DISORDERS OF CALCIUM,

INORGANIC PHOSPHATE AND

MAGNESIUM METABOLISM
OYELAMI LEKAN AKINKUNMI
OUTLINES
• Introduction
• Calcium Metabolism
• Regulation of Calcium metabolism
• Disorders of Calcium metabolism
• Phosphate Metabolism
• Regulation of Phosphate metabolism
• Disorders of Phosphate metabolism
• Magnesium metabolism
• Regulation of Magnesium metabolism
• Disorders of Magnesium metabolism
• Conclusion
INTRODUCTION
• Calcium, phosphate and magnesium are essential body electrolytes
which are important in normal functioning of the body.
• Disorders of these electrolytes results due to the failure of different
regulatory mechanisms controlling their metabolism
CALCIUM METABOLISM
• Calcium is an essential mineral required for bone mineralization,proper
functioning of muscle contraction,nerve conduction, cell signalling,
hormone release and blood coagulation
• Total body calcium is about 1000g. 99% of this is found in
skeleton(predominantly as hydroxyapatite crystals).
• Extraosseous fraction although amounting to only 1% is essential
because of its effect on neuromuscular excitability and cardiac muscle.
• Maintenance of body calcium depends on the calcium stores which in
turn depends on:
• Dietary Calcium intake
• Absorption of calcium from the GI tract
• Renal calcium excretion
CALCIUM METABOLISM
CALCIUM METABOLISM
• Foods rich in calcium include: milk, cheese, meat, leafy vegetables, soybeans
etc
• About 25mmol(1g) of calcium is ingested per day of which about 12mmol is
absorbed (dependent on 1,25DHCC). About 7mmol is secreted into the GIT
and 20mmol excreted in faeces.
• Calcium is absorbed in the small intestine by both passive diffusion and
active transport. Amount absorbed is determined largely by cellular
concentration of a specific calcium binding protein regulated by 1,25 DHCC.
Presence of excessive oxalate,phosphate and fatty acids reduce calcium
absorption.
• There is constant state of flux between bone and available calcium pool due
to bone resorption and remodelling.
CALCIUM METABOLISM
• Large quantity of calcium are filtered by the glomerulus of which
about 99% are reabsorbed from the renal tubules.
• 65% reabsorption occur in proximal tubule coupled to sodium
reabsorption.
• About 20% reabsorption occur at the thick ascending limb of loop of
Henle along a paracellular route also coupled to Na reabsorption.
• Remaining 15% reabsorption is at the distal tubule which is the site of
regulation of Calcium reabsorption by PTH. Reabsorption here is not
coupled to Na reabsorption
PLASMA CALCIUM
• Total plasma calcium concentration is around 2.15-2.55 mmol/L and
consists of three components:
1. Protein bound calcium(40-45%)
2. Free ionized Calcium (45-50%)
3. Calcium complexed to citrate, phosphate and bicarbonate(5-10%)
• Factors that alter these forms include:
1. Changes in plasma protein conc.(alter the total calcium in the same
direction as protein conc. This does not affect ionized calcium conc.
2. Acid-base abnormalities :Albumin has 12 calcium bindung sites and H⁺
compete for these so in acidosis, there is increase in ionized calcium.
Alkalosis causes the reverse. This pH change will not affect the Total plasma
calcium.
CALCIUM MEASUREMENT
• The physiologically active fracton is the free ionized fraction so its
measurement is the one of importance.
• The best way to do this is by measuring directly with ion sensitive
electrode but is technically demanding.
• More commonly, Total calcium is measured. Due to the effect of albumin
conc, corrected calcium is calculated from the measured total calcium
using the Payne's formula which corects the total plasma to a standadized
albumin concentration of 40g/L.
• It is calculated as follows:
• corrected calcium(mmol/L)=[Total calcium]+0.02(40-[albumin])
REGULATION OF PLASMA CALCIUM
• Calcium homeostasis involves coordinated interactions of 3 organs
(bone, kidney and intestine) and 3 hormones (PTH, Vitamin D and
Calcitonin)
• It follows the general rule that extracellular concentration are
controlled rather than the total body content and the effectiveness of
this control depends on the normal functioning of the above organs
and adequate supply of hormone
PTH
• PTH is a single-chain polypeptide with 84 amino acids secreted by the
chief cells of parathyroid glands.
• The biological activity is largely determined by its 34 N- terminal amino
acids.
