In the clinical setting, measurement of the electrolytes, or solutes, in the blood is one of the most frequently ordered laboratory tests. The test is known by many names, including electrolytes, ‘lytes, basic metabolic profile (BMP), serum chemistries, CHEM‐7, CHEM‐10, and sequential multiple analysis‐7 (SMA‐7). Interpretation of the results provides information about volume status, acid‐base status, and baseline renal function. Evaluating any disequilibrium in electrolytes can be challenging and requires an understanding of the pathophysiology of diseases that can cause electrolyte imbalances; the counterregulatory pathways of the body to correct the imbalance; and the various approaches to augmenting the specific electrolyte through use of medications, specific electrolyte replacement, or removal of the electrolyte. Understanding these disturbances can improve patient care, be cost‐effective, prevent complications from primary disease, and ultimately reduce mortality and morbidity.
Dysnatremias, or alterations in sodium (Na+) concentration, are less about the amount of circulating sodium and more about the amount of free water in the serum. Osmolarity is defined as the concentration of solutes per liter of solution. In the human body, serum osmolarity ranges from 280 to 300 mOsm/L.1 Increased serum osmolarity suggests fluid depletion with concentration of solutes, while decreased serum osmolarity suggests an increase in fluid with dilution of solutes. A simple calculation can be performed using sodium, BUN, and glucose to determine a patient's serum osmolarity (mOsm/L): 2(Na+ [mEq/L]) + (BUN [mg/dL]/2.8) + (glucose [mg/dL]/18).2 Water regulation is primarily controlled by secretion of antidiuretic hormone (ADH) from the posterior hypothalamus via a mechanism of absorption and excretion of fluid within the nephrons.3 As a consequence of this regulation, dysnatremias primarily occur through alterations in water homeostasis.
Hyponatremia (Na+ <135 mEq/L) can occur in conditions with low, normal, or elevated osmolarity, as well as in hypovolemic, hypervolemic, or euvolemic conditions.4 The most common type of hyponatremia is hypo‐osmolar hypervolemia, which is due to fluid overload5 and can be attributed to acute illness, heart failure, cirrhosis, renal failure, or aggressive administration of IV fluid.4 Hyperglycemia can cause a hyperosmolar hyponatremia by causing water to shift from the intracellular compartment to the extracellular compartment, thus causing a dilution of sodium.5 Syndrome of inappropriate antidiuretic hormone (SIADH) causes a hypo‐osmolar, euvolemic hyponatremia that is the result of an increase in circulating ADH due either to hypersecretion from the posterior pituitary or an ectopic source.6 The degree of the hyponatremia and the rapidity with which it develops are the most important determinants in onset of symptoms.7,8 Signs and symptoms generally begin to develop once the serum sodium has reached 125 to 130 mEq/L;5 if the decline is slow to develop, however, the patient may be asymptomatic until levels fall below 110 mEq/L.9 Clinical manifestations are the result of CNS dysfunction due to cerebral edema and include headache, nausea, vomiting, weakness, lethargy, seizure, coma, and permanent brain damage.5,8‐10 Mild or asymptomatic hyponatremia can be treated with fluid restriction only, while severe or symptomatic disease requires fluid restriction and sodium replacement.5,8,10 This correction must be done slowly, usually over a period of 1 to 3 days, and the rate of sodium administration should not exceed 1 to 2 mEq/L/hour during replacement infusion. The resultant serum sodium level should not be greater than 135 mEq/L.5,8,10,11 If the correction occurs too quickly, an osmotic demyelinating injury called central pontine myelinolysis (CPM) can occur and manifest as quadriplegia, flaccid paralysis, dysarthria, or seizures.4,8,11
Hypernatremia (Na+ >145 mEq/L) can occur in either hypervolemic or hypovolemic conditions.4,5,10,12 The most common cause of hypernatremia is volume depletion with a total body free water deficit that occurs with insensible losses from fever, sweating, vomiting, diarrhea, or primary hypodipsia.4,6,10,12 Diabetes insipidus can cause a hypovolemic hypernatremia through one of two mechanisms: decreased secretion of AD H from the posterior pituitary or increased renal resistance to ADH, with resultant inability to concentrate urine.6 Hypervolemic hypernatremia is often seen in the hospital setting as a result of aggressive IV administration of 0.9% saline or infusion of hypertonic fluids,4,5 but it can also be seen in primary hyperaldosteronism.4,13 Signs and symptoms due to the increase in serum sodium include altered mental status, seizures, hyperreflexia, spasticity, and lethargy.9,10,12 If volume depletion is the cause of the hypernatremia, patients may have orthostatic hypotension, tachycardia, poor skin turgor, and dry mucous membranes.14 The goal of treatment for hypernatremia is to normalize the serum sodium and restore the extracellular and intracellular fluid compartments with either hypotonic or isotonic fluids.10,12 Rapid correction of an elevated serum sodium can cause severe fluid shifts and result in cerebral edema, seizures, permanent brain damage, and death from cerebral herniation.12,15
- Understanding of the pathophysiology of diseases that can cause electrolyte imbalances, the counterregulatory pathways of the body to correct the imbalance, and the various approaches to correcting the imbalance is paramount to treatment.
