70% of Total Body Magnesium is filtered as 30% is protein bound
96% is reabsorbed
PCT- 10-30% Reabsorbed unknown mechanism
Thick Ascending Loop of Henle-( 40-70%) of Magnesium reabsorbed paracellularly by positive transluminal voltage caused Na/K/Cl and ROMK channel clckb and na/k/atpase
claudin 16/19 are tight junctions responsible for magnesium absorption
Kidney dominate control of mg hemodtasis , freely filtered across glomerulus ;70% reabsorbed in TALH strongly negative paracellular protein paracellin-1 allow efficient absorption of mg under control of PTH . In DCT transmembrane trans cellular protein TRPM6 allow further uptake .
loss of paracellin 1 or TRPM6 lead to urinary mg wasting and hypoMG
30% of total serum Mg is protein bound, 70% is available for glomerular filtrate, assuming a normal GFR, the kidney filters ~2000-2400mg/d, 96% of which is reabsorbed as follows:
10-30% in PCT by paracellular tight junction proteins claudin 16 & 19 following Na and water,
40-70% in CTALH via paracellular route following NKCC2, ROMK, which are regulated also by CaSR
5-10% in DCT via transcellular route mediated by TRPM6
Renal Regulation of Magnesium:
Assuming a normal GFR, the kidney filters approximately2000–2400 mg of magnesium per day. This takes into account the fact that only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration. Under normal conditions, 96% of filtered magnesium is reabsorbed in the renal tubules.
10%–30% of the filtered magnesium is absorbed in the proximal tubule via a paracellular pathway aided by a chemical gradient generated by Na gradient– driven water transport that increases intraluminal magnesium as well as lumen-positive potential.
Thick Ascending Limb: A paracellular pathway in the:thick ascending limb absorbs 40%–70% of filtered magnesium, mostly enhanced by lumen-positive transepithelial voltage, in which claudin-16 and claudin-19 play an important role.
Distal Convoluted Tubule: The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6.
How do the kidneys control Magnesium levels?Renal Regulation of Magnesium
Assuming a normal GFR, the kidney filters approximately 2000–2400 mg of magnesium per day. This takes into account the fact that only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration. Under normal conditions, 96% of filtered magnesium is reabsorbed in the renal tubules by several coordinated transport processes and magnesium transporters Proximal Tubule 10%–30% of the filtered magnesium is absorbed in the proximal tubule.The exact mechanisms are not known, magnesium is believed to be absorbed via a paracellular pathway aided by a chemical gradient generated by Na gradient– driven water transport that increases intraluminal magnesium as well as lumen-positive potential. Thick Ascending Limb. A paracellular pathway in the thick ascending limb absorbs 40%–70% of filtered magnesium, mostly enhanced by lumen-positive transepithelial voltage, in which claudin-16 and claudin-19 play an important role. The NKCC2 cotransporter mediates apical absorption of Na, K, and Cl. The apical ROMK mediates apical recycling of K back to the tubular lumen and generation of lumen-positive voltage. The Cl channel ClC-Kb mediates Cl exit through the basolateral membrane. Na, K,-ATPase also mediates Na exit through the basolateral membrane and generates the Na gradient for Na absorption. The tight junction proteins claudin-16 and claudin-19 play a prominent role in magnesium absorption. The CaSR has also been determined to regulate magnesium transport in this segment: upon stimulation, magnesium transport is decreased. Basolateral receptor activation inhibits apical K channels and possibly Na-2C1-K cotransport in the rat thick ascending limb Distal Convoluted Tubule. The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6. Bone. At least 50% of the total body magnesium content resides in bone as hydroxyapatite crystals. Dietary magnesium restriction causes decreased bone magnesium content
How do the kidneys control Magnesium levels? Kidney filters 2g of Mg per day, 70% of total serum Mg is filtered by the glomeruli (30% are protein bound), 96% reabsorbed by the renal tubules, 10 to 30% by PCT presumably through paracelluar pathway, 40 to 70% thick ascending limb mediated by of claudin 16,19 & CaSR, 5 to 10% by the DCT, active transcelluar process mediated by TRPM6, basolateral K channel and Mg/Na exchanger (SLC41A1 family) Factors that alter renal regulation of Mg Increase absorption: Low Mg diet, Hormonal factors e.g., PTH, glucagon, calcitonin, vasopressin, and aldosterone, & insulin, Drugs e.g., amiloride, Metaboilc alkalosis Decrease absorption: Electrolytes e.g., High Mg, High Ca, low Pi, low K, Metaboic acidosis, Drugs e.g., diuretics, aminoglycosides, ampho B, foscarnet, cisplatin, CNIs, Genetic mutations e.g., Bartter’s syndrome
Assuming a normal GFR, the kidney filters approximately 2000–2400 mg of magnesium per day. This takes into ac- count the fact that only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration.
Proximal Tubule:
10%–30% of the filtered magnesium is absorbed in the proximal tubule. via a paracellular pathway aided by a chemical gradient generated by Na gradient– driven water transport that increases intraluminal magnesium as well as lumen-positive potential.