• It acts on bone, kidney and intestine to bring about increased
concentration of free ionized calcium
• on BONE, PTH stimulates osteoclast activity causing bone resorption
releasing calcium and phosphate. It does this by stimulating osteoblast
to release RANK ligand which activates osteoclasts via the RANK-L/RANK
pathway
• Activated osteoclasts through H⁺ and cathepsin-K dissolves bone
minerals leading to the release of Calcium and phosphates
• Osteoprotegerin serves as handbrake to the RANK/RANK-L system.
Osteoclast activation
PTH
• On the KIDNEY, PTH binds with the basolateral receptor(GPCR) in the
distal tubule activating adenylyl cyclase thereby producing cAMP
which activate protein kinase C
• PKC promotes insertion of calcium channels(TRPV5) into the apical
membrane thus enhancing calcium reabsorption
• At the proximal tubule, PTH-induced cAMP activate protein kinase A
which phosphorylate specific intracellular proteins which inhibit Na⁺-
phosphate cotransport leading to decreased phosphate reabsorption
and phosphaturia
• This phosphaturic action is needed because the phosphate
reabsorbed from bone would have complexed Ca²⁺.
PTH
• On small intestine, PTH does not have a direct action. It stimulates
intestinal calcium reabsorption via activation of Vitamin D
• PTH stimulates renal 1α hydroxylase which convert 25 hydroxyl
cholecalciferol to 1,25DHCC(stimulates intestinal calcium reabsorption).
REGULATION OF SECRETION
• Plasma calcium concentration(the free ionized fraction)
• Calcium-sensing receptor(CaSR)
• A GPCR found primarily in the Parathyroid gland, also in the kidney, brain and
thyroid gland.
• Senses extracellular calcium levels to adjust PTH secretion
• Facilitate calcium excretion
• 1,25 DHCC
VITAMIN D
• Vitamin D is derived from diet(ergocalciferol) or from 7-
dehydrocholesterol in the skin by action of UV light.
• It is transported in the plasma bound to specific carrier potein. It is
inactive until metabolized.
• In the liver, cholecalciferol is hydroxylated to 25-hydroxyl cholecalciferol
by 25-hydroxylase. This is followed by 1-α hydroxylation in the proximal
renal tubules to its active form 1,25 DHCC by 1-α hydroxylase.
• 1-α hydroxylase is stimulated by : ↓plasma calcium conc., ↑plasma PTH
conc and ↓plasma phosphate conc. It is inhibited by:
Hyperphosphatemia, high level of free ionized calcium, FGF-23 and1,25
DHCC.
• In the state of calcium sufficiency, 24-hydroxylase becomes active and
convert the precursor to 24,24 DHCC(less active metabolite)
VITAMIN D
• 1,25 DHCC is transported in the blood bound to VDBP to its main
target tissue (intestine, bone and kidney).
• It is a steroid hormone; its mechanism of action involves binding to
nuclear receptors stimulating gene transcription and synthesis of new
proteins which have the following actions:
• In the INTESTINE, there is increase absorption of Ca²⁺ and phosphate.
This is due to the synthesis of Calbindin D-28K (a vitamin D-
dependent calcium binding protein) in the intestinal cells.
• KIDNEY: stimulates both calcium and phosphate reabsorption
• BONE: Act synergistically with PTH to stimulate bone resorption by
osteoclast activity.
• Overall result is increase in plasma calcium and phosphate
concentration
CALCITONIN
• A 32 amino acid polypeptide secreted by the parafollicular cells of the thyroid
gland.
• It decreases osteoclastic activity, slows calcium release from bone and has
opposite effect of PTH however, it has less importance on calcium homeostasis.
• Exogenous calcitonin has been used to treat hypercalcaemia and Paget's disease
of bone

• Miscellaneous mechanism of calcium regulation includes:

• Thyroid hormone: excess may be associated with increase rate of calcium removal from
bones
• Estrogen, Prolacin and growth hormone which may increase 1,25 DHCC production and
increase calcium absorption during pregnancy, lactation and growth.
DISORDERS OF CALCIUM
METABOLISM
• Disorders of serum calcium conc. are relatively common in clinical
settings and often serve as harbinger of underlying disease.
• They results from failure of regulatory processes of calcium
metabolism.
• They are:
1. Hypercalcaemia
2. Hypocalcaemia
HYPERCALCAEMIA
• Hypercalcaemia is a condition in which there is elevated albumin-
adjusted plasma calcium concentration above 2.60mmol/L or ionized
serum calcium >1.30mmol/L.
