Hypokalemia and Hypomagnesemia

Mild hypokalemia (Plasma [K] 3.3-3.8 mmol liter^1) and metabolic alkalosis occurs in up to 20% of patients and will appear within the first 6 weeks of starting therapy. Significant hypokalemia (<3.2 mmol liter-1) should not be ignored and warrants further investigation (e.g., underlying hyperaldosteron-ism) and/or potassium supplementation (especially in elderly patients on di-goxin and those with a history of ischemic heart disease and liver cirrhosis). Hypokalemia is thought to predispose to rhabdomyolysis and acute renal failure, especially in young subjects engaged in heavy physical exertion; hypokalemia should be monitored closely in young and physically active hypertensives. While mild hypokalemia is well tolerated and not associated with an increased risk of cardiac dysrhythmias, it may be a factor in diuretic-induced glucose intolerance and hyperlipidemia, and as already mentioned, potassium depletion has been causally linked to hypertension and stroke. Therefore, it is probably advisable to avoid even mild hypokalemia during long-term diuretic therapy. Hypomagnesemia is more likely with a long-term loop diuretic than a thiazide, because magnesium is absorbed mainly along the thick ascending limb. Moreover, chronic magnesium deficiency prevents correction of associated hypokalemia and this is one reason why potassium-sparing diuretics, which are also magnesium-sparing (particularly amiloride and triamterene), are more effective in treating hypokalemia than oral KC1 supplements. Hypokalemia, hypomagnesemia, and hypertriglyceridemia are more likely to be found in hypertension associated with excessive alcohol intake.

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