Hypocalcemia
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The presentations of patients with hypocalcemia vary widely, from asymptomatic to life-threatening situations. Hypocalcemia is frequently encountered in patients who are hospitalized. Depending on the cause, unrecognized or poorly treated hypocalcemic emergencies can lead to significant morbidity or death. [48]
A 70-kg person has approximately 1.2 kg of calcium in the body, more than 99% of which is stored as hydroxyapatite in bones. Less than 1% (5-6 g) of this calcium is located in the intracellular and extracellular compartments, with only 1.3 g located extracellularly. The total calcium concentration in the plasma is 4.5-5.1 mEq/L (9-10.2 mg/dL). Fifty percent of plasma calcium is ionized, 40% is bound to proteins (90% of which binds to albumin), and 10% circulates bound to anions (eg, phosphate, carbonate, citrate, lactate, sulfate).
At a plasma pH of 7.4, each gram of albumin binds 0.8 mg/dL of calcium. This bond is dependent on the carboxyl groups of albumin and is highly dependent on pH. Acute acidemia decreases calcium binding to albumin, whereas alkalemia increases binding, which decreases ionized calcium. Clinical signs and symptoms are observed only with decreases in ionized calcium concentration (normally 4.5-5.5 mg/dL). [1, 2]
Calcium regulation is critical for normal cell function, neural transmission, membrane stability, bone structure, blood coagulation, and intracellular signaling. The essential functions of this divalent cation continue to be elucidated, particularly in head injury/stroke and cardiopulmonary disorders.
Symptomatic patients with classic clinical findings of acute hypocalcemia require immediate resuscitation and evaluation. However, most cases of hypocalcemia are discovered by clinical suspicion and appropriate laboratory testing. (See Presentation and Workup.)
The treatment of hypocalcemia depends on the cause, the severity, the presence of symptoms, and how rapidly the hypocalcemia developed. Most hypocalcemic emergencies are mild and require only supportive treatment and further laboratory evaluation. On occasion, severe hypocalcemia may result in seizures, tetany, refractory hypotension, or arrhythmias that require a more aggressive approach, including intravenous infusions of calcium. (See Treatment and Medication.)
For more information on hypocalcemia, see the Medscape Reference articles Hypocalcemia in Emergency Medicine and Pediatric Hypocalcemia.
Ionized calcium is the necessary plasma fraction for normal physiologic processes. In the neuromuscular system, ionized calcium facilitates nerve conduction, muscle contraction, and muscle relaxation. Calcium is necessary for bone mineralization and is an important cofactor for hormonal secretion in endocrine organs. At the cellular level, calcium is an important regulator of ion transport and membrane integrity.
Calcium turnover is estimated to be 10-20 mEq/day. Approximately 500 mg of calcium is removed from the bones daily and replaced by an equal amount. Normally, the amount of calcium absorbed by the intestines is matched by urinary calcium excretion. Despite these enormous fluxes of calcium, the levels of ionized calcium remain stable because of the rigid control maintained by parathyroid hormone (PTH), vitamin D, and calcitonin through complex feedback loops. These compounds act primarily at bone, renal, and GI sites. Calcium levels are also affected by magnesium and phosphorus. [3]
PTH stimulates osteoclastic bone reabsorption and distal tubular calcium reabsorption and mediates 1,25-dihydroxyvitamin D (1,25[OH]2 D) intestinal calcium absorption. [4] Vitamin D stimulates intestinal absorption of calcium, regulates PTH release by the chief cells, and mediates PTH-stimulated bone reabsorption. Calcitonin lowers calcium by targeting bone, renal, and GI losses.
The parathyroid gland has a remarkable sensitivity to ionized serum calcium changes. These changes are recognized by the calcium-sensing receptor (CaSR), a 7-transmembrane receptor linked to G-protein with a large extracellular amino-terminal region. Binding of calcium to the CaSR induces activation of phospholipase C and inhibition of PTH secretion. On the other hand, a slight decrease in calcium stimulates the chief cells of the parathyroid gland to secrete PTH.
CaSR is crucial in PTH secretion. A loss of CaSR function leads to pathologic states, such as familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. In renal failure, CaSR agonists suppress the progression of hyperparathyroidism and parathyroid gland growth.