CAUSES OF HYPERCALCAEMIA
• Overall, thiazides are one of the most comon causes of mild
hypercalcaemia. However, Primary hyperthyroidism and Malignancy
are the major causes of severe hypercalcaemia
HYPERCALCAEMIA OF MALIGNANCY
• In hospitalized patient, malignancy is the commonest cause of
hypercalcaemia and in most instances, it is a late complication of the
disease.
• The presentation is usually abrupt and serum calcium level is very
high (3.5mmol/L)
• Carcinoma of the breast, bronchus, kidneys,thyroid and hematological
malignancies (myeloma, leukaemia, lymphoma, Hodgkin's disease)
are tumors commonly associated with hypercalcaemia.
• They are classified into three based on their pathophysiology
1. Tumors with bone metastasis
2. Tumors without bone metastasis
3. 1,25 DHCC secreting tumors
 HYPERCALCAEMIA OF MALIGNANCY
1. Tumors with bone metastasis
• Here, there is direct bone resorption due to direct invasion by metastatic
tumors(breast, lung, prostate, thyroid tumors and multiple myeloma).
• They do this with the help of osteoclast activating factors like IL- 1 amd 6, TGF β,
TNF, PG E2
2. Tumors without bone metastasis
• Squamous cell carcinoma of lung and oesophagus, carcinomas of kidney and
ovary
• Here, there is secretion of PTHrP(a polypeptide of 141 amino acid residue) by
malignant tumors and it is not subject to normal feedback control
• PTHrP binds to PTH receptors in bone and kidney and produce same biologic
effect as PTH
3. 1,25DHCC secreting tumors(lymphoma)
• There is overproduction of 1,25 DHCC due to poduction of 1α hydroxylase by
lymphoma tissue
• There is hypercalcaemia and hyperphosphataemia with low PTH level
HYPERPARATHYROIDISM
Primary hyperparathyroidism
• Commonest cause of hyperclcaemia after malignancy
• Has a female:male propenderance of 3:1
• Incidence increases with age
• Commonest cause is solitary adenoma, occasionally due to hyperplasia of
all 4 parathyroid glands and rarely due to parathyroid carcinoma.
• It may also present as familial disease (as part of multiple endocrine
neoplasia)
• There is high plasma calcium concentration and hypophosphataemia with
phosphaturia
HYPERPARATHYROIDISM
Tertiary Hyperparathyroidism
• Occurs in long standing secondary hyperparathyroidism (chonic
kidney disease, vitamin D deficiency) which have been subsequently
corrected
• Here, the parathyroid gland hypertrophy; PTH secretion becomes
autonomous and is not sensitive to negative feedback by the
hypercalcaemia.
Diseases affecting CaSR
Familial Benign Hypocalciuric Hypercalcaemia
• Autosomal dominant inherited loss of function of CaSR in the
Parathyroid gland and kidney thus high level of calcium is needed to
suppress PTH secretion.
• There is hypercalcaemia, normal or high PTH and hypocalciuria
• Diagnosis is suspected when there is a strong family history of
hypercalcaemia. Diagnosis is made by measuring FECa (<1% in FBHH)
Lithium therapy
• Chronic lithium therapy interferes with CaSR
• Same findings as in FBHH
EXCESSIVE 1,25 DHCC PRODUCTION
Vitamin D intoxication
• Can occur with overvigorous treatment of hypocalcaemia
• Increased calcium absorption leading to hypercalcaemia
Granulomatous diseases
• Sarcoidosis, tuberculosis, histoplasmosis, leprosy
• There is increased secretion of 1α hydroxylase by the macrophages of
the granuloma
Lymphoma
High bone resorptiom
Immobilization
• High bone resorption compared to formation due to reduced axial
pressure
Hyperthyroidism
• There is increase in osteoclastic activity thereby raising calcium level
and causing osteoporosis
Vitamin A intoxication
DRUGS
• Thiazide diuretics: reduce renal calcium excretion
• Milk-Alkali syndrome: excessive use of calcium antacids for dyspepsia
Clinical features
CNS effects
• Lethargy, muscle weakness, confusion, depression, Coma
Renal effects
• Polyuria, Renal calculi, AKI, CKD
GI effects
• Constipation, abdominal pain, nausea and vomiting.
CVS effects
• Arrhythmia, hypertension, bradycardia, shortened QT interval,
broadened T waves on ECG.
