HYPOKALEMIA
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Major causes of hypokalemia are outlined in Table 1-3. Atrial and ventricular arrhythmias are the most serious health consequences of hypokalemia. Pts with concurrent Mg deficit and/or digoxin therapy are at a particularly increased risk of arrhythmias. Hypokalemia can directly prolong the QT interval and is a significant cofactor in arrhythmias due to other causes of a prolonged QT interval. Other clinical manifestations include muscle weakness, which may be profound at serum [K+] <2.5 mmol/L, and, if hypokalemia is sustained, hypertension, ileus, polyuria, renal cysts, and even renal failure.
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The cause of hypokalemia is usually obvious from history, physical examination, and/or basic laboratory tests. However, persistent hypokalemia may require a more thorough, systematic evaluation (Fig. 1-2). Initial laboratory evaluation should include electrolytes, BUN, creatinine, serum osmolality, Mg2+, and Ca2+, a complete blood count, and urinary pH, osmolality, creatinine, and electrolytes. Serum and urine osmolality are required for calculation of the transtubular K+ gradient (TTKG), which should be <3 in the presence of hypokalemia (see also Hyperkalemia). Alternatively, a urinary K+-to-creatinine ratio of >13-mmol/g creatinine (>1.5-mmol/mmol creatinine) is compatible with excessive K+ excretion. Further tests such as urinary Mg2+ and Ca2+ and/or plasma renin and aldosterone levels may be necessary in specific cases.
The diagnostic approach to hypokalemia. See text for details. bp, blood pressure; DKA, diabetic ketoacidosis; FH-I, familial hyperaldosteronism type I; FHPP, familial hypokalemic periodic paralysis; HTN, hypertension; PA, primary aldosteronism; RAS, renal artery stenosis; RST, renin-secreting tumor; RTA, renal tubular acidosis; SAME, syndrome of apparent mineralocorticoid excess; TTKG, transtubular potassium gradient. (Reprinted with permission from Mount DB, Zandi-Nejad K: Disorders of potassium balance. In: Brenner and Rector’s The Kidney, 8th ed, Brenner BM [ed]. Philadelphia, Saunders, 2008.)
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Major causes of hypokalemia are outlined in Table 1-3. Atrial and ventricular arrhythmias are the most serious health consequences of hypokalemia. Pts with concurrent Mg deficit and/or digoxin therapy are at a particularly increased risk of arrhythmias. Hypokalemia can directly prolong the QT interval and is a significant cofactor in arrhythmias due to other causes of a prolonged QT interval. Other clinical manifestations include muscle weakness, which may be profound at serum [K+] <2.5 mmol/L, and, if hypokalemia is sustained, hypertension, ileus, polyuria, renal cysts, and even renal failure.
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The cause of hypokalemia is usually obvious from history, physical examination, and/or basic laboratory tests. However, persistent hypokalemia may require a more thorough, systematic evaluation (Fig. 1-2). Initial laboratory evaluation should include electrolytes, BUN, creatinine, serum osmolality, Mg2+, and Ca2+, a complete blood count, and urinary pH, osmolality, creatinine, and electrolytes. Serum and urine osmolality are required for calculation of the transtubular K+ gradient (TTKG), which should be <3 in the presence of hypokalemia (see also Hyperkalemia). Alternatively, a urinary K+-to-creatinine ratio of >13-mmol/g creatinine (>1.5-mmol/mmol creatinine) is compatible with excessive K+ excretion. Further tests such as urinary Mg2+ and Ca2+ and/or plasma renin and aldosterone levels may be necessary in specific cases.
The diagnostic approach to hypokalemia. See text for details. bp, blood pressure; DKA, diabetic ketoacidosis; FH-I, familial hyperaldosteronism type I; FHPP, familial hypokalemic periodic paralysis; HTN, hypertension; PA, primary aldosteronism; RAS, renal artery stenosis; RST, renin-secreting tumor; RTA, renal tubular acidosis; SAME, syndrome of apparent mineralocorticoid excess; TTKG, transtubular potassium gradient. (Reprinted with permission from Mount DB, Zandi-Nejad K: Disorders of potassium balance. In: Brenner and Rector’s The Kidney, 8th ed, Brenner BM [ed]. Philadelphia, Saunders, 2008.)
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