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FGF23, fibroblast growth factor 23; RTA, renal tubular acidosis
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levels Loop diuretics (eg, furosemide) cause substantial renal potassium and magnesium losses Magnesium depletion should be suspected in persistent hypokalemia refractory to potassium repletion
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Magnesium deficiency also needs to be corrected at the same time, particularly in refractory hypokalemia
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Coca SG et al The cardiovascular implications of hypokalemia Am J Kidney Dis 2005 Feb;45(2):233 47 [PMID: 15685500] Groeneveld JH et al An approach to the patient with severe hypokalemia: the potassium quiz QJM 2005 Apr;98(4):305 16 [PMID: 15760922] Schaefer TJ et al Disorders of potassium Emerg Med Clin North Am 2005 Aug;23(3):723 47 [PMID: 15982543] Sherman FT The 3 hypo s of hospitalization Geriatrics 2005 May;60(5):9 10 [PMID: 15877479] Welfare W et al Challenges in managing profound hypokalemia BMJ 2002 Feb 2;324(7332):269 70 [PMID: 11823358]
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Clinical Findings
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A Symptoms and Signs
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Muscular weakness, fatigue, and muscle cramps are frequent complaints in mild to moderate hypokalemia Smooth muscle involvement may result in constipation or ileus Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis may be seen with severe hypokalemia (< 25 mEq/L) The presence of hypertension may serve as a clue to the diagnosis of hypokalemia from aldosterone or mineralcorticoid excess (Table 21 5)
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B Laboratory Findings
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Urinary potassium concentration is low (< 20 mEq/L) as a result of extrarenal fluid loss (eg, diarrhea, vomiting) and inappropriately high (> 40 mEq/L) with urinary losses (eg, mineralocorticoid excess, Bartter s syndrome, Liddle s syndrome) (Table 21 4) The transtubular [K+] gradient (TTKG) is a simple and rapid evaluation of net potassium secretion TTKG is calculated as follows: + + Urine K /Plasma K TTKG = -------------------------------------------------Urine osm/Plasma osm Hypokalemia with a TTKG > 4 suggests renal potassium loss with increased distal K+ secretion In such cases, plasma renin and aldosterone levels are helpful in differential diagnosis The presence of nonabsorbed anions, including bicarbonate, also increases TTKG Loop diuretics may cause hypomagnesemia as well as hypokalemia
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HYPERKALEMIA
ESSENTIALS OF DIAGNOSIS
Hyperkalemia may develop in patients taking ACE inhibitors, ARBs, potassium-sparing diuretics, or their combination, even with no or only mild renal dysfunction The ECG may show peaked T waves, widened QRS and biphasic QRS T complexes, or may be normal despite life-threatening hyperkalemia Measurement of plasma potassium level differentiates potassium leak from blood cells in cases of clotting, leukocytosis, and thrombocytosis from elevated serum potassium Rule out extracellular potassium shift from the cells in acidosis and assess renal potassium excretion
C Electrocardiogram
The electrocardiogram (ECG) shows decreased amplitude and broadening of T waves, prominent U waves, premature ventricular contractions, and depressed ST segments
General Considerations
Hyperkalemia usually develops in patients with advanced renal dysfunction but can also develop with no or only mild renal dysfunction (Table 21 6) Intracellular potassium shifts to the ECF in hyperkalemia associated with acidosis Serum potassium concentration rises about 07 mEq/L for every decrease of 01 pH unit during acidosis The common practice of repeatedly clenching and unclenching a fist during venipuncture may raise the potassium concentration by 1 2 mEq/L by causing acidosis and consequent potassium loss from cells In the absence of acidosis, serum potassium concentration rises about 1 mEq/L when there is a total body potassium excess of 1 4 mEq/kg However, the higher the serum potassium concentration, the smaller the excess necessary to raise the potassium levels further Mineralocorticoid deficiency from Addison s disease (high renin) or chronic kidney disease (CKD) (low renin) is another cause of hyperkalemia with decreased renal excretion of potassium Mineralocorticoid resistance due to genetic disorders, interstitial renal disease, or urinary tract obstruction also leads to hypokalemia ACE inhibitors or ARBs, commonly used in patients with congestive heart failure or CKD, may cause hyperkalemia The simultaneous use of spironolactone or eplerenone, or -blockers further increases the risk of hyperkalemia
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