Skeletal effects
• Bone and joint pain
INVESTIGATIONS
• Establish the albumin concentration and check albumin adjusted
calcium concentration
• Serum PTH
• Plasma phosphate concentration
• USS or MRI of neck
• Vitamin D Levels
• FECa
• PTHrP
• FBC, ESR
• Serum protein electrophoresis
• Steroid suppression test
• Thyroid function test
INVESTIGATIONS
Treatment
Asymptomatic Patients:
• Causes of mild to moderate hypercalcemia (<3.5mmol/L) are investigated
and treated;
• If primary hyperparathyroidism, surgery is indicated.
• Normal saline to correct hemodilution
• Bisphosphonates
Severe Hypercalcaemia: >3.5mmol/L
• Rehydration
• Furosemide
• Bisphosphonates e.g palmidronate
• Address underlying cause
• Steroids in malignancy, sarcoidosis, vit D intoxication
• Calcitonin
• Denosumab
HYPOCALCAEMIA
• Hypocalcaemia is a condition where the albumin adjusted plasma
calcium is below the lower limit of the reference range (<2.15mmol/L)
CAUSES AND CLASSIFICATION OF HYPOCALCAEMIA
• In a clinical settings, one of the most common cause of low calcium
level in the blood is hypoalbuminaemia so it is necessary to estimate
the plasma albumin conc. to exclude hypoalbuminaemic state
• Another cause to exclude is artefactual cause(EDTA in blood sample
tube)
• Based on the plasma phosphate concentration, hypocalcaemia can be
classified into two:
1. Hypocalcaemia with hypophosphataemia
2. Hypocalcaemia with hyperphosphataemia
Causes of Hypocalcaemia with Hypophosphataemia
1. Vitamin D and Calcium deficiency
• Dietary deficiciency
• Malabsorption
• Inadequate exposure to UV light
2. Impaired Vitamin D metabolism
• Decreased 25-hydroxylation as seen in chronic liver disease and prolonged
anticonvulsion therapy(phenytoin, barbiturate)
• Decreased 1α-hydroxylation seen in renal disease, type 1 Vitamin D-dependent ricket
3. Resistance to 1,25 DHCC
• Anticonvulsion therapy, type 2 Vitamin D-dependent ricket
4. Increased clearance of 1,25 DHCC
• Nephrotic syndrome, phenytoin, alcohol
In all these conditions, there is ↓action of 1,25 DHCC→↓calcium
absorption→hypocalcaemia→↑increased PTH
secretion→hypophosphataemia
Hypocalcaemia with hyperphosphataemia
1. Renal dysfunction
• Decreased 1α-hydroxylation
• Impaired phosphate excretion
2. Primary Hypoparathyroidism: Here, there is deficient PTH production by
the parathyroid glands. This leads to decreased calcium absorption and
phosphate excretion. Causes iclude:
• Surgical damage from thyroidectomy, laryngectomy, partial parathyroidectomy
• Congenital absence of parathyroid gland (DiGeorge's syndrome)
• Autoimmune disorder
3. Infiltrative diseases e.g. hemochromatosis
4. Pseudohypoparathyroidism: Inborn error associated with resistance to
circulating PTH. Associated phenotype may show short stature, obesity,
round face, shorth 3rd and 4th metacarpals.
5. Magnesium deficiency:Hypomagnesaemia impairs PTH scretion causing
hypocalcemia resistant to calcium and Vitamin D therapy
Clinical features
• Muscle spasm
• Carpopedal spasm
• Facial grimacing
• Laryngeal spasm
• Convulsion
• Depression
• Prolonged QT interval
• Arrhythmia
• Cataract
• Positive Chvostek's and Trosseau's sign
• Dry and scaly skin, brittle nails and coarse hair
Investigations
• Albumin conc.
• Plasma PTH assay
• Plasma phosphate conc.
• Urea and creatinine
• Plasma 25HCC and 1,25DHCC
• Plasma magnesium level
Treatment
• For asymptomatic hypoclcaemia, give oral calcium spplement and
vitamin D supplement
• For hypoclcaemia with life threatening symptoms, intravenous
calcium, usually as 10 mL of 10 per cent calcium gluconate, should be
given over about 5 min.
PHOSPHATE METABOLISM
• Phosphate is a divalent anion; approximately 80% of which is found in
the bony skeleton and 20% in soft tissue and muscle
FUNCTIONS
• Combination with calcium to form the mineral component
(hydroxyapatite) of bones and teeth
• Participation as essential agents (high energy phosphate bonds) in
energy transfer and in the metabolism of carbohydrate and fat
• Crucial urinary buffer
• Maintenance of cell wall integrity
• Enzyme regulation
• Regulation of oxygen transport through 2,3- diphosphoglycerate
PHOSPHATE METABOLISM
• Daily intake is about 30mmol with about 80% being absorbed in the
jejunum. Protein rich food like cereals,nuts are major source of
phosphate intake.
