Here are the key points about ionized calcium levels: - Ionized calcium is the biologically active form of calcium and provides a more accurate assessment of calcium status compared to total calcium levels. - Low ionized calcium levels are common in critically ill patients and those with conditions affecting calcium homeostasis like renal failure. - Ionized calcium levels below 2.8 mg/dL increase the risk of cardiac arrest, so calcium replacement therapy is generally started once levels fall below this threshold. - Measurement of ionized calcium is particularly important for monitoring unconscious or anesthetized patients where changes in calcium levels may not produce early warning signs. - Ionized calcium can also be useful for evaluating conditions like neonatal hypocal

1. Osteopetrosis (malignant)
Pseudohypoparathyroidism type 1a
Hypocalcaemia Pseudohypoparathyroidism type 1b
Autosomal recessive conditions
Links : http://www.diseasesdatabase.com/links1.asp?glngUserChoice=6412
Cystinosis
"Reduction of the blood calcium below normal. Manifestations include
Intestinal hypomagnesemia type 1
hyperactive deep tendon reflexes, Chvostek's sign, muscle and
Metaphyseal dysplasia
abdominal cramps, and carpopedal spasm. (Dorland, 27th ed)" Osteopetrosis (malignant)
Vitamin D dependent rickets type 1
Vitamin D dependent rickets type 2a
Nutritional conditions
Cow milk, baby feed
Malabsorption syndrome
Vitamin D deficiency
Endocrine conditions
Hyperparathyroidism, secondary
Hyperthyroidism
Hypoparathyroidism
Inflammatory conditions
Pancreatitis, acute
Hypocalcaemia may be caused by or feature of the following ... Bacteria and bacterial conditions
_
Artifacts Neisseria meningiditis
Citrated blood sample Iatrogenic conditions
EDTA blood sample
Oxalate blood sample Blood transfusion and complications
Tumor lysis syndrome
Miscellaneous syndromes Chemicals
Malabsorption syndrome Ethylene glycol
Osteomalacia
Proximal renal tubular acidosis Drugs, hormones and mediators
Renal failure, acute
Renal failure, chronic Actinomycin D
Rhabdomyolysis Alendronate
Bumetanide
Biochemical abnormalities Cinacalcet
Dasatinib
Hyperphosphataemia Edetate disodium
Hypomagnesemia Ethotoin
Foscarnet
Mendelian inherited conditions Frusemide
Gallium nitrate
Kenny-Caffey-Linarelli syndrome Mithramycin
Pamidronate
Autosomal dominant conditions Phenytoin

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Potassium Serum
Paraneoplastic Autoantibodies
Parathyroid Hormone
Parathyroid Hormone Introperative Potassium is the major intracellular cation, with a 20 fold greater concentration in the cells
Parathyroid Related Protein than in the extracellular fluid. Only 2% of total body potassium circulates in the plasma. The
Parietal Cell Antibodies sodium potassium ATPase pump is largely responsible for maintaining this important ratio. The
Paroxysmal Nocturnal Hemoglobinuria kidneys are also important in regulating potassium balance. Proximal tubules reabsorb nearly
Partial Thromboplastin Time all of the filtered potassium. Under the influence of aldosterone, additional potassium is
Parvovirus B19 Antibodies secreted by the distal tubules and collecting ducts in exchange for sodium. Maintaining normal
Penicillin Antibody potassium levels is important for regulation of neuromuscular excitability, cardiac contractility
Peptide Nucleic Acid FISH for Blood and rhythm, extracellular volume, and acid base balance.
Culture Identification
Pernicious Anemia
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Phosphatidyl Glycerol
Phosphorus
Plasma Cell Enumeration by Flow
Cytometry Hypokalemia is defined as a plasma potassium concentration less than 3 meq/L. The primary
Plastic Blood Collection Tubes mechanisms are excessive GI or urinary loss of potassium, increased cellular uptake, or
Platelet Aggregation inadequate dietary intake. GI loss results from vomiting, diarrhea, gastric suction, or intestinal
Platelet Antibody fistula discharge. Diuretics, such as thiazides and furosemide, promote potassium secretion in
Platelet Count the distal tubules. Kidney disorders, such as renal tubular acidosis, cause excessive urinary loss
Platelet Function Screen of potassium. Hyperaldosteronism leads to excessive urinary secretion of potassium and
Pneumococcus Urine Antigen metabolic acidosis. Hypomagnesemia causes hypokalemia by promoting both urinary and fecal
Pneumocystis loss of potassium. Magnesium deficiency diminishes sodium potassium ATPase activity and
Polycythemia enhances aldosterone secretion. Alkalemia and insulin are the two major causes of increased
Porphyrins cellular uptake of potassium. Alkalemia promotes intracellular loss of hydrogen ion. To
Potassium Serum preserve electroneutrality, both potassium and sodium enter cells. Plasma potassium decreases
Potassium Urine by 0.4 meq/L for every 0.1 unit rise in pH. Insulin promotes the entry of potassium into muscle
Prealbumin and hepatocytes. Reduced dietary intake of potassium is a rare cause of hypokalemia, but may
Pregnancy Test be an important factor in patients taking diuretics.
