20200910

HYPOMAGNESEMIA
Hypomagnesemia is an electrolyte disturbance in which there is an abnormally
low level of magnesium in the blood

symptoms may include:

 nausea,
 vomiting,
 muscle cramps,
 abnormal heart rhythms
 Hypomagnesemia during pregnancy can contribute to
malformations in the developing fetus

Causes of hypomagnesemia:
1. Related to decreased Mg intake
2. Related to Gastrointestinal Mg loss: Diarrhea, severe vomiting,
Hypomagnesemia with secondary hypocalcemia (HSH)
3. Related to renal Mg loss:
4. Drugs: Diuretics, Antimicrobials, Chemotherapeutic agents,
Immunosuppressants
HYPOMAGNESEMIA

Renal magnesium losses can be differentiated from intestinal losses by

evaluating the fractional excretion of magnesium (FEMg):

→ If FEMg is more than 2%

consistent with renal magnesium wasting.
→ If FEMg is less than 2%
extrarenal cause of magnesium loss
HYPERMAGNESEMIA

Causes of hypermagnesemia:
1.Mostly, Renal failure: In the presence of a decline in renal function with a
GFR less than 30 mL/min

2. ingestion of antacids, cathartics, or laxatives,

3. Lithium therapy

symptoms include:
 Neuro-psychiatrical: confusion; ↓ DTR
 Cardiovascular: bradycardia, heart block, cardiac arrest ↑PR, ↑QRS,
↑QT
 Bone: ↓PTH; PTH resistance
 Hypocalcemia
MAGNESIUMABSORPTION

1.Intestinal magnesium absorption

1.Absorption ranges from 25% - 75%

(typical absorption is 120 mg/d)
2. Mg2+ is mainly absorbed in the small
bowel (jejunum and
ileum)
3. Mg2+ absorption occurs via two different
pathways:
A. a saturable, active transcellular
transport
B. a nonsaturable passive paracellular
pathway
4. Transcellular channels, TRPM6
(mutations lead to hypomagnesemia and
hypocalcemia)
MAGNESIUM ABSORPTION

2. Renal magnesium conservation

 Mg2+ enters the blood stream and is filtered within the

Kidneys
 Approximately 95% to 99% of filtered Mg2+ is
reabsorbed
along the kidney tubule
 Different segments of the nephron are tasked with
magnesium reabsorption
(1). 10-20% proximal convoluted tubule

(2). 70% loop of Henle

(3). 10% distal convoluted tubule

MAGNESIUM ABSORPTION
Magnesium and the TAHL
1.Responsible for 40-70% of magnesium
reabsorption 
2.Magnesium reabsorption is passive and
occurs through the paracellular pathway
3. Furosemide diminishes Mg2+ absorption
by inhibiting the Na-Cl-K cotransporter and
the transepithelial voltage
4. parathyroid hormone (PTH), calcitonin,
and glucagon enhance magnesium
reabsorption in the cTAL
5. Claudin 16, a tight junction protein, is
involved with paracellular permeability
6. Casr
• The extracellular Ca21/ Mg2+
sensing receptor
• modulates Mg2+ transport through
changes in transepithelial voltage
and alteration of the permeability of
the paracellular pathway
Magnesium and the Distal Convoluted Tubule

1. Responsible for 5-10% of magnesium

reabsorption
2. Active transcellular transport
3. Process coupled to potassium and
sodium transport
4. Peptide hormones such as PTH,
calcitonin and glucagon enhance
magnesium reabsorption in the DCT
5. The extracellular Casr modulates
hormone-stimulated Mg21 transport through
Gi protein coupling
6. anti-EGF drugs used in oncology are
associated with hypomagnesemia
7. The epidermal growth factor is an
important controller of the process
Thanks for your attention