Homeostasis is maintained by an extracellular-to-intracellular gradient, which is largely due to abundant high-energy phosphates intracellularly. Intracellular calcium regulates cyclic adenosine monophosphate (cAMP)–mediated messenger systems and most cell organelle functions. Ion pumps control levels. Extracellular calcium levels are maintained at 8.7-10.4 mg/dL. Variations depend on serum pH, protein and anion levels, and calcium-regulating hormone function.
Patients with a decrease in total serum calcium may not have “true” hypocalcemia, which is defined as a decrease in ionized calcium. A reduction in total serum calcium can result from a decrease in albumin secondary to liver disease, nephrotic syndrome, or malnutrition.
Hypocalcemia causes neuromuscular irritability and tetany. Alkalemia induces tetany due to a decrease in ionized calcium, whereas acidemia is protective. This pathophysiology is important in patients with renal failure who have hypocalcemia because rapid correction of acidemia or development of alkalemia may trigger tetany. [5, 6, 7]
The causes of hypocalcemia include the following:
Hypoalbuminemia
Hypomagnesemia
Hyperphosphatemia
Multifactorial enhanced protein binding and anion chelation
Medication effects
Surgical effects
PTH deficiency or resistance
Vitamin D deficiency or resistance
Hypoalbuminemia is the most common cause of hypocalcemia. Causes include cirrhosis, nephrosis, malnutrition, burns, chronic illness, and sepsis. In patients who are critically ill, low calcium levels can be simply due to hypoalbuminemia, which has no clinical significance because the active fraction (ionized) is not affected. However, to prevent missing a second hypocalcemic disorder, measure the ionized calcium level whenever the albumin level is low.
In a patient with hypocalcemia, measurement of the serum albumin is essential to distinguish true hypocalcemia, which involves a reduction in ionized serum calcium, from factitious hypocalcemia, meaning decreased total, but not ionized, calcium. To correct for hypoalbuminemia, add 0.8 mg/dL to the total serum calcium for each 1.0 g/dL decrease in albumin below 4.0 g/dL.
Hypoparathyroidism can be hereditary or acquired. The hereditary and acquired varieties share the same symptoms, although hereditary hypoparathyroidism tends to have a gradual onset. [8]
Acquired hypoparathyroidism may result from the following:
Neck irradiation/radioiodine therapy [9]
Postparathyroidectomy in dialysis patients [10]
Inadvertent surgical removal (can be transient or permanent)
Infiltrative disease (eg, hemochromatosis, granulomatous disease [sarcoidosis], thalassemia, amyloidosis, or metastatic malignant infiltration
Late-onset hypoparathyroidism can be seen as a part of a complex autoimmune disorder involving ovarian failure and adrenal failure. Mucocutaneous candidiasis, alopecia, vitiligo, and pernicious anemia are associated with this disorder, which is referred to as polyglandular autoimmune disease (PGA I).
Hereditary hypoparathyroidism may be familial or sporadic, and it can occur as an isolated entity or can be associated with other endocrine manifestations. The familial forms include autosomal dominant and autosomal recessive, as well as a sex-linked form of early onset, for which the gene has been located on the long arm of the X chromosome.
Sporadic, late-onset hypoparathyroidism is a feature of several hereditary syndromes. These syndromes, and their associated features, are as follows:
DiGeorge syndrome: congenital heart disease, cleft palate/lip, and abnormal facies
Kearns-Sayre syndrome: heart block, retinitis pigmentosa, and ophthalmoplegia
Kenny-Caffey syndrome: medullary stenosis of the long bones and growth retardation
Pseudohypoparathyroidism is characterized by end-organ resistance to the effects of PTH. PTH binds to the PTH receptor, which, in turn, activates cAMP through guanine nucleotide regulatory proteins (Gs). These proteins consist of alpha, beta, and gamma subunits.
Pseudohypoparathyroidism is classified into types I and II. Type I is further subdivided into Ia, Ib, and Ic. [8]
Type Ia
Type Ia pseudohypoparathyroidism results from a decrease in the Gs-alpha protein. This disorder comprises the biochemical features of pseudohypoparathyroidism along with the following somatic features of Albright hereditary osteodystrophy (AHO):
Short stature
Mental retardation
Obesity
Round-shaped face
Brachymetacarpia
Brachymetatarsia
Subcutaneous bone formation
Laboratory findings in AHO include hypocalcemia, hyperphosphatemia (with normal or high PTH levels), and low calcitriol. Vitamin D may be decreased because of inhibition by elevated levels of phosphorus and by decreased PTH stimulation of 25-hydroxyvitamin D 1-alpha-hydroxylase. The low calcitriol levels, in turn, may cause the resistance to the hypercalcemic effects of PTH in the bone.