Preoperative Hemostasis Testing
Preoperative Testing Hyperkalemia occurs frequently in hospitalized patients with a reported incidence of 1 to 10%.
Primidone A recent article investigated the causes of 242 episodes of hyperkalemia in 206 inpatients at
Procainamide & Nacetylprocainamide the University of Pittsburgh Medical Center between February 15 and June 30, 1996 (Arch
Progesterone Intern Med 1998; 158: 917-24). Hyperkalemia was defined as a critical plasma potassium level
Proinsulin of 6 meq/L or more. The incidence of hyperkalemia in this study was 2.3%. Approximately 2
Prolactin hyperkalemic episodes occurred per day during the study period. Most of the elevated
Prostate Specific Antigen potassium levels fell between 6.0 and 7.1 meq/L, but a few values were as high as 9.0 meq/L.
Prostate Specific Antigen Free Further investigation revealed that most cases of hyperkalemia were multifactorial in origin.
Protein C
Protein Electrophoresis
Cause % of Cases
Protein Electrophoresis Spinal Fluid
Protein Electrophoresis Urine
Protein S Renal failure 77
Protein Total Serum
Protein Total Spinal Fluid Hyperglycemia 49
Protein Urine Quantitative
Prothrombin Gene Mutation Potassium supplements/ TPN 15
Prothrombin Time
Prothrombin Time Significant Change Medications 63
Psoriasis & T Cell Monitoring
PTT or Plasma Thromboplastin Time
Cyclosporine/ Tacrolimus 27
Pyruvate Kinase Screen RBC
Beta Blockers 17
Trimethoprim 15
ICPbio International
Ltd. ACE inhibitors 15
Plasma proteins from
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Quality and Performance
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3. K sparing diuretics 5
Iron Overload Heparin 5
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Medical Renal failure was present in more than two thirds of the patients. Hyperglycemia was the
second most common contributor to hyperkalemia. Medications contributed to the development
Coagulation and
of hyperkalemia in 63% of cases. The drugs most often implicated are listed in the table.
Hemostasis reagents Heparin causes hyperkalemia by suppressing aldosterone.
Human Plasmas for
Diagnostic Use Another recent study revealed that 194 of 1818 (11%) medical outpatients using angiotensin
www.kingbiomed.com converting enzyme (ACE) inhibitors developed hyperkalemia, which was defined as a potassium
level above 5.1 meq/L (Arch Intern Med 1998; 158:26-32). The majority of patients had
potassium levels between 5.1 and 5.5 meq/L, but one fifth of the patients had higher levels.
Proteome Independent risk factors for developing hyperkalemia included a serum creatinine level above
Quantification 1.5 mg/dL, BUN greater than 18 mg/dL, congestive heart failure, and the use of long acting
Sensitive and ACE inhibitors. Patients over the age of 70 with a BUN of 25 mg/dL or higher were more likely
reproducible quantitative to develop severe hyperkalemia (potassium > 6.0 meq/L).
proteome analyses
Hyperkalemia can cause muscle weakness by decreasing the ratio of intra to extracellular
www.proteomescience.de
potassium, which alters neuromuscular conduction. Muscle weakness does not usually develop
until plasma potassium reaches 8 meq/L. Hyperkalemia disturbs cardiac conduction, which can
cause arrhythmias. Plasma potassium levels between 6 and 7 meq/L may alter the ECG, while
levels greater than 10 meq/L may precipitate cardiac arrest.
Factitious causes of hyperkalemia include:
In vitro hemolysis
Traumatic phlebotomy
Too small bore of needle
Butterfly needle w/ excessive syringe pressure
Vacutainer tubes placed directly on large bore catheter
Collection with syringe and injection into Vacutainer tubes
Elevated platelet count
0.15 mEq/L increase for every 100,000 cells/uL increase
Elevated leukocyte count
Contamination with IV fluids
Contamination with anticoagulant (K3EDTA concentration exceeds 15 mEq/L)
Aged specimens
More accelerated at 4oC than at 25oC
Serum sitting on clot
Respun serum separator tube
Plasma is the preferred specimen for patients with platelet counts greater than 600,000/uL.
Erroneously high potassium results are also produced by centrifugation of SST tubes in fixed
angle centrifuges. Under these conditions, the separation gel does not form a complete barrier
and potassium leaks out of red blood cells into the plasma during specimen storage.
Reference range is 3.6 to 5.0 mEq/L (Vitros analyzer). Levels < 3.0 and > 6.0 mEq/L are
considered critical values. Serum potassium levels run slightly higher (0.4 mEq/L) than plasma
levels, even in patients with normal platelet counts.
Specimen requirement is one SST tube of blood. Hemolysis should be avoided because it will
cause false elevation of potassium.
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Potassium Urine
Paraneoplastic Autoantibodies
Parathyroid Hormone
Parathyroid Hormone Introperative In healthy individuals, nearly all potassium filtered by the kidney is reabsorbed. Potassium
Parathyroid Related Protein excretion reflects distal tubule secretion of potassium, which is stimulated by aldosterone and
Parietal Cell Antibodies the rate of potassium entry into the plasma from the diet and from cells. Urine potassium
Paroxysmal Nocturnal Hemoglobinuria levels are generally helpful only in evaluation of patients with unexplained hypokalemia. Urine
Partial Thromboplastin Time potassium levels between 0 and 10 mEq/L suggest the GI tract is the source of potassium loss,
Parvovirus B19 Antibodies while levels >10 mEq/L suggest renal potassium loss.
