Diuretics in the therapy of hypertension

Reyes, Ariel J.

doi:10.1038/sj.jhh.1001349

Cited by 27 publications

(14 citation statements)

References 39 publications

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“…Thiazides also induce hyperuricemia, even at low dose [50]. The elevation in mean serum uric acid caused by low dose of diuretics (12.5mg hydrochlorothiazide, or 1.25 mg of bendrofluazide) may occur without any significant changes in serum potassium concentration [51-53], thereby suggesting that alterations in serum uric acid may be more sensitive to the action of diuretics than serum potassium.…”

Section: Hyperuricemia and Hypokalemia: Common Abnormalities Even Witmentioning

confidence: 99%

Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia

Reungjui

Pratipanawatr²,

Johnson³

et al. 2008

Current Opinion in Nephrology and Hypertension

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Purpose of review-1. To review the current controversies related to the use of thiazide diuretics as first-line treatment of hypertension 2. To discuss the causal roles for hyperuricemia and hypokalemia on the adverse consequences of thiazide usage Recent findings-Thiazides significantly reduce morbidity and mortality in hypertensive subjects. However, there remains debate about thiazide usage as first line treatment of hypertension. This negative impact of thiazides may be partially attributed to the ability of thiazides to exacerbate features of metabolic syndrome and/or increase the risk for developing diabetes. Several clinical trials suggest that thiazide-induced hyperuricemia and hypokalemia may account for some of these negative effects. Thiazide treatment is also associated with a decline of renal function in spite of a lowering blood pressure. In this review, we discuss the clinical and experimental evidence supporting a potential role of hyperuricemia and hypokalemia on the development of renal injury and worsening of the metabolic syndrome..Summary-Hyperuricemia and hypokalemia may have pivotal roles in the exacerbation of the metabolic syndrome in response to thiazides. We propose that controlling serum uric acid and serum potassium could improve thiazide efficacy and also reduce its risk for inducing metabolic syndrome or diabetes.

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Section: Hyperuricemia and Hypokalemia: Common Abnormalities Even Witmentioning

confidence: 99%

Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia

Reungjui

Pratipanawatr²,

Johnson³

et al. 2008

Current Opinion in Nephrology and Hypertension

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“…The increase in serum UA concentration caused by diuretics is apparent at low doses and increases in dose‐dependent fashion [79,86,87]. Antihypertensive treatments with dosages of diuretics that are substantially lower than those used in the past, including 12.5 mg of hydrochlorothiazide [88,89], 12.5–25 mg of chlorthalidone [38,90,91] and 1.25 mg of bendrofluazide [86] once daily, increase serum UA concentration.…”

Section: Diuretics and Uric Acidmentioning

confidence: 99%

The increase in serum uric acid concentration caused by diuretics might be beneficial in heart failure

Reyes¹

2005

European J of Heart Fail

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Patients with mild-moderate chronic heart failure (CHF) often have raised levels of serum uric acid (UA). This is due, amongst other factors, to reduced UA excretion by the kidneys, which is partly explained by restriction of sodium intake and treatment with diuretics. The decline in renal function that parallels worsening cardiac function also contributes to elevated serum UA in patients with advanced CHF. However, UA production also appears to be augmented in CHF. Because UA scavenges various reactive oxygen species, diureticinduced elevations in serum UA could be beneficial in patients with CHF. This concept is supported by the superior performance of antihypertensive therapy with diuretics in preventing heart failure. The present hypothesis may be tested by examining the effects of add-on treatment with a thiazide-type diuretic on morbidity and mortality, or surrogate variables, in asymptomatic patients with left ventricular dysfunction but without fluid retention.

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“…Considered together with the aforementioned studies, the fall in arterial pressure recorded in the present study was clinically significant and more than a subtle change. Although increasing the dose of trichlormethiazide might achieve further reduction in blood pressure, we only used a low dose of trichlormethiazide, because the adverse effects on metabolism are more common with higher doses of thiazide diuretics 14,22 .…”

Section: Discussionmentioning

confidence: 99%

Comparison of effects of azelnidipine and trichlormethiazide in combination with olmesartan on blood pressure and metabolic parameters in hypertensive type 2 diabetic patients

Yoshii

Mita²,

Sato

et al. 2011

Journal of Diabetes Investigation

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Aims/Introduction: Angiotensin II type 1 receptor blockers (ARB) are regarded as first‐line treatment for type 2 diabetes with hypertension. However, lowering blood pressure to the target level often requires more than one antihypertensive agent as recommended by the guideline. In this open‐label, prospective, crossover clinical trial, we compared the effects of combination treatment of ARB with a calcium channel blocker (CCB) or with a low‐dose thiazide diuretic on blood pressure (BP) and various metabolic parameters in hypertensive patients with type 2 diabetes.Materials and Methods: A total of 39 Japanese type 2 diabetics with hypertension treated with olmesartan (20 mg/day) for at least 8 weeks were recruited to this study. At study entry, treatment was switched to either olmesartan (20 mg/day)/azelnidipine (16 mg/day) or olmesartan (20 mg/day)/trichlormethiazide (1 mg/day) and continued for 12 weeks. Then, the drugs were switched and treatment was continued for another 12 weeks. We measured clinical blood pressure and various metabolic parameters before and at the end of each study arm.Results: Compared with the olmesartan/trichlormethiazide treatment, treatment with olmesartan/azelnidipine achieved superior clinical blood pressure and pulse rate control. In contrast, the treatment with olmesartan/trichlormethiazide resulted in increased HbA1c, serum uric acid and worsening of estimated glomerular filtration rate, though there were no differences in other metabolic parameters including urine 8‐hydroxy‐2′‐deoxyguanosine, C‐reactive protein and adiponectin between the two treatments.Conclusions: Our results show that the combination of ARB with azelnidipine is more beneficial with regard to blood pressure control and metabolic outcome than the combination of olmesartan with low dose trichlormethiazide. This trial was registered with UMIN clinical trial registry (no. UMIN000005064). (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2011.00135.x, 2011)

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Diuretics in the therapy of hypertension

Cited by 27 publications

References 39 publications

Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia

Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia

The increase in serum uric acid concentration caused by diuretics might be beneficial in heart failure

Comparison of effects of azelnidipine and trichlormethiazide in combination with olmesartan on blood pressure and metabolic parameters in hypertensive type 2 diabetic patients

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