- Changes in sodium concentration are less about the amount of circulating sodium and more about the amount of free water in the serum, and dysnatremias primarily occur through alterations in water homeostasis.
- When replacing potassium intravenously, replacement should not exceed 10 mEq/hour, and patients should be placed on continuous cardiac telemetry to monitor for arrhythmias.
- Imbalances in potassium and calcium can result in abnormal ECG findings.
- Calcium, magnesium, phosphorus, and parathyroid hormone are all very intimately related, and fluctuations from the norm of one can have a major impact on the levels of another.
Potassium (K+) is the most abundant intracellular cation. The ratio of its intracellular and extracellular levels is vital for cell metabolism as well as neuromuscular and cardiac electrical transmission.16,17 The kidneys are the main regulator of potassium homeostasis and must adjust quickly to fluctuations in potassium level by altering the secretion or reabsorption within the nephron.18 The most common causes of dyskalemias include medication side effects, dietary intake, and renal dysfunction.19,20
Hypokalemia (K+ <3.5 mEq/L) is frequently due to increased renal excretion of potassium resulting from diuretic use, hyperaldosteronism, and hypomagnesemia.4,19 Insulin, beta2‐adrenergic agonists, and alkalosis can also cause extracellular potassium to be shifted into the intracellular compartment.4,19 Signs and symptoms of hypokalemia include muscle weakness, constipation, palpitations, and fatigue.5,9,19 ECG can show flat T waves, ST‐segment depression, and U‐wave formation.19,21 Mild, asymptomatic hypokalemia can be managed with oral replacement using potassium chloride (KCl), while severe or symptomatic hypokalemia requires IV replacement.19,21 When replacing potassium intravenously, care should be taken to avoid rebound hyperkalemia. Replacement should not exceed 10 mEq/hour, and patients should be placed on continuous cardiac telemetry to monitor for arrthymias.19,21 If a concomitant hypomagnesemia is present, magnesium levels must be repleted prior to potassium replacement because of the role of magnesium in regulating the sodium‐potassiumadenosine triphosphate (Na‐K‐ATPase) pump.5
Hyperkalemia (K+ >5.0 mEq/L) is a common complication seen with renal insufficiency, acidosis, and medication side effects of ACE inhibitors, angiotensin II receptor blockers (ARBs), and aldosterone antagonists.4,20 Pseudohyperkalemia must be ruled out as a cause of false laboratory elevation of potassium. This phenomenon can be caused by hemolysis (in vivo or during the phlebotomy process), extreme erythrocytosis, and/or thrombocytosis and does not reflect actual serum potassium levels.22 Common physical manifestations of hyperkalemia include muscle weakness, muscle cramping, and paresthesias.5,9,21 ECG may show tall or peaked T waves, prolonged PR interval, ST depression, widened QRS complex, or loss of the P wave.9,21 The initial medication given to a patient with symptomatic hyperkalemia is IV calcium (Ca2+), as either gluconate or chloride, to stabilize the cardiac membranes and prevent arrhythmias while awaiting definitive treatment.4 The treatment of hyperkalemia involves shunting extracellular potassium into the intracellular compartment, giving oral or rectal resins that bind to the potassium and are excreted in the stool, or hemodialysis.20
Ca2+ is one of the most prevalent cations in the human body and is primarily stored in the bones and teeth. The physiologic processes that require calcium include blood coagulation; nerve excitability; and development of action potentials for skeletal, cardiac, and smooth muscle contractions.23 Calcium levels are regulated by a complex feedback mechanism involving parathyroid hormone (PTH) secretion, calcitonin secretion of the thyroid, and calcitriol secretion of the kidneys. Along with vitamin D and phosphorus, these substances play crucial roles in the osteoclastic activity in bone and in the ability of the intestines and kidneys to absorb and store calcium that is ingested.23 Three forms of calcium are found in the human body: ionized, bound, and complexed; ionized calcium is the most physiologically significant.23,24