Penicillin Antibody
Peptide Nucleic Acid FISH for Blood Reference range is 25 - 123 mEq/24 hr.
Culture Identification
Pernicious Anemia Specimen requirement is a 24-hour urine collection in a container without preservative.
pH Specimen should be refrigerated during and after the collection.
Phenobarbital
Phenytoin
Phosphatidyl Glycerol
Phosphorus
Plasma Cell Enumeration by Flow
Cytometry
Plastic Blood Collection Tubes
Platelet Aggregation
Platelet Antibody
Platelet Count
Platelet Function Screen
Pneumococcus Urine Antigen
Pneumocystis
Polycythemia
Porphyrins
Potassium Serum
Potassium Urine
Prealbumin
Pregnancy Test
Preoperative Hemostasis Testing
Preoperative Testing
Primidone
Procainamide & Nacetylprocainamide
Progesterone
Proinsulin
Prolactin
Prostate Specific Antigen
Prostate Specific Antigen Free
Protein C
Protein Electrophoresis
Protein Electrophoresis Spinal Fluid
Protein Electrophoresis Urine
Protein S
Protein Total Serum
Protein Total Spinal Fluid
Protein Urine Quantitative
Prothrombin Gene Mutation
Prothrombin Time
Prothrombin Time Significant Change
Psoriasis & T Cell Monitoring
PTT or Plasma Thromboplastin Time
Pyruvate Kinase Screen RBC
IgE and Autoimmmune EIA ICPbio International Ltd. Manage High Iron
The right technology For your lab Plasma proteins from New Zealand Read About Exjade®: An Effective
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Calcium Ionized
C1 Esterase Inhibitor
C Reactive Protein
C Reactive Protein High Sensitivity Low ionized calcium levels are common in critically ill patients with sepsis, renal failure, cardiac
CA 125 failure, pulmonary failure, post-surgery or burns. Monitoring of ionized calcium is particularly
CA 153 important in the unconscious or anesthetized patient, in whom unrecognized changes in
CA 19.9 calcium homeostasis may result in serious cardiovascular dysfunction with little of no prior
CA 27.29 warning signs. Decreased ionized calcium levels between 3 and 4 mg/dL are usually well
Caffeine tolerated, but the risk of cardiac arrest increases when ionized calcium levels approach 2.5
Calcitonin mg/dL. An ionized calcium level below 2.8 mg/dL is a reasonable threshold to begin calcium
Calcium replacement therapy. Patients with hypotension or low cardiac output may require calcium
Calcium Ionized replacement when ionized calcium falls below 3.2 to 3.6 mg/dL. Replacement therapy should
Carbamazepine be monitored with Ionized calcium levels.
Carbon Dioxide
Carbon Monoxide
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Cardiovascular Risk Panel
Carotene
CCP Antibody
CD4 Enumeration Measurement of ionized calcium may also be helpful in evaluating neonatal hypocalcemia, and
Celiac Disease Panel for monitoring hypo- or hypercalcemia associated with malignancy and pancreatitis. Ionized
Centromere Antibody calcium is valuable in establishing a diagnosis of hyperparathyroidism, especially in borderline
Cephalothin Antibody cases where total calcium levels may be normal but ionized calcium increased.
Cerebrospinal Fluid
Ceruloplasmin In these clinical situations, total calcium is often difficult to interpret or misleading due to
Chemistry Panels decreased albumin and other proteins, acid-base disturbances, and transfusion of citrated
Chlamydia Detection blood. Alterations in serum albumin during an acute illness may change the total serum
Chloride calcium by as much as 30%. Nomograms and formulas for indirect prediction of free calcium
Cholesterol levels are inaccurate and may under-diagnose hypocalcemia. The percentage of protein bound
Cholinesterase calcium may vary from 30 to 50% during illness. Acute acidosis decreases protein binding,
Clindamycin Resistance while acute alkalosis increases it. Free fatty acids often increase during illness and after
Clostridium Difficile administration of heparin, isproterenol and insulin. They increase calcium binding to albumin.
Coagulation Factor Assays Changes in the concentration of anions such as phosphate, bicarbonate, and citrate also
Coagulation Factor Inhibitor change ionized calcium levels. Transfusion of large numbers of blood components, containing
Coagulation Screen excess citrate, may chelate calcium. Total calcium levels may only be slightly decreased, even
Cold Agglutinin Titer though ionized calcium levels are markedly decreased.
Colloid Osmotic Pressure
Complement Profile High Ferritin Levels Detoxamin
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Cord Blood Studies
Corticotropin Releasing Hormone
Stimulation Test
Reference range is 4.5 - 5.3 mg/dL. Critical values are < 3.5 mg/dL and >6.5 mg/dL.