The defect of the Gs-alpha protein is not confined to the effects of PTH but also affects other hormonal systems (eg, resistance to glucagon, thyroid-stimulating hormone, gonadotropins). The gene for the Gs-alpha protein is located on chromosome 20. Some family members carry the mutation and display the AHO phenotype but do not have pseudohypoparathyroidism. This is termed pseudo-pseudohypoparathyroidism.
Types Ib and Ic
In type Ib pseudohypoparathyroidism, patients do not present with the somatic features of AHO. These patients have normal Gs-alpha protein, with hormonal resistance to PTH—an impaired cAMP response to PTH, suggesting that the defect lies on the receptor. At what level the receptor is affected is not yet clear.
In type Ic pseudohypoparathyroidism, patients present with resistance to multiple hormonal receptors. However, Gs-alpha protein expression is normal.
Type II
In type II pseudohypoparathyroidism, PTH raises cAMP normally but fails to increase levels of serum calcium or urinary phosphate excretion, suggesting that the defect is located downstream of the generation of cAMP. These patients present with hypocalcemia, hypophosphaturia, and elevated immunoreactive PTH (iPTH) levels. These findings also occur in vitamin D deficiency, but in patients with a vitamin D deficiency, all parameters return to normal after vitamin D administration.
Severe hypomagnesemia can lead to hypocalcemia that is resistant to the administration of calcium and vitamin D. The usual cause of hypomagnesemia is loss via the kidneys (eg, osmotic diuresis, drugs) or the gastrointestinal tract (eg, chronic diarrhea, severe pancreatitis, bypass or resection of small bowel). These patients present with low or inappropriately normal PTH levels in the presence of hypocalcemia.
The mechanism of hypocalcemia includes resistance to PTH in the bone and kidneys, as well as a decrease in PTH secretion. Acute magnesium restoration rapidly corrects the PTH level, suggesting the hypomagnesemia affects the release of PTH, rather than its synthesis.
Vitamin D is a necessary cofactor for the normal response to PTH, and vitamin D deficiency renders PTH ineffective. Poor nutritional intake, chronic renal insufficiency, or reduced exposure to sunlight may cause vitamin D deficiency.
Current Recommended Dietary Allowances (RDAs) for vitamin D are 600 IU of vitamin D per day for adults for individuals from 1 to 70 years of age and 800 IU per day for those over 70 years. [11] Studies have demonstrated that despite adequate intake, that vitamin D insufficiency can still occur and lead to an increased PTH and subsequent bone turnover. Studies have also shown that dietary intake of vitamin D varies greatly by race and age. In a review of National Health and Nutrition Examination Survey (NHANES) III data from 2001-2006, 32% of African-American women were at risk for vitamin D deficiency—defined as serum 25-hydroxyvitamin D (24[OH]D) levels < 30 nmol/L—as compared with only 3% of white women. [12]
An observational study in elderly adults found that 74% of those studied were deficient in vitamin D, defined as 25(OH)D concentrations < 32 ng/mL, despite intake of more than 400-600 IU/d, which was the recommended RDA at the time. [13] The authors of this study suggested that elderly individuals may require as much as 1000 IU per day.
Mild hypovitaminosis D may not be trivial. In an elderly population with an increased PTH and osteoporosis, response to alendronate was attenuated. This attenuation was improved when vitamin D was administered. [14, 15]
Impaired absorption
Numerous conditions can impair the absorption of vitamin D. Small bowel diseases, such as celiac disease, gastric bypass (particularly long limb Roux-en-Y gastric bypass), steatorrhea, and pancreatic diseases can all lead to low vitamin D levels. [16]
Pseudovitamin D deficiency rickets
This condition is secondary to an autosomal mutation of the 1-hydroxylase gene. Ultimately, calcidiol is not hydroxylated to calcitriol, and calcium is not absorbed appropriately. This condition is considered a pseudovitamin D deficiency because high doses of vitamin D can overcome the clinical and biochemical findings of this disease.
Hereditary vitamin D resistance rickets
This condition is extremely rare and is caused by a mutation in the vitamin D receptor. Typically, this condition presents within the first 2 years of life.
