A 55-year-old woman with diabetes, hypertension, and chronic kidney disease (CKD) stage 4 is admitted to the hospital for treatment of left lower-extremity cellulitis. Laboratory studies on admission show a creatinine level of 2.5 mg/dL (glomerular filtration rate [GFR] is 20 mL/min per 1.73 m2
She is put on renally dosed vancomycin to treat her cellulitis. As the hospitalist, how should you manage her multiple electrolyte abnormalities?
Overview of the issue
Chronic kidney disease is progressively becoming a common disease, already affecting an estimated 15% of the U.S. adult population. Although CKD is traditionally viewed as an outpatient issue, it is an increasingly documented problem in the hospital setting. This is reflected in the fact that, as CKD advances, rates of admissions increase.
CKD is also an important risk factor for acute kidney injury. Additionally, rates of readmission for CKD patients are higher than those without CKD. Given that CKD is a “silent disease” that many patients do not realize they have, it is very possible that the first documentation of CKD could happen during an acute hospitalization.
Among the various manifestations of CKD, electrolyte abnormalities are the most likely ones hospitalists will run into.
Overview of the data
Hypokalemia and Hypomagnesemia
Hypokalemia (potassium levels less than 3.5 mEq/L) is not as common as hyperkalemia (potassium levels greater than 5.0 mEq/L) in CKD, which is the result of impaired renal excretion of potassium. Hypokalemia can occur as a result of GI losses, urinary losses, or decreased intake and can be worsened by the use of certain drugs, such as non–K-sparing diuretics.
In the setting of diuretic use involving thiazides and loop diuretics, hypokalemia is dose and sodium-intake dependent. Potassium deficiency worsens the effects of detrimental sodium excess, which plays a role in hypertension and its associated complications. Potassium also has a protective vascular effect, which is a major reason why potassium should be kept normal in patients with CKD.
Acutely, hypokalemia can cause arrhythmias, ileus, and paralysis, which are all indications for immediate repletion. In these cases, hypokalemia must be repleted carefully in small increments (some suggest 20 mEq doses), and the patient must be monitored frequently to avoid hyperkalemia. If patients are persistently hypokalemic, several options can be considered based on the underlying cause. Dietary modifications with foods rich in potassium (containing 250mg/100g) can be suggested. Daily potassium chloride supplementation can be used in those on diuretic therapy who have hypokalemia and metabolic alkalosis (bicarbonate levels greater than 30 mEq/L). Alkalinizing salts, containing citrate or bicarbonate, can be used in hypokalemia without metabolic alkalosis. Initiation of angiotensin-converting-enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), beta-adrenergic blockers, and K-sparing diuretics can be used as well.
Potassium supplementation and K-sparing diuretics should be used with extreme caution in CKD 3 and 4 given the risk of overcorrection. If potassium supplements or drugs to raise serum potassium are initiated in house, potassium should be rechecked within a week. These treatments should be avoided in individuals with diabetes, who are at highest risk for hyperkalemia given hyporeninemic hypoaldosteronism (type IV renal tubular acidosis).
Hypomagnesemia (magnesium levels less than 1.8 mEq/L) is also a common occurrence with diuretic therapy. Urinary magnesium losses parallel those of potassium in loop-diuretic treated CKD patients, so deficiency in total body magnesium is likely in most diuretic-treated patients with hypokalemia. Additionally, hypomagnesemia increases tubular secretion of potassium, causing hypokalemia.
There is emerging evidence that hypomagnesemia can play a part in progression to end-stage renal disease. In the setting of cardiovascular disease, which often co-exists with CKD, the risk of hypomagnesemia precipitating arrhythmia necessitates repletion to a normal level. Any of the magnesium salts and antacids can be used for treatment. K-sparing diuretics are also magnesium sparing. An important side effect of magnesium repletion is diarrhea, which can potentiate electrolyte losses and reduce long-term adherence rates.
Acid-base balance is maintained by the kidney through urinary excretion of hydrogen ions both as titratable acids and ammonium. In CKD, renal excretion of the daily acid load is impaired, primarily from decreased ammonium excretion caused by there being too few functioning nephrons.