Cortisol
Cortisol in Critical Illness
Specimen requirement is one SST tube of blood. Tourniquet time should not exceed one
Cortisol Salivary
minute. The tube must remained capped and should be transported in wet ice. Hemolysis will
Cortisol Urine Free
falsely lower ionized calcium values.
Cortrosyn Stimulation Test
Cotinine
Creatine Kinase
Creatine Kinase MB
Creatinine
Creatinine Clearance
Creatinine Kinase Isoenzymes
Crossmatch
CRP
Cryoglobulin
Cryptococcal Antigen
Cryptosporidium Antigen
Crystal Identification
Cushing Syndrome
Cyclosporine
Cystic Fibrosis
Cytogenetic Studies

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Calcium, Total
C1 Esterase Inhibitor
C Reactive Protein
C Reactive Protein High Sensitivity Plasma calcium exists in the blood in three forms; 50% is ionized, 40-45% is protein bound,
CA 125 and 5-10% is complexed to anions such as bicarbonate, citrate, sulfate, phosphate, and
CA 153 lactate. Plasma ionized calcium is the biologically active moiety. Total calcium levels are
CA 19.9 maintained between 8.8 and 10.2 mg/dL. Parathyroid hormone and vitamin D regulate normal
CA 27.29 plasma calcium levels by their actions on kidney, intestine, and bone ion transport.
Caffeine
Calcitonin
Cytokine Center Protein Evolution
Calcium Recombinant cytokines, ELISPOT Kits ELISA Kits, Superior to Directed Evolution Next Generation
Calcium Ionized related antibodies Technologies
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Carbon Dioxide
Carbon Monoxide
Carcinoembryonic Antigen
Carcinoid Syndrome The main causes of hypercalcemia are primary hyperparathyroidism, malignant disease, and
Cardiac Marker Panel chronic renal failure. The differential diagnosis of hypercalcemia depends on the clinical setting.
Cardiovascular Risk Panel Overall, primary hyperparathyroidism and malignancy account for 80 - 90% of hypercalcemia
Carotene cases. However, primary hyperparathyroidism is the cause of ~60% of ambulatory cases and
CCP Antibody of ~25% of inpatient cases, whereas malignancy causes ~35% of ambulatory cases and 65%
CD4 Enumeration of inpatient cases.
Celiac Disease Panel
Centromere Antibody Malignancies can raise serum calcium levels by either direct bone destruction or secretion of
Cephalothin Antibody calcemic factors. Patients with squamous cell carcinoma of the lung, metastatic breast cancer,
Cerebrospinal Fluid multiple myeloma, and renal cell carcinoma are most prone to hypercalcemia. These tumors
Ceruloplasmin may produce PTH related protein (PTH-rp) which binds to PTH receptors, but is not detected by
Chemistry Panels standard intact PTH immunoassays. Specific assays for PTH-rp are available.
Chlamydia Detection
Chloride The prevalence of hyperparathyroidism in the general population is 1 to 2 cases per 1000
Cholesterol people, but is more frequent in the elderly and in women. The most common pathological
Cholinesterase lesion is a single parathyroid adenoma (85% of cases) or chief cell hyperplasia (10%).
Clindamycin Resistance Parathyroid carcinoma occurs in 1 to 3% of cases. Hyperparathyroidism also occurs in multiple
Clostridium Difficile endocrine neoplasia type 1 and 2A. Patients identified by laboratory screening are commonly
Coagulation Factor Assays asymptomatic. Presentation with kidney stones is unusual today, but 5% of patients with
Coagulation Factor Inhibitor kidney stone disease have primary hyperparathyroidism. Finding an elevated PTH level in a
Coagulation Screen patient with hypercalcemia makes the diagnosis.
Cold Agglutinin Titer
Colloid Osmotic Pressure The signs and symptoms of hypercalcemia are summarized in the following table.
Complement Profile
Complete Blood Count
Mental Neurological & Skeletal GI & Urological
Congenital Adrenal Hyperplasia
Cord Blood Gases
Cord Blood Studies Fatigue Reduced muscle tone Nausea
Corticotropin Releasing Hormone
Stimulation Test Obtundation Muscle weakness Vomiting
Cortisol
Cortisol in Critical Illness
Cortisol Salivary Apathy Myalgia Polyuria
Cortisol Urine Free
Cortrosyn Stimulation Test Lethargy Pain Polydipsia
Cotinine
Creatine Kinase
Confusion Deep tendon reflexes Dehydration
Creatine Kinase MB
Creatinine
Creatinine Clearance Disorientation Anorexia
Creatinine Kinase Isoenzymes
Crossmatch Coma Constipation
CRP
Cryoglobulin
Cryptococcal Antigen
Cryptosporidium Antigen Evaluation of hypercalcemia usually begins with measurement of total calcium. If total calcium
Crystal Identification is markedly elevated, an ionized calcium level is usually not needed. Slightly to moderately
Cushing Syndrome elevated total calcium should be confirmed by measurement of ionized calcium. The patient's
Cyclosporine history may indicate the cause, such as; immobilization for more than a week, drug therapy,
Cystic Fibrosis hyperthyroidism, adrenal insufficiency, or familial hypocalciuric hypercalcemia. If time permits,
Cytogenetic Studies

7. total calcium levels should be repeated two more times to rule out a transient cause of
Cytomegalovirus Antibody hypercalcemia before undertaking a complete work-up. If hypercalcemia is still evident, serum
Cytomegalovirus Culture albumin and total protein should be determined. Calcium levels should be corrected for
Cytomegalovirus PCR Qualitative elevated albumin levels (see below). If total protein is high, but albumin is normal or low, a
Cytomegalovirus PCR Quantitative monoclonal gammopathy should be ruled out by serum protein electrophoresis. Serum
chloride, phosphorus and intact PTH are also useful in diagnosing the most frequent causes of
hypercalcemia; malignancy and hyperparathyroidism. Serum chloride is mildly elevated in
primary hyperparathyroidism.