Hypocalcemia (Ca2+ <8.5 mg/dL) can occur if any of the previously mentioned pathways is altered. This can be seen with primary thyroid or parathyroid diseases, after thyroid or parathyroid surgery, in chronic renal failure, or with vitamin D deficiency. Since calcium is bound to albumin in serum, hypoalbuminemia can cause a pseudohypocalcemia.4,5,25 Determining a true hypocalcemia requires calculation of a calcium level that has been corrected for albumin or measurement of ionized calcium.4 In the hospital setting, chelation of calcium can occur if citrated blood products have been given or if citrate is being used as an anticoagulant with continuous renal replacement therapy.4 Severe hypocalcemia may result in a prolonged QT interval and can precipitate torsades de pointes.24,25 Symptoms begin to develop when Ca2+ levels fall below 7.5 mg/dL and can include paresthesias, hyperreflexia, tetany, muscle spasm, muscle cramps, and seizures.5,9,24 Classic physical examination findings of hypocalcemia include Chvostek sign (facial spasms following percussion on the facial nerve) and Trousseau sign (carpopedal spasms of the hand elicited by inflation of a sphygmomanometer above systolic BP for several minutes).9,26 Oral replacement is the treatment of choice for asymptomatic hypocalcemia, and IV supplementation is used for severe or symptomatic deficiency.5,24 Because of the effect of magnesium on calcium balance, any magnesium deficit must be replenished prior to calcium administration.27
“Understanding and managing electrolyte imbalances can be cost‐effective and help to prevent primary disease complications.”
Hypercalcemia (Ca2+ >10.5 mg/dL) is most commonly caused by hyperparathyroidism, bone malignancy, or prolonged immobilization.25 Patients are generally asymptomatic until levels exceed 12 mg/dL.5 Common symptoms associated with hypercalcemia include abdominal/flank pain, bone pain, muscle weakness, and nephrolithiasis, with less common findings of lethargy, confusion, depression, and fatigue.9,25 The classic medical phrase referring to stones, bones, moans, psychic groans, and fatigue overtones describes this constellation of symptoms.28 Treatment of hypercalcemia involves restriction of calcium‐containing medications or foods; IV fluid administration with loop diuretics to facilitate calcium excretion; and, as a last resort, hemodialysis.5
Magnesium (Mg2+) is the second most abundant intracellular cation and is vital for many cell processes, including ATP processing, macronutrient and energy metabolism, and neuromuscular transmission.29 Levels are regulated by intestinal absorption, renal excretion, and tubular reabsorption of magnesium to maintain homeostasis.18
Hypomagnesemia (Mg2+ <1.5 mEq/L) is commonly seen in chronic alcoholism from poor dietary intake, reduced intestinal absorption, and increased renal excretion from the ethanol effect.29 It can also be caused by excessive GI loss (vomiting, diarrhea, fistulae) and intracellular shifts from refeeding syndrome.27 Symptoms of lethargy, confusion, tremors, convulsions, hyperreflexia, and paresthesias do not develop until levels fall below 1.0 mg/dL.9,27,29 Oral replacement is acceptable for mild, asymptomatic conditions; exercise caution to avoid osmotic diarrhea from the magnesium salts.5 Intravenous replacement is reserved for severe or symptomatic deficiency, with careful monitoring for rebound hypermagnesemia and arrhythmias.27,29
Hypermagnesemia (Mg2+ >2.5 mEq/L) is much less common than hypomagnesemia and is generally seen only in renal failure patients, supratherapeutic replacement, and antacid abuse.27,29 Symptoms begin to manifest once levels exceed 4.0 mg/dL and can range from decreased deep tendon reflexes, bradycardia, and hypotension to flaccid paralysis and cardiac arrest.9,27 Dietary restriction, elimination of magnesium‐containing medications, loop diuretics, and dialysis are the mainstays of treatment.4
Phosphorus, or phosphate, (PO43−) is involved in many essential intracellular functions, such as ATP synthesis, phospholipid membrane formation, and 2,3 diphosphoglycerate (DPG) formation for oxygen delivery to tissues. Other functions include bone development and macronutrient metabolism.27,30 Phosphorus is primarily stored in bone and teeth; more than 90% of circulating phosphate is excreted by the kidneys in the proximal tubules.18,27 Calcium, magnesium, phosphorus, and PTH are all intimately related, and fluctuations from the norm of one can have a major impact on the levels of another.