• The rate of absorption is increased by PTH and 1,25 DHCC
• The major route of excretion is the kidney (90%), GI loss accounts for the
remaining 10%.
• About 100-200mmol of phosphate is filtered daily by the glomerulus;
80-90% is reabsorbed in the proximal tubule and remainder excreted in
the urine.
• This reabsorption is accomplished by Na⁺-phosphate co-transporter in
the luminal membrane of the proximal tube
• Increased renal excretion is associated with;
• Increased PTH secretion, Increased phosphate intake, Increased ECV, Increased
sodium intake and calcitonin
PHOSPHATE METABOLISM
• Decreased renal excretion is associated with
• Decreased PTH secretion, Decreased phosphate intake,Decreased ECV,
Increased growth hormone secretion
• Plasma conc. of phosphate in adult is ranges from
0.8-1.4mmol/L(Higher in children and neonates)
• Short-term changes in phosphate concentrations occur with rapid
exchange between intracellular and extracellular phosphate pools.
This exchange is influenced by
• Insulin, glucose, catecholamines, alkalosis (decrease)
• Rapid cell breakdown (increases)
• Rapid growth and repair (decreases)
PHOSPHATE REGULATION
• Phosphate concentration is regulated by 3 hormones which are:
• 1,25 DHCC , PTH and FGF-23
1. 1,25 DHCC: act on the intestine, kidney and bone to increase
phosphate absorption
2. PTH: net effect is to decrease phosphate conc.
• It stimulates internalization of Na⁺-phosphate co-transporter leading to
phosphaturia.
• By stimulating 1α hydroxylase activity and bone resorption, It increases
plasma phosphate conc.
3. FGF-23: Secreted by osteoblasts in response to high phosphate
levels. It decreases phosphate conc. by the following mechanism;
• Decreases the number of Na⁺-phosphate co-transporter in the luminal
membrane of proximal renal tubules
• Inhibit 1α hydroxylase activity
DISORDERS OF PHOSPHATE METABOLISM
HYPERPHOSPHATAEMIA
• Hyperphosphataemia is a medical condition characterized by elevated
levels of phosphate in the blood.
• It is typically defined in adult as serum phosphate concentration
greater than 1.46mmol/L
• Causes may be due to:
• Impaired renal phosphate excretion as seen in renal insufficiency,
Hypoparathyroidism and Parathyroid suppression, acromegaly and tumoral
calcinosis
• Massive ECF phosphate loads as seen in overzealous exogenous phosphate
therapy, extensive soft tissue injury or necrosis (crush injuries,
rhabdomyolysis, hyperthermia, fulminant hepatitis, cytotoxic chemotherapy),
extensive hemolytic anemia, and transcellular phosphate shifts induced by
severe metabolic or respiratory acidosis
CLINICAL FEATURES
They are mainly due to widespread formation of calcium phosphate
precipitates and resulting hypocalcaemia(reduced intestinal absoption)
• Tetany
• Seizures
• Accelerated nephrocalcinosis (with renal failure, hyperkalemia,
hyperuricemia, and metabolic acidosis)
• Pulmonary calcification
• Cardiac calcification
Investigations
• Plasma phosphate concentration
• Plasma creatinine conc.
• Plasma calcium conc.
• Urinary phosphate excretion rate
Treatment
• Volume expansion
• Oral phosphate binding agent (calcium carbonate, magnesium
hydroxide,sevelamer)
• Haemodialysis
HYPOPHOSPHATAEMIA
• Hypophosphataemia is
characterized by low level of
phosphate in blood i.e
serum phosphate <
0.8mmol/L
Clinical features
• CVS- cardiomyopathy,
• CNS:
• seizures,
• drowsiness,
• paresthesia
• Musculoskeletal system:
• muscle weakness,
• myopathy
• rhabdomyolysis,
• impaired diaghramatic contractility,
• Hematology:
• Impaired leucocyte function,
• impaired clotting,
• left shift of Hb/O2 curve
Investigations
• FePi%
• PTH level
• Calcium conc.
• FGF-23 serum level
Treatment
• Oral phosphate salts
• IV 9mmol of monobasic potasium phosphate in half normal
saline over 12 hours.