Serum IgE v. skin Test Hyperparathyroidism Malignancy
testing
Practical information For Total calcium (mg/dL) <12.4 >12.4
healthcare professionals
www.hycorbiomedical.com Chloride (meq/L) >103 <103
Phosphorus normal to low normal
Calcium Phosphate
Chloride : phosphorus ratio 29 or greater <29
Powders, Solids,
Coatings for Dental,
Intact PTH elevated suppressed
Medical, Laboratory Uses
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PTH-rp normal elevated
Renal Epithelials - Calcitriol elevated low
Normal
ATCC Primary Cell
Solutionsâ„¢ LGC Hypocalcemia most commonly results from PTH deficiency or failure to produce 1,25 dihydroxy
Standards partnered with vitamin D. The most common causes of hypoparathyroidism are parathyroid or thyroid surgery
ATCC and parathyroid infiltration by cancer, sarcoid, amyloid or hemochromatosis. Acute illnesses
www.lgcstandards-atcc.org such as pancreatitis, hepatic failure, sepsis, and various medications can also cause
hypocalcemia. The normal response to a fall in the plasma ionized calcium level is increased
PTH secretion and 1,25 dihyroxy vitamin D synthesis, leading to increased calcium absorption
Iron Toxicity from the intestine and increased resorption from bone and kidneys.
Read The Benefits Of
Prescribing Exjade® Some drugs are associated with hypocalcemia. Gentamicin and cisplatin cause renal
For Oral Chelation magnesium loss, which leads to hypocalcemia. Heparin therapy releases fatty acids that bind
calcium ions and cause transient hypocalcemia. Anticonvulsants such as dilantin and
Therapy
phenobarbital induce the microsomal oxidase pathway which accelerates inactivation of vitamin
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D. Loop diuretics such as furosemide enhance renal calcium excretion. Phosphate salts bind up
calcium ions causing hypocalcemia.
Cytokine Center The laboratory evaluation of a low total plasma calcium level should include measurement of
Recombinant cytokines, ionized calcium, magnesium, and phosphorus levels. Low ionized calcium rules out artefactual
causes of hypocalcemia, such as hypoalbuminemia. Abnormally high or low magnesium levels
ELISPOT Kits ELISA should be excluded because they can inhibit PTH secretion. A low serum phosphorus level is
Kits, related antibodies consistent with vitamin D deficiency, while a high level suggests chronic renal failure or
www.cellsciences.com pseudohypoparathyroidism. Measurement of intact PTH levels helps to differentiate between
conditions caused by PTH and vitamin D defects. The demonstration of an inappropriately low
intact PTH level in the presence of hypocalcemia is consistent with the diagnosis of
hypoparathyroidism. Serum 25-hydroxyvitamin D levels can be measured to confirm vitamin D
deficiency.
Total calcium levels are effected by changes in plasma protein concentrations. Most of the
protein bound fraction of calcium is bound to albumin; each 1 g/dL of albumin binds 0.8 mg/dL
of calcium. Three formulas have been used to correct calcium for decreased serum albumin
levels:
%Calcium bound = 8 (albumin) + 2(globulin) + 3
Corrected calcium = measured Calcium /0.6 + [total protein/8.5]
Corrected calcium = Calcium - albumin + 4
Each formula will give a slightly different value for corrected calcium. A better approach is to
directly measure ionized calcium levels.
Two of the four approved gadolinium based magnetic resonance (MR) imaging contrast agents,
gadodiamide (Omniscan) and gadoversetamide (OptiMARK), have recently been shown to
interfere with calcium measurements on some chemistry analyzers, resulting in falsely low
values. Patients with normal renal function may have spuriously low calcium measurements up
to 24 hours after administration of these contrast agents, but patients with renal insufficiency
may be affected for up to 4.5 days. However, the Vitros chemistry analyzers used throughout
the Saint Luke's Health System are not adversely affected (Am J Clin Pathol 2004;121:282-
92).
Reference range is 8.8 - 10.2 mg/dL. Calcium levels less than 6.0 mg/dL or greater than 13.0
mg/dL are considered critical values.

8. Specimen requirement is one SST tube or one green top (heparin) tube of blood. Prolonged
venous stasis should be avoided because it can produce artefactual hypercalcemia.