Liver disease with decreased synthetic function can cause vitamin D deficiency from several sources, as follows:
Impaired 25-hydroxylation of vitamin D
Decreased bile salts with malabsorption of vitamin D
Decreased synthesis of vitamin D–binding protein
Other factors
Patients with cirrhosis and osteomalacia have low or normal levels of calcitriol, suggesting that other factors may interfere with vitamin D function or are synergistic with malabsorption or decreased sun exposure. These patients require administration of calcidiol or calcitriol for the treatment of hypocalcemia.
Chronic kidney disease leads to a decrease in the conversion of 25-hydroxyvitamin D to its active form 1,25-dihydroxyvitamin D, particularly when the glomerular filtration rate (GFR) falls below 30 mL/min. This results in an increase in PTH. Ultimately, the increased absorption of phosphorus and calcium can lead to calcium-phosphorus mineral deposition in the soft tissues. In the early stages of renal failure, hypocalcemia can occur because of the decrease in calcitriol production and a subsequent decrease in the intestinal absorption of calcium.
Surgical correction of primary or secondary hyperparathyroidism may be associated with severe hypocalcemia due to a rapid increase in bone remodeling. Hypocalcemia results if the rate of skeletal mineralization exceeds the rate of osteoclast-mediated bone resorption.
A less severe picture is also observed after correction of thyrotoxicosis, after institution of vitamin D therapy for osteomalacia, and with tumors associated with bone formation (eg, prostate, breast, leukemia). All of these disease states result in hypocalcemia due to mineralization of large amounts of unmineralized osteoid. [17]
Pancreatitis can be associated with tetany and hypocalcemia. It is caused primarily by precipitation of calcium soaps in the abdominal cavity, but glucagon-stimulated calcitonin release and decreased PTH secretion may play a role.
When the pancreas is damaged, free fatty acids are generated by the action of pancreatic lipase. Insoluble calcium salts are present in the pancreas, and the free fatty acids avidly chelate the salts, resulting in calcium deposition in the retroperitoneum. In addition, hypoalbuminemia may be a part of the clinical picture, resulting in a reduction in total serum calcium. In patients with concomitant alcohol abuse, a poor nutritional intake of calcium and vitamin D, as well as accompanying hypomagnesemia, may predispose these patients to hypocalcemia. [18]
Hyperphosphatemia may be seen in critical illness and in patients who have ingested phosphate-containing enemas. Phosphate binds calcium avidly, causing acute hypocalcemia. Acute hypocalcemia secondary to hyperphosphatemia may also result from renal failure or excess tissue breakdown because of rhabdomyolysis or tumor lysis.
In acute hyperphosphatemia, calcium is deposited mostly in the bone but also in the extraskeletal tissue. In contrast, in chronic hyperphosphatemia, which is nearly always from chronic renal failure, calcium efflux from the bone is inhibited and the calcium absorption is low, because of reduced renal synthesis of 1,25-dihydroxyvitamin D. However, other consequences of renal failure, including a primary impairment in calcitriol synthesis, also contribute to hypocalcemia.
Patients receiving the calcimimetic agent cinacalcet to help control secondary hyperparathyroidism in renal failure may experience hypocalcemia as a result of acute inhibition of PTH release. Clinically significant hypocalcemia occurs in approximately 5% of patients treated with cinacalcet. [19]
Hypocalcemia can also occur in patients treated with some chemotherapeutic drugs. For example, cisplatin can induce hypocalcemia by causing hypomagnesemia, and combination therapy with 5-fluorouracil and leucovorin can cause mild hypocalcemia (65% of patients in one series), possibly by decreasing calcitriol production. [20]
Hypocalcemia may result from the treatment of hypercalcemia with bisphosphonates, particularly zoledronic acid, which is significantly more potent than other bisphosphonates in suppressing the formation and function of osteoclasts. Patients who are affected appear to lack an adequate PTH response to decreasing serum calcium levels. [21]
Hypocalcemia and osteomalacia have been described with prolonged therapy with anticonvulsants (eg, phenytoin, phenobarbital). [22] The mechanisms differ according to the class of anticonvulsants; for example, phenytoin induces cytochrome P450 enzymes and enhances vitamin D catabolism.
Foscarnet is a drug used to treat refractory cytomegalovirus and herpes infections in patients who are immunocompromised, and it complexes ionized calcium and, therefore, lowers ionized calcium concentrations, potentially causing symptomatic hypocalcemia. Therefore, the ionized calcium concentration should be measured at the end of an infusion of foscarnet.
