Prevention and Treatment of Diuretic Induced Hypokalemia

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The first approach to preventing diuretic-induced hypokalemia is to use the lowest dose possible (Table 1). With regard to thiazide diuretics, the majority of the blood pressure lowering effect is seen at doses of 12.5-25 mg/day. At higher doses, further blood pressure lowering is minimal, but rather, metabolic side-effects such as hypokalemia, hyperglycemia, and hypercholesterolemia become more prevalent.

Dietary manipulations can also be utilized in the prevention and treatment of diuretic-induced hypokalemia. As discussed earlier, overly strict dietary Na restriction as well as excess Na intake will tend to exacerbate renal K wasting. As a result, dietary Na should only be moderately restricted. If hypokalemia does develop, the patient can be initially tried on a diet of potassium rich foods. While mild potassium deficits may correct with dietary manipulation, this approach is not generally effective for patients with more severe hypokalemia. In this setting, food intake in amounts that would replenish a large potassium deficit would be complicated by excess caloric intake, potentially resulting in unwanted weight gain.

A more feasible approach to the hypokalemic patient is to administer potassium chloride supplements at doses of 20 to 40 mEq/day. Therapy is particu-

TABLE 1 Treatment and Prevention of Diuretic-Induced Hypokalemia

Use low doses of the diuretic

Moderate Na restriction (70-100 mEq/24 hr)

Correct magnesium deficit if present

Oral K supplements (20-40 mEq/24 hr)

Combined therapy with an angiotensin-converting enzyme inhibitor Combined therapy with an angiotensin II receptor antagonist Combined therapy with a potassium-sparing diuretic larly indicated for patients taking cardiac glycosides and patients with underlying cardiac disease. In these high risk patients even mild hypokalemia should be treated as more severe reductions in the serum K concentration can rapidly develop under conditions of increased stress. In this setting, stress-induced increases in catecholamines can result in a shift of K into the intracellular compartment, predisposing such a patient to complex ventricular arrhythmias. In patients who appear resistant to oral supplements, magnesium levels should be checked. Chronic use of both thiazide and loop diuretics can lead to magnesium deficiency which, in turn, can result in renal K wasting. In the setting of magnesium deficiency renal K wasting will continue unabated until the magnesium deficit is first corrected.

An alternative approach is to coadminister an agent which will counteract diuretic-induced renal potassium wasting. One such class of drugs are the an-giotensin-converting enzyme inhibitors. These drugs limit the development of hypokalemia when given with diuretics and provide the advantage of further lowering the blood pressure. These agents block the conversion of angiotensin I to angiotensin II and thereby decrease circulating levels of aldosterone normally provoked by diuretic-induced renin release. The angiotensin II receptor antagonists will similarly decrease aldosterone levels and minimize diuretic-induced hypokalemia but do so by acting one step further down the renin-angiotensin-aldosterone cascade.

Potassium-sparing diuretics can also be utilized to counteract the effects of diuretic-induced hyperaldosteronism. Spironolactone is the most direct acting of these in that it blocks aldosterone binding to its cytoplasmic receptor. Triamterene and amiloride indirectly inhibit the kaliuretic effect of aldosterone. As discussed below these agents decrease the luminal electronegativity in the aldosterone sensitive distal nephron, thereby creating a less favorable electrochemical gradient for potassium secretion. The potassium sparing diuretics also diminish net acid excretion which has the effect of minimizing the development of metabolic alkalosis characteristically associated with use of loop and thiazide diuretics. By limiting the development of an alkaline pH renal K losses will be further minimized since metabolic alkalosis increases distal K secretion. Another advantage of these agents is that they decrease magnesium excretion, allowing for the correction of any magnesium deficit that might underlie loop or thiazide diuretic-induced hypokalemia. All of these agents can be given alone or in fixed-dose combinations with the thiazide diuretics. The most important complication associated with use of these agents is the development of fatal hyperkalemia. As a result, patients should be evaluated carefully for any factors which might predispose to the development of hyperkalemia. Furthermore the serum K concentration should be followed closely during the initiation of therapy and whenever the clinical condition of the patient changes.

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