Calcium carbonate Cytokine Center Atherosclerosis testing
Ground calcium carbonate (GCC) fillers & Recombinant cytokines, ELISPOT Kits Coronary artery disease Stroke Risk Novel
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B. Pseudo-Hypoparathyroidism
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Serum Creatinine F. Renal osteodystrophy
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Phosphorus
Disorders
Serum Phosphorus
Hypercalciuria (C0020438)
Potassium abnormally high calcium in the urine; may be due to
Definition
Disorders hyperabsorption of calcium, with the formation of
(CSP)
Fractional Excretion calcium oxalate or calcium phosphate renal stones.
of Potassium Definition Excretion of abnormally high level of CALCIUM in the
Serum Potassium (MSH) URINE, greater than 4 mg/kg/day.
Transtubular
Potassium Gradient Concepts Disease or Syndrome (T047)

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Magnesium
Macrocytosis
Magnesium
Malaria Blood Smear Magnesium is the fourth most abundant cation in the body, behind sodium, potassium, and
Manganese calcium. It is the second most prevalent intracellular cation after potassium. The normal body
Mean Platelet Volume magnesium content is approximately 1000 mmol or 25 g, of which about half is in bone and
Menorrhagia Coagulation Workup the other half is intracellular in soft tissue and muscle. Less than 1% of the total body
Mercury magnesium is present in blood. Magnesium is essential for the function of many important
Metanephrines for Pheochromocytoma enzymes, including reactions involving ATP synthesis and DNA replication and transcription.
Metapneumovirus Magnesium is also required for cellular energy metabolism, membrane stabilization, nerve
Methanol Poisoning conduction, calcium channel activity and ion transport. Magnesium deficiency results in a
Methemoglobin variety of metabolic abnormalities and clinical consequences.
Methicillin Resistant Staphylococcus
Aureus No-Risk Prenatal Test Magnesium Sulphate-Turkey
Methotrexate Paternity test- mother's blood only Call Now Toll Fertilizer & Industrial MgSO4-7H2O Over 20 years
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Microsomal Antibodies
Minimum Bactericidal Concentration
Minimum Inhibitory Concentration
Mitochondrial Antibody GI absorption and renal excretion regulate total body magnesium levels. The average daily
Monoclonal B Cell Lymphocytosis dietary intake is about 325 mg and intestinal absorption is inversely proportional to the amount
Multiple Sclerosis Panel ingested. Most magnesium is absorbed in the ileum and colon. Cereal, grains, nuts legumes,
Mumps Virus IgG & IgM Antibodies and chocolate are relatively rich in magnesium. Vegetables, fruits, meats and fish have
Mycobacteria DNA Sequencing intermediate amounts and dairy products are low in magnesium. The kidney is the major
Mycobacterial Blood Cultures excretory organ for magnesium. Approximately 70% of plasma magnesium is filtered through
Mycoplasma Pneumoniae Antibody the glomerular membrane. Only about 6% of filtered magnesium (120 mg) is excreted daily
Mycoplasma Pneumoniae PCR into the urine, because of reabsorption in the Loop of Henle. The major regulator of tubular
Myeloperoxidase Antibodies reabsorption is the plasma magnesium concentration. Hypermagnesemia inhibits and
Myeloproliferative Disorders hypomagnesemia stimulates renal transport.
Myoglobin
Myoglobin Urine Serum magnesium exists in three states: approximately 60% is ionized (free), 33% is protein
bound, and 7% is complexed to phosphate, citrate, and other anions. Approximately 75% of
the protein bound fraction is bound to albumin and 25% to globulins. Serum magnesium
concentration does not correlate very well with tissue magnesium levels. Serum levels are
useful for assessing acute changes in magnesium states, especially in patients with cardiac
arrhythmias, acute onset of seizures, and diabetic ketoacidosis.
Serum IgE v. skin
testing Hypomagnesemia is found in 12 to 20% of hospitalized patients and up to 65% of patients in
Practical information For intensive care units. The usual reason is loss of magnesium from the GI tract or the kidney.
The causes of magnesium depletion can be remembered as the "D" factors:
healthcare professionals
www.hycorbiomedical.com Diarrhea: Lower GI secretions are rich in magnesium. Diarrhea, malabsorption, bowel
resection, steatorrhea and acute pancreatitis are common causes of magnesium
depletion.
Diuretics: Loop diuretics can rapidly induce magnesium wasting. Long term thiazide
Manage High Iron diuretics can also cause hypomagnesemia.
Read About Exjade®: Diabetes: This is the most common cause probably due to glycosuria and osmotic
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Drugs: mostly nephrotoxic drugs such as aminoglycosides, amphotericin B, cyclosporine,
Chelation Therapy cisplatin, foscarnet, pentamidine.
www.Exjade.com Delivery: Magnesium normally declines by 10% in pregnancy and further during labor.
Severe depletion is associated with eclampsia.
Denuded Skin: Burns are associated with a general loss of electrolytes.
offer magnesium Dietary: Hypomagnesemia becomes evident after 7 days of dietary magnesium
restriction. Clinical signs are observed after 42 days.
sulfate
Drinking: Alcohol inhibits renal tubular reabsorption of magnesium. Thirty percent of
manufacture magnesium alcoholics admitted to the hospital have low magnesium.
sulfate aluminum sulfate,
monensin sodium Hypocalcemia is common in patients with severe hypomagnesemia, usually appearing when the
www.jinxingchem.com serum magnesium level is less than 1.0 mEq/L. PTH levels are usually low and rise rapidly
following magnesium replacement. Hyokalemia also frequently accompanies hypomagnesemia.