Denosumab is a fully human monoclonal antibody to the receptor activator of nuclear factor kappaB ligand (RANKL), an osteoclast differentiating factor. It inhibits osteoclast formation, decreases bone resorption, increases bone mineral density (BMD), and reduces the risk of fracture. See the Fracture Index WITH known Bone Mineral Density (BMD) calculator.
In the denosumab trials, all women were supplemented with daily calcium (1000 mg) and vitamin D (400-800 U). A small proportion of women in the denosumab trials had a decrease in the serum calcium level to less than 8.5 mg/dL. However, in patients with conditions that predispose to hypocalcemia, such as chronic kidney disease, malabsorption syndromes, or hypoparathyroidism, symptomatic hypocalcemia may occur. The nadir in serum calcium occurs approximately 10 days after administration. Thus, denosumab should not be given to patients with preexisting hypocalcemia until it is corrected. In addition, patients with conditions predisposing to hypocalcemia (ie, chronic kidney disease and creatinine clearance < 30 mL/min) should be monitored for hypocalcemia. [23]
Symptomatic hypocalcemia during transfusion of citrated blood or plasma is rare, because healthy patients rapidly metabolize citrate in the liver and kidney. However, a clinically important fall in serum ionized calcium concentration can occur if citrate metabolism is impaired due to hepatic or renal failure or if large quantities of citrate are given rapidly, for example, during plasma exchange or massive blood transfusion.
Sodium phosphate preparations, which come in aqueous and tablet forms, are used to cleanse the bowel prior to GI procedures such as colonoscopy. In certain populations, these agents can lead to acute hyperphosphatemia and subsequent hypocalcemia. [24, 25] Risk factors include the following:
Renal failure
Advanced age
Chronic heart failure
Hepatic insufficiency
Volume depletion
Use of angiotensin-converting enzyme (ACE) inhibitors or nonsteroidal anti-inflammatory drugs (NSAIDS)
Some radiographic contrast dyes may contain ethylenediaminetetraacetic acid (EDTA), which chelates calcium in serum, thereby reducing serum ionized calcium concentration, resulting in hypocalcemia. Gadolinium-based contrast material can falsely lower serum calcium levels and should be considered if levels are drawn shortly after magnetic resonance imaging.
Rarely, an excess intake of fluoride can cause hypocalcemia; this effect is presumably mediated by inhibition of bone resorption. Overfluorinated public water supplies and ingestion of fluoride-containing cleaning agents have been associated with low serum calcium levels. In this case, hypocalcemia is thought to be due to excessive rates of skeletal mineralization secondary to formation of calcium difluoride complex.
Proton pump inhibitors (PPIs) and histamine-2 receptor blockers (eg, cimetidine) reduce gastric acid production; this slows fat breakdown, which is necessary to complex calcium for gut absorption. An association with these medicines and an increased risk for hip fractures in elderly patients has been made because of decreased calcium absorption.
Other medication effects that may lead to hypocalcemia are as follows:
Calcitonin and bisphosphonates cause chelation and end-organ inhibition
Ethylene glycol complexes with calcium
Estrogen inhibits bone resorption
Aluminum and alcohol suppress PTH
Protein binding is enhanced by elevated pH and free fatty acid release in high catecholamine states. Anion chelation is seen in high phosphate states (eg, renal failure, rhabdomyolysis, mesenteric ischemia, oral administration of phosphate-containing enemas); high citrate states (eg, massive blood transfusion, radiocontrast dyes); and high bicarbonate, lactate, and oxalate levels.
Multifactorial causes are probably the most clinically relevant in hypocalcemic emergencies in the emergency department (ED). These include the following:
Rhabdomyolysis: increased phosphates from creatine phosphokinase (CPK) and other anions (ie, lactate, bicarbonate) chelate calcium
Toxic shock syndrome can cause hypocalcemia
High calcitonin levels cause low calcium
Malignancy: osteoblastic metastases (eg, breast cancer, prostate cancer) and tumor lysis syndrome may cause hypocalcemia (by differing mechanisms)
Infiltrative disease: sarcoidosis, tuberculosis, and hemochromatosis may infiltrate the parathyroids, causing dysfunction
Toxicologic causes include hydrofluoric acid burn or ingestion
Trauma patients with massive transfusion will have hemostasis impairment as one effect of hypocalcemia [26]
Acute illness may lead to hypocalcemia for multiple reasons. In one study, the 3 most common factors identified in patients with hypocalcemia associated with acute illness were hypomagnesemia, acute renal failure, and transfusions.