Hypophosphatemia (PO43− <2.6 mg/dL) can be caused by intracellular shifting, as seen with refeeding syndrome or respiratory alkalosis; increased renal excretion resulting from diuretic use or hyperparathyroidism; and increased intestinal loss or malabsorption, as occurs with diarrhea, vitamin D deficiency, or high‐output fistulae.4,27,30 The signs and symptoms that develop from hypophosphatemia are mainly from decreases in ATP and 2,3‐DPG synthesis and can include decreased muscle strength, respiratory failure, hypoxemia, paresthesias, hemolysis, and lethargy.30 Treatment is directed at the cause of the deficiency. Since most conditions that cause hypophosphatemia are transient in nature, treating the primary condition will often stabilize phosphate levels. If patients are symptomatic from the hypophosphatemia, oral replacement should be attempted before IV formulations are used because of the possibility of hyperphosphatemia.4
Hyperphosphatemia (PO43− >4.5 mg/dL) is most commonly caused by chronic renal failure as a result of decreased renal excretion of phosphate, but the condition can also be seen in vitamin D toxicity and hematopoietic malignancies.27,30 Calcium and phosphate have an inverse relationship, and the signs and symptoms of hyperphosphatemia are similar to those of hypocalcemia: conduction disturbances, tetany, muscle weakness, and hyperreflexia.27,30 Hyperphosphatemia can be managed with oral binding resins taken with meals but often requires dialysis to protect against cardiac arrhythmias.4,30
CHLORIDE AND BICARBONATE
Chloride (Cl−) and bicarbonate (HCO3−) are prevalent anions in serum and are primarily involved in acid‐base regulation and fluid osmotic pressure balance.5,27 Chloride levels are augmented by adjusting the absorption of chloride from dietary sources in the duodenum and proximal jejunum and from hydrochloric acid secretion of the stomach and by altering the secretion and reabsorption of chloride in the renal tubules of the kidneys.31,32 Bicarbonate levels are maintained by varying production, secretion, and reabsorption within the renal tubule.33 Because of the intimate relationship between these electrolytes and the acid‐base regulation of the kidneys and lungs, chloride and bicarbonate levels will be adjusted based on changes in the serum pH. The signs and symptoms of these alterations are caused by the acid‐base disturbances, not by the electrolytes themselves.
Hypochloremia (Cl− <95 mEq/L) is a decrease in available chloride within the GI tract and can result from intractable vomiting, nasogastric tube suctioning, high‐dose acidsuppression therapy, and duodenal fistulae.27 This decrease in chloride will result in a primary metabolic alkalosis or act as compensation for a respiratory or metabolic acidosis. Hyperchloremia (Cl− greater than 105 mEq/L) is primarily caused by aggressive administration of IV fluids or profound volume depletion. Normal saline (0.9%) contains 154 mEq/L of sodium chloride (NaCl) and can quickly overload the ability of the renal tubules to excrete additional chloride. This most commonly presents as a primary metabolic acidosis or as a compensatory response to an alkalosis.