It does not respond to potassium replacement until the magnesium deficit is corrected.
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Hypermagnesemia is rare and usually iatrogenic. The most common causes are IV magnesium
High Purity Magnesium and magnesium containing cathartics or antacids. Patient most at risk are the elderly and those
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Specimen requirement is one SST tube of blood.
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Test Interpretations Transfusion Quality Control Utilization Method Evaluation Test Significant Change Q&A Blog
Sodium Urine
Sd70 Antibody
Secretin Provocative Test
Semen Analysis Dietary intake greatly influences the urinary excretion of sodium. The rate of sodium excretion
Severe Acute Respiratory Syndrome during the night is only one fifth of the peak rate during the day, indicating a large diurnal
Sickle Cell Screen variation. Measurement of urinary sodium is helpful in the differential diagnosis of
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Synovial Fluid Analysis
Fluid Volume Urinary Sodium Causes
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Hypovolemia >20 Renal losses due to diuretics, aldosterone deficiency, salt
losing nephropathy, osmotic diuresis, ketonuria, RTA
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Normal <20 Extra renal losses due to vomiting, diarrhea, third spacing of
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Hypovolemia <20 Excess sweating, burns, diarrhea, fistulas
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chemistry distribution Reference range is 43 - 217 mEq/24 hours.
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Specimen requirement is a 24 hour urine collection in a container without preservative.
Specimen should be refrigerated during an after the collection.
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Sodium, Serum
Sd70 Antibody
Secretin Provocative Test
Semen Analysis Sodium is the most abundant cation in the extracellular fluid. Serum sodium with its
Severe Acute Respiratory Syndrome accompanying anions accounts for most of the osmotic activity of the plasma. Serum sodium
Sickle Cell Screen and osmolality are controlled by two separate but related systems. Serum sodium is
Smith Antibody maintained by a feedback loop involving the kidney and adrenal glands. A decrease in serum
Smooth Muscle Antibody sodium concentration or in blood pressure results in the release of renin by the kidney. Renin
Sodium catalyzes the conversion of angiotensinogen to angiotensin I, which in turn is converted to
Sodium Urine angiotensin II by angiotensin converting enzyme in the lung. Angiotensin II stimulates the
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Stenotrophomonas Maltophilia stimulus to renin secretion.
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Serum osmolality is maintained by a feedback system involving the hypothalamus, pituitary
gland, and the kidney. An increase in serum osmolality is sensed by osmoreceptors located in
the anterior hypothalamus resulting in release of antidiuretic hormone (ADH) from the posterior
Manage High Iron pituitary gland. ADH acts on the distal nephron to cause retention of water, which reduces
Read About Exjade®: serum osmolality and removes the stimulus to ADH secretion. Conversely, a decrease in serum
An Effective Iron osmolality inhibits ADH release, and excess water is excreted in the urine until serum
osmolality returns to normal.
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Hyponatremia is the most common electrolyte abnormality in hospitalized patients and is
defined as a serum sodium concentration less than 135 mEq/L. Symptoms are due to the
relative excess of water that results in overhydration of cells. The severity of symptoms
depends on the degree of hyponatremia and the rate at which it develops. A patient with mild
Sulfo Isophthalic Acid hyponatremia (sodium >125 mEq/L) may be asymptomatic or experience malaise and nausea.
Sulfo Isophthalic Acid As the hyponatremia worsens, headaches, lethargy, confusion, and a decreasing level of
Sodium Salt Professional consciousness may develop. Seizures and coma usually occur only if there is a sudden
decrease in sodium to less than 120 mEq/L.
chemistry distribution
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Hyponatremia can be categorized by its effect on blood volume. The initial evaluation of
hyponatremia should include measurement of plasma osmolality, electrolytes, glucose and
BUN. When serum osmolality is reduced, the next step is to determine the extracellular fluid
volume of the patient. If it is reduced, hyponatremia is defined as depletional. The patient has
Buy DCA lost sodium and water, and the sodium loss is proportionately greater than the water loss.
Measurement of urinary sodium concentration helps to identify the site of sodium and fluid
Sodium Dichloroacetate loss. Urinary sodium concentration greater than 20 mEq/L indicates renal loss of sodium while
Ships Immediately urinary sodium concentration less than 20 mEq/L indicates extrarenal loss. The most common
www.buyDCA.com/ causes are thiazide diuretics; prolonged vomiting or diarrhea; third spacing of fluids secondary
to burns, pancreatitis or trauma; potassium depletion, and aldosterone deficiency.
