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Published on: July 21, 2011
Potassium Magnesium Citrate Is Superior to Potassium Chloride in Reversing Metabolic Side Effects of Chlorthalidone
Wanpen Vongpatanasin1,2, John M Giacona1,3, Danielle Pittman1
1Department of Internal Medicine, Hypertension Section (W.V., J.M.G., D.P., A.M., G.K.), University of Texas Southwestern Medical Center, Dallas.
Insights
Potassium magnesium citrate (KMgCit) can prevent thiazide diuretic-induced hyperglycemia, unlike potassium chloride (KCl). This finding may enhance the cardiovascular safety and tolerability of hypertension treatments.
Area of Science:
- Endocrinology and Metabolism
- Cardiovascular Medicine
- Pharmacology
Background:
- Thiazide diuretics (TD) are first-line hypertension treatments, effective in lowering blood pressure and cardiovascular risk.
- TD use is associated with an increased risk of diabetes, potentially limiting long-term adherence.
- While potassium depletion was a suspected cause of TD-induced hyperglycemia, magnesium depletion is also triggered, with its role uninvestigated.
Purpose of the Study:
- To investigate the effect of potassium magnesium citrate (KMgCit) on fasting plasma glucose and liver fat during TD therapy.
- To compare KMgCit with potassium chloride (KCl) in modulating metabolic side effects of TD.
Main Methods:
- A double-blinded randomized controlled trial (RCT) was conducted with 60 non-diabetic hypertension patients.
- Patients received chlorthalidone alone for 3 weeks, followed by randomization to receive either KCl or KMgCit for 16 weeks.
- The primary endpoint was the change in fasting plasma glucose.
Main Results:
- Chlorthalidone monotherapy significantly increased fasting plasma glucose and decreased serum potassium and magnesium levels.
- KMgCit supplementation significantly attenuated the rise in fasting plasma glucose by 7.9 mg/dL compared to KCl.
- No significant differences in liver fat were observed between the KMgCit and KCl groups.
Conclusions:
- Potassium magnesium citrate (KMgCit) is more effective than potassium chloride (KCl) in preventing thiazide diuretic-induced hyperglycemia.
- This improved metabolic profile may enhance the tolerability and cardiovascular safety of TD therapy in hypertensive patients.
Background:
Thiazide diuretics (TD) are the first-line treatment of hypertension because of its consistent benefit in lowering blood pressure and cardiovascular risk. TD is also known to cause an excess risk of diabetes, which may limit long-term use. Although potassium (K) depletion was thought to be the main mechanism of TD-induced hyperglycemia, TD also triggers magnesium (Mg) depletion. However, the role of Mg supplementation in modulating metabolic side effects of TD has not been investigated. Therefore, we aim to determine the effect of potassium magnesium citrate (KMgCit) on fasting plasma glucose and liver fat by magnetic resonance imaging during TD therapy.
Methods:
Accordingly, we conducted a double-blinded RCT in 60 nondiabetic hypertension patients to compare the effects of KCl versus KMgCit during chlorthalidone treatment. Each patient received chlorthalidone alone for 3 weeks before randomization. Primary end point was the change in fasting plasma glucose after 16 weeks of KCl or KMgCit supplementation from chlorthalidone alone.
Results:
The mean age of subjects was 59±11 years (30% Black participants). Chlorthalidone alone induced a significant rise in fasting plasma glucose, and a significant fall in serum K, serum Mg, and 24-hour urinary citrate excretion (all P<0.05). KMgCit attenuated the rise in fasting plasma glucose by 7.9 mg/dL versus KCl (P<0.05), which was not observed with KCl. There were no significant differences in liver fat between the 2 groups.
Conclusions:
KMgCit is superior to KCl, the common form of K supplement used in clinical practice, in preventing TD-induced hyperglycemia. This action may improve tolerability and cardiovascular safety in patients with hypertension treated with this drug class.
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