Primary conditions of bicarbonate alterations are rare. Instead, most disequilibrium involving bicarbonate is seen only as a result of other conditions. Hypobicarbonatemia (HCO3− <22 mEq/L) is seen with renal failure, various metabolic acidoses, and compensation for a respiratory alkalosis.34 Hypercarbonatemia (HCO3− >27 mEq/L) most commonly occurs with compensation for a chronic respiratory acidosis, contraction alkalosis from volume depletion, and aggressive IV administration of bicarbonate‐containing or acetate‐containing fluids.34
BUN AND CREATININE
While BUN and creatinine are not true electrolytes, they are included in a basic metabolic panel and can provide vital information on the function of the renal filtration system. BUN levels are the result of balance between urea production by the liver35 and reabsorption and secretion within the nephron.3 Creatinine is secreted at a constant rate based on skeletal muscle mass and is excreted only by the kidney. This accounts for the inverse relationship between creatinine levels and renal function.36
Elevations of BUN (>20 mg/dL), ie, azotemia, without elevations in creatinine are due to increased urea production and absorption. This is most commonly the result of overfeeding of protein, RBC digestion within the intestines from upper GI bleeding and the anabolic effect of systemic corticosteroids.36 Elevation of BUN and creatinine in tandem is evaluated based on the ratio of BUN to creatinine. A ratio greater than 20:1 suggests prerenal causes, such as dehydration or volume depletion due to increased rates of urea absorption in the proximal tubule in the nephron, while a ratio less than 20:1 implies intrinsic renal causes, such as acute tubular necrosis, glomerulonephritis, or chronic kidney disease (CKD).36
Medicine has come a long way since Peters and Van Slyke published their classic textbook on clinical chemistry interpretations more than 60 years ago.37 The electrolyte imbalances summarized in Table 1 are common occurrences throughout every subspecialty in medicine. Understanding these disturbances can improve patient care, be cost‐effective, prevent complications from primary disease, and ultimately reduce mortality and morbidity. JAAPA
1. Guyton AC, Hall JE. The body fluid compartments: extracellular and intracellular fluids; interstitial fluid and edema. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:291-306.
2. Isakow W. Common equations and rules of thumb in the intensive care unit. In: Kollef MH, Bedient TJ, Isakow W, Witt CA, eds. The Washington Manual of Critical Care.
Philadelphia, PA: Lippincott Williams and Wilkins; 2008:522-525.
3. Guyton AC, Hall JE. Regulation of extracellular fluid osmolarity and sodium concentration. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:348-364.
4. Sambandam KK. Electrolyte abnormalities. In: Kollef MH, Bedient TJ, Isakow W, Witt CA, eds. The Washington Manual of Critical Care.
Philadelphia, PA: Lippincott Williams and Wilkins; 2008: 153-177.
5. Rhoda KM, Porter MJ, Quintini C. Fluid and electrolyte management: putting a plan in motion. JPEN J Parenter Enteral Nutr.
6. Singer GG, Brenner BM. Fluid and electrolyte disturbances. In: Kasper DL, Braunwald E, Hauser SL, et al. Harrison's Principles of Internal Medicine.
16th ed. New York, NY: McGraw-Hill; 2005: 252-263.
7. Yeates KE, Singer M, Morton AR. Salt and water: a simple approach to hyponatremia. CMAJ.
8. Adrogué HJ, Madias NE. Hyponatremia. NEngl J Med.
9. WeinerM, Epstein FH. Signs and symptoms of electrolyte disorders. Yale J Biol Med
. 1970; 43(2):76-109.
10. Whitmire SJ. Nutrition-focused evaluation and management of dysnatremias. Nutr Clin Pract.
11. Adrogué HJ. Consequences of inadequate management of hyponatremia. Am J Nephrol.
12. Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med.
13. Williams GH, Dluhy RG. Disorders of the adrenal cortex. In: Kasper DL, Braunwald E, Hauser SL, et al. Harrison's Principles of Internal Medicine.