Euvolemic hyponatremia is the most commonly encountered sodium disorder in hospitalized
LianXing Chemical patients. It typically indicates a problem with water balance. The most common etiologies are
Co.,Lt inappropriate ADH secretion, severe hyperglycemia, polydipsia, adrenal (cortisol) insufficiency,
and pregnancy. The syndrome of inappropriate ADH secretion (SIADH) is the commonest cause
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of hyponatremia in hospital patients and is associated with malignancies, pulmonary disease,
Sodium Hypopho- sphite CNS disorders, and HIV infection. Hyponatremia is common after surgery and is characterized
(quantity is 5000MT/year) by high levels of circulating ADH. Hyperglycemia accounts for 15% of hyponatremia in
www.lianxingchem.com inpatients. Plasma sodium falls by 1.6 mEq/L for every 100 mg/dL increase in plasma glucose.
Drug induced hyponatremia can be caused by drugs that stimulate the release of ADH or
potentiate its action. Drugs causing hyponatremia include psychoactive agents (fluoxetine,
sertraline, thiothixene, haloperidol, and amitriptyline), some anti-cancer agents (vincristine,
Kidney Failure Cure vinblastine, and high dose cyclophosphamide), and carbamazepine, bromocriptine, lorcainide,
Your Kidney Failure. . . chlorpropamide, and IV vasopressin.
Absolutely Gone Forever.
. . Never To Return. Hypervolemic hyponatremia is nearly always a problem of water overload, which causes
www.TheKidneyDiseaseSolution.c edema. Total body sodium is increased, but total body water is increased even more. The most
common causes are congestive heart failure, cirrhosis, advanced renal failure, and nephrotic
syndrome. In congestive heart failure, impaired perfusion of the kidney causes retention of
sodium and water, with water retained in excess of sodium. In renal failure, the impaired

14. kidney is unable to excrete normal amounts of water. Hypoalbuminemia due to cirrhosis or
nephrotic syndrome decreases oncotic pressure and causes water to leave the intravascular
space, resulting in decreased blood pressure. Homeostatic mechanisms lead to retention of
water in the extracellular fluid compartment.
Approach to Diagnosis of Hyponatremia
Pseudohyponatremia is an artifactual hyponatremia most commonly caused by severe
hypertriglyceridemia (>1500 mg/dL), or less often, by severe hyperproteinemia (>10 g/dL).
Sodium is most commonly measured with an ion specific electrode (ISE). Two types of ISE
exist; indirect and direct. Sodium is dissolved only in the water portion of plasma. When
triglyceride or protein levels are extremely high, they occupy more space in a given volume of
plasma, resulting in a decreased in the percentage of water with its sodium content.
Consequently, an artifactually low sodium concentration is obtained because less sodium is
present in a given volume of plasma, even though the concentration of sodium in the water
phase is unaltered. Pseudohyponatremia can occur when sodium is measured with an indirect
ISE, which is the method used by most automated chemistry analyzers. This phenomenon is
not seen when sodium is measured with an instrument that uses direct ISE, such as point of
care instruments and blood gas analyzers. These instruments use whole blood, instead of
plasma, and do not require predilution of the sample. Pseudohyponatremia can be confirmed
by measuring sodium on an instrument using direct ISE and also measuring serum osmolality
and comparing the result to a calculated osmolality. In a patient with hyponatremia, an
increased osmolal gap suggests the presence of pseudohyponatremia.
Hypernatremia is far less common than hyponatremia. Patients at highest risk include infants,
elderly patients, patients with altered mental status, uncontrolled diabetics, and hospitalized
patients receiving hypertonic infusions, tube feedings, osmotic diuretics, lactulose, or
mechanical ventilation. Hypernatremia always reflects a hyperosmolar state so CNS symptoms
are prominent. The signs and symptoms include; altered mental status, lethargy, irritability,
restlessness, seizures, muscle twitching, hyerreflexia, spasticity, fever, nausea, labored
respiration, and intense thirst. In adults, a plasma sodium level above 160 mEq/L is associated
with a 60 to 75% mortality.
Hypernatremia usually results from excessive loss of water relative to sodium. Loss of
hypotonic fluid may be secondary to kidney disease or profuse sweating or diarrhea. The renal
concentrating mechanism is the first line of defense against water depletion and
hyperosmolarlity. Thirst is an important backup defense. Measurement of urine osmolality is
helpful in evaluating the cause of hypernatremia Urine osmolality is normal or low after renal
loss and increased after extrarenal losses. Patients fall into three broad categories.
Urine osmolality < 300 mOsm/kg
Diabetes insipidus (central or nephrogenic)
Urine osmolality 300 to 800 mOsm/kg
Defect in ADH release -
Diuretics
Osmotic diuresis
Urine osmolality >800 mOsm/kg
Excess intake of sodium
Insensible water loss - infants, dementia, fever, burns, heat exposure
GI loss of hypotonic fluid
Loss of thirst
Sodium levels above 160 mEq/L are unusual and may be due to a preanalytical error.
Vacutainer tubes containing a sodium based anticoagulant such as sodium heparin, sodium

15. fluoride, sodium citrate, or sodium EDTA can markedly elevate plasma sodium levels. Cardiac
patients whose specimen are collected from catheters containing benzalkonium heparin can
also have falsely elevated heparin levels.
Reference range is 134 - 144 mEq/L. Sodium concentrations < 120 mEq/L or >155 mEq/L are
considered critical values.
Specimen requirement is one SST tube of blood.
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