In gram-negative sepsis, there is a reduction in total and ionized serum calcium. The mechanism for this remains unknown, but it appears to be associated with multiple factors, including elevated levels of cytokines (eg, interleukin-6, interleukin-1, TNF-alpha), hypoparathyroidism, and vitamin D deficiency or resistance.
Mortality rates are increased in patients with sepsis and hypocalcemia, compared with patients who are normocalcemic. [27, 28] However, there is no clear evidence that treating critically ill patients with supplemental calcium alters outcomes. [29]
The following surgical procedures may result in hypocalcemia:
Parathyroid adenoma resection causes a transient hypocalcemia due to end-organ PTH resistance in the first postoperative day; in addition, vascular/parathyroid injury may occur as an operative mishap
Pancreatectomy prevents calcium absorption in the duodenum and the jejunum by eliminating necessary enzymes
Bowel resection may cause hypocalcemia by reducing the surface available to absorb fatty acids and calcium
Epidemiologic studies of hypocalcemia versus other electrolyte abnormalities have not been performed. During the last 20 years, laboratory tests have quantified serum and ionized calcium and PTH levels, enabling easier diagnosis. The incidence of ionized hypocalcemia is difficult to quantify. In intensive care patients, reported rates have ranged from 15-88%. [30] A systematic review and meta-analysis of hypocalcemia after thyroidectomy found that the median incidence of transient hypocalcaemia was 27% (range, 19-38%) and that of permanent hypocalcemia was 1% (range, 0-3%). [31] In a series of 500 postsurgical patients operated on for hyperparathyroidism, 2% had permanent hypocalcemia. [32]
In order of frequency, hypocalcemia occurs in the following settings:
Chronic and acute renal failure
Vitamin D deficiency
Magnesium deficiency
Acute pancreatitis
Hypoparathyroidism and pseudohypoparathyroidism
Infusion of phosphate, citrate, or calcium-free albumin
Death is rare but has been reported. The disease causing hypocalcemia may have greater impact on morbidity than hypocalcemia itself.
Complications of chronic hypocalcemia predominantly are those of bone disease. In addition, severe hypocalcemia may result in cardiovascular collapse, hypotension unresponsive to fluids and vasopressors, and dysrhythmias. Some patients may manifest digitalis insensitivity. Neurologic complications of hypocalcemia include acute seizures or tetany, basal ganglia calcification, parkinsonism, hemiballismus, and choreoathetosis. Although some patients with hypocalcemia may improve with treatment, the calcification typically is not reversible.
The age distribution of hypocalcemia is contingent on the underling disorder. In children, nutritional deficiencies are more frequent; in adults, renal failure predominates. However, the recognition of the high prevalence of vitamin D deficiency, particularly in elderly patients, may change the understanding of hypocalcemia in the general population.
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Manish Suneja, MD, FASN, FACP Clinical Professor of Internal Medicine, Director, Internal Medicine Residency Program, Co-Strand Director of Clinical and Professional Skills, Dr William and Sondra Myers Professor, Department of Internal Medicine, Division of Nephrology, University of Iowa Hospitals and Clinics
Manish Suneja, MD, FASN, FACP is a member of the following medical societies: American College of Physicians, American Society of Nephrology, National Kidney Foundation
Disclosure: Editor for the book DeGowins Diagnostic examination for: McGraw Hills.
Heather A Muster, MD, MS Medical Director, Davita Clinical Research
Heather A Muster, MD, MS is a member of the following medical societies: American College of Physicians, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Minnesota Medical Association, National Kidney Foundation
Disclosure: Nothing to disclose.
Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital
Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc<br/>Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.
Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.
Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center
Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians
Disclosure: Nothing to disclose.
Christopher B Beach, MD, FACEP, FAAEM Associate Professor and Vice Chair of Emergency Medicine, Department of Emergency Medicine, Associate Professor of Institute for Healthcare Studies, Institute for Patient Safety, Feinberg School of Medicine, Northwestern University
Christopher B Beach, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University
Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Dept of Veterans Affairs Grant/research funds Research
James W Lohr, MD Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences
James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Genzyme Honoraria Speaking and teaching
Alfredo A Pegoraro, MD Consulting Staff, Nephrology Associates
Alfredo A Pegoraro, MD is a member of the following medical societies: American Medical Assocation, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.
Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
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