MAGNESIUM METABOLISM
• Magnesium is predominantly an intracellular divalent cation
• The body contains about 1mol of Mg mostly in bone and muscle
• ECF contains only about 1% of total body Mg
• Normal serum Mg conc ranges from 0.7-1.1mmol/L
FUNCTIONS
• It is an essential cofactor to many enzymes
• contributes to maintenance of structure of ribosomes, nucleic acids
and proteins
• Plays a major role in preventing hyperexcitability of nerve cells
MAGNESIUM METABOLISM
• Maintenance of serum magnesium conc. is largely a funtion of dietary
intake and effectie rena land intestinal conservation.
• RDA for adult is about 4.5mg/Kg. Rich sources include; whole cereal,
nuts and vegetables
• About 30% is absorbed majorly in the upper small
intestine(absorption not vitamin D dependent unlike calcium)
• Major excretory route is via kidney, about 20-30% of filtered Mg is
reabsorbed in the proximal renal tube and 60-70% in the thick
ascending limb of the loop of Henle. Small percentage(<5%) is
reabsorbed in the distal tube.
MAGNESIUM METABOLISM
There are no well defined mechanism controlling Mg metabolism
unlike calcium but the rate of excretion is infuenced by many factors
including:
• Body magnesium: a low intake or deficiency causes increased
reabsorption
• Plasma calcium levels: hypercalcaemia decreases reabsorption
• Phosphate: depletion decreases reabsorption
• PTH, calcitonin, ADH, glucagon: all of which increase reabsorption
• Extracellular volume: an increased ECV increases renal excretion
• Drugs: Alcohol and a number of drugs such as diuretics and various
chemotherapeutic agents also increase the excretion rate
Disorders of Magnesium Metabolism
HYPERMAGNESAEMIA
• Characterized by elevated level of magnesium in the blood i.e. serum
level>1.1mmol/L
CAUSES
1. Increased intake
• Antacids, Purgatives, Parenteral nutrition
2. Impaired Renal excretion
• Renal failure (AKI or CKD), FHH, Lithium treatment
3. Rapid mobilization from soft tissues
• Trauma, shock, sepsis, cardiac arrest, burns
Clinical features
• Cardiac arrhythmias
• Cardiac arrest
• Seizures
• Reduced tendon reflexes
• Paralytic ileus
• Respiratory depression
• Hypotension.
Treatment
• Identifying and interrupting the source of Magnesium
• Magnesium free cathartics
• IV injection of 10 mL of 10% calcium gluconate
• Insulin and glucose
• Dialysis
HYPOMAGNESAEMIA
• Characterized by reduced level of magnesium in the blood i.e. serum level <
0.7mmol/L
CAUSES
• Decreased intake and absorption
• Starvation, parenteral nutrition, malabsorption syndrome, prolonged gastric suction,
PPI.
• Increased cell uptake
• Excess of catecholamines, Hungry bone syndrome, Refeeding syndrome
• Increased renal loss
• Dialysis, alcoholism, Bartter’s and Gitelman’s syndromes
• Drugs: diuretics, amphotericin B, gentamycin, cis-platinum, ciclosporin, pentamidin
and tacrolimus
• Primary hyperaldosteronism, hyperparathyroidism, SIADH
• Extrarenal losses
• Prolonged diarrhoea, laxative abuse, GI fistula
Clinical features
• Arrhythmia
• Digoxin sensitivity
• Abdominal discomfort
• Tremor
• Paraesthesiae
• Vertigo
• Tetany,
• Seizures
• Confusion
• Weakness
• Ataxia.
INVESTIGATION
• 24 h urinary magnesium excretion rate
• Plasma calcium
• Plasma electrolytes
TREATMENT
• Oral magnesium salts,
• magnesium gluconate 12 - 48mmol/day in 3 to 4 divided doses
• Magnesium sulfate I.V 0.5 mmol/Kg
CONCLUSION
• Calcium, phosphate and magnesium are essential electrolytes needed
in optimal concentration for normal functioning of the body.
• Kidney, intestine and bone with hormones like PTH, 1,25 DHCC, FGF-
23 are essential in maintaining this optimal concentration.
• Disorders of these electrolytes results due to the failure of different
regulatory mechanisms controlling their metabolism
• A carefully taken history,laboratory investigations and treatment helps
prevent long term complication and death.
REFERENCES
• Martin A. Crook, Clinical Biochemistry and Metabolic Medicine. 8th
ed
• A Primer of Chemical Pathology
• University of Cape Town Chemical Pathology Lecture note
• Costanzo Physiology