16th ed. New York, NY: McGraw-Hill; 2005:2127-2148.
14. Heitz UE, Horne MM. Disorders of sodium balance. In: Heitz UE, Horne MM, eds. Pocket Guide to Fluid, Electrolyte, and Acid-Base Balance.
4th ed. St. Louis, MO: Mosby; 2001:90-99.
15. Fried LF, Palevsky PM. Hyponatremia and hypernatremia. Med Clin North Am.
16. Guyton AC, Hall JE. Heart muscle; the heart as a pump and function of the heart valves. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:103-115.
17. Guyton AC, Hall JE. Membrane potentials and action potentials. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:57-71.
18. Guyton AC, Hall JE. Renal regulation of potassium, calcium, phosphate, and magnesium; integration of renal mechanisms for control of blood volume and extracellular fluid volume. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:365-382.
19. Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a clinical perspective. Nat Rev Nephrol.
20. Elliott MJ, Ronksley PE, Clase CM, et al. Management of patients with acute hyperkalemia. CMAJ.
21. Heitz UE, Horne MM. Disorders of potassium balance. In: Heitz UE, Horne MM, eds. Pocket Guide to Fluid, Electrolyte, and Acid-Base Balance.
4th ed. St. Louis, MO: Mosby; 2001:100-112.
22. Sevastos N, Theodossiades G, Archimandritis AJ. Pseudohyperkalemia in serum: a new insight into an old phenomenon. Clin Med Res.
23. Guyton AC, Hall JE. Parathyroid hormone, calcitonin, calcium and phosphate metabolism, vitamin D, bone, and teeth. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:978-995.
24. Murphy E, Williams GR. Disorders of calcium metabolism. Practitioner.
25. Heitz UE, Horne MM. Disorders of calcium balance. In: Heitz UE, Horne MM, eds. Pocket Guide to Fluid, Electrolyte, and Acid-Base Balance.
4th ed. St. Louis, MO: Mosby; 2001:113-136.
26. Urbano FL. Signs of hypocalcemia: Chvostek's and Trousseau's signs. Hosp Physician.
27. Lau A, Chan L-N. Electrolytes, other minerals, and trace elements. In: Lee M, ed. Basic Skills in Interpreting Laboratory Data.
4th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2009:119-160.
28. Younes NA, Shafagoj Y Khatib F, Ababneh M. Laboratory screening for hyperparathyroidism. Clin Chim Acta.
29. Heitz UE, Horne MM. Disorders of magnesium balance. In: Heitz UE, Horne MM, eds. Pocket Guide to Fluid, Electrolyte, and Acid-Base Balance.
4th ed. St. Louis, MO: Mosby; 2001:137-147.
30. Heitz UE, Horne MM. Disorders of phosphorus balance. In: Heitz UE, Horne MM, eds. Pocket Guide to Fluid, Electrolyte, and Acid-Base Balance.
4th ed. St. Louis, MO: Mosby; 2001:125-136.
31. Guyton AC, Hall JE. Urine formation by the kidneys: II. Tubular processing of the glomerular filtrate. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:327-347.
32. Guyton AC, Hall JE. Digestion and absorption in the gastrointestinal tract. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:808-818.
33. Guyton AC, Hall JE. Regulation of acid-base balance. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:383-401.
34. Hall TG. Arterial blood gases and acid base balance. In: Lee M, ed. Basic Skills in Interpreting Laboratory Data.
4th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2009: 179-190.
35. Guyton AC, Hall JE. Protein metabolism. In: Guyton AC, Hall JE, eds. Textbook of Medical Physiology.
11th ed. Philadelphia, PA: Elsevier Saunders; 2006:852-858.
36. Trombetta DP, Foote EF. The kidneys. In: Lee M, ed. Basic Skills in Interpreting Laboratory Data.
4th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2009:161-177.
37. Peters JP, Van Slyke DD. Quantitative Clinical Chemistry Interpretations.
2nd ed. Baltimore, MD: Williams and Wilkins; 1946.
EARN CATEGORY I CME CREDIT by reading this article and the article beginning on page 50 and successfully completing the posttest on page 55. Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of January 2013.