Pharmacology
- Cardiology
Background:
- Thiazide diuretics are commonly prescribed for hypertension.
- The impact of thiazide diuretics on serum uric acid and creatinine levels requires further investigation.
- Baseline and therapy-induced changes in uric acid may influence kidney function and mortality.
Purpose of the Study:
- To examine the interaction between thiazide diuretics, serum uric acid, and serum creatinine levels.
- To assess the relationship between baseline uric acid, creatinine, and mortality.
- To determine if changes in uric acid levels due to therapy affect kidney function or mortality.
Main Methods:
- Analysis of 3693 participants from the Hypertension Detection and Follow-up Program.
- Stratification of participants by baseline uric acid levels (quartiles).
- Observation of serum creatinine and uric acid levels before and after thiazide diuretic therapy.
Main Results:
- Thiazide diuretics increased uric acid and creatinine, with a lesser increase in those with higher baseline uric acid.
- Baseline uric acid was a weak predictor of mortality, primarily in those with elevated creatinine.
- Changes in uric acid after therapy were inversely correlated with mortality in men.
- No significant kidney injury was observed related to baseline or therapy-induced uric acid changes.
Conclusions:
- Neither baseline nor therapy-induced changes in uric acid appear to cause kidney injury in hypertensive patients.
- Pharmacological lowering of uric acid is not indicated for non-gouty hypertensive patients on thiazide diuretics.
- Further research is needed to clarify the predictive value of baseline uric acid independent of other cardiovascular risk factors.
Abstract:
Interaction of thiazide diuretics and the serum uric acid and creatinine levels was studied in 3693 stepped care participants in the Hypertension Detection and Follow-up Program not receiving treatment at baseline. Among men grouped into quartiles by their level of uric acid at baseline, the upper quartile (average uric acid, 7.7 mg/dL [458 mumol/L]) had an average serum creatinine level of 1.2 mg/dL (106 mumol/L) and the lowest quartile (uric acid, 4.9 mg/dL [291 mumol/L]) had an average serum creatinine level of 1.1 mg/dL (97 mumol/L). Similar findings were present in women. Therapy with chlorthalidone or other thiazide-type diuretics tended to increase levels of uric acid and creatinine, but the increase in both was less in the upper quartile than in the lower quartile. Among individuals who were prescribed uric acid-lowering drugs, the level of serum creatinine increased just as much as in those whose uric acid level was not pharmacologically lowered. Baseline uric acid level was a weak predictor of mortality in men; the introduction of an interaction term for creatinine suggested that this effect was primarily restricted to those with elevated levels of both uric acid and creatinine at baseline. Change in uric acid level at one year after therapy was inversely correlated with mortality in men. There were few episodes of gout (only 15 recorded in five years among 3693 participants at risk). These results suggest that neither the baseline uric acid level nor the change in uric acid level produced by therapy injures the kidney. These results suggest no reason to lower uric acid levels pharmacologically in the treated hypertensive patient who is not gouty. They leave unanswered whether there is a predictive value to baseline uric acid level not explainable by other correlated cardiovascular risk factors.