Thick Ascending Limb :
A paracellular pathway in the thick ascending limb absorbs 40%–70% of filtered magnesium.
The CaSR has also been determined to regulate magnesium transport in this segment: upon stimulation, magnesium transport is decreased.
Distal Convoluted Tubule:
The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6.
Bone:
At least 50% of the total body magnesium content resides in bone as hydroxyapatite crystals .Dietary magnesium restriction causes decreased bone magnesium content .
The kidney filters approximately 2000–2400 mg of magnesium per day. Only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration. Under normal conditions, 96% of filtered magnesium is reabsorbed in the renal tubules.
Proximal Tubule: 10%–30% of the filtered magnesium is absorbed in the proximal tubule. magnesium is believed to be absorbed via a paracellular pathway aided by a chemical gradient generated by Na gradient–driven water transport that increases intraluminal magnesium as well as lumen-positive potential.
Thick Ascending Limb: A paracellular pathway in the thick ascending limb absorbs 40%–70% of filtered magnesium, mostly enhanced by lumen-positive transepithelial voltage, in which claudin-16 and claudin-19 play an im- portant role. The CaSR has also been determined to regulate magnesium transport in this segment: upon stimulation, magnesium transport is decreased.
Distal Convoluted Tubule. The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6.
The kidneys control Magnesium levels through
The important segment for Mg2+ reabsorption is the cortical thick ascending limb of Henle’s loop. In this segment, about 40–70% of Mg2+ is reabsorbed active and passive process .
In The proximal tubule reabsorbs about 20% of the filtered Mg2+ passive .
In the distal convoluted tubule reabsorbs 5–10% of the filtered Mg2+,which active transport .very little reabsorption occurs in the collecting duct. Under steady state conditions, the urinary excretion of Mg2+ is about 5% of the filtered load
How do the kidneys control Magnesium levels?
important segment for Mg2+ reabsorption is the cortical thick ascending limb of Henle’s loop. In this segment, about 40–70% of Mg2+ is reabsorbed .
The transport of Mg2+ in the cortical TALH is both passive and active. Passive transport is dependent on the lumen-positive voltage difference secondary to Na/K/2Cl cotransporter activity and back-leak of K+ into the lumen via ROMK.
This positive voltage difference facilitates paracellular movement of Mg2+
in The proximal tubule reabsorbs about 20% of the filtered Mg2+ (passive ).
in The distal convoluted tubule reabsorbs 5–10% of the filtered Mg2+,which transport from the lumen to the cell occurs via an epithelial Mg2+ channel called the TRPM6.
very little reabsorption occurs in the collecting duct. Under steady state conditions, the urinary excretion of Mg2+ is about 5% of the filtered load.
In normal kidney function, 2000-2400 mg of Mg is filtered per day.
70% of total magnesium is filtered and the remaining 30% is protein bounded.
96% of filtered Mg is reabsorbed in the renal tubules.
Proximal tubule
via a paracellular pathway. 2. Thick ascending loop of Henle
A paracellular pathway absorbs 40-70% of filtered Mg.
A transcellular pathway mediated via apical absorption of Na, K, and Cl.
CaSR also mediates absorption in the loop of Henle.
Loop diuretics inhibit chloride absorption by NKCC2 and also decrease basolateral Cl efflux.
Barriers syndrome (hypomagnesemia) is caused by mutations in (NKCC2, or ROMK, CIC-Kb, Barrtin and or CaSR.
Familial hypomagnesemia (Autosomal recessive) with hypercalciuria and nephrocalcinosis, caused by a mutation in CLDN16 or CLDN19 encoding the tight junction.
Hypermagnesemia and nephrocalcinosis; resulted from a mutation in claudin-10.
3. DCC
5-10% is reabsorbed in the DCC by active transcellular transport mediated by TRPM6.
EGF inhibitors (anticancer treatment) induce hypomagnesemia by interfering with magnesium reabsorption.
The kidneys filter magnesium every day and reabsorb most of it(96%). Different parts of the renal tubules work together to achieve this. The proximal tubule (10-30%)and the thick ascending limb absorb (40-70%)a large amount of magnesium through a paracellular route, helped by receptors such as Claudine 16, Claudine 19, and NKCC2. The distal convoluted tubule absorbs the remaining magnesium through active transport mediated by TRPM6 and the Kv1 receptor.
Renal Regulation of Mg
In normal GFR, the kidney filter 2000-2400mg /day, 96% reabsorped bt renal tubule
Proximal tubule : 10-30% reabsorped in Proximal CT through a paracellular transport induced by chemical gradient by Na gradient driven water transport.
Thick ascending limb of loop of henle :
40-70%of filtered Mg through paracellular transport enhanced by lumen positive Trans epithelial voltage in which Claudine 16 and claudin 19 in the tight junction play an important role in Mg absorption.
The lumen positive voltage provided by the NKCC2, ROMK and ClC/Kb which enhance absorption.
Stimulation of CaSR will decrease Mg transport
Caudin 10 determines paracellular Na permeability and if lost lead to hyperMg an NC.
Distal convoluted tubule :
Cause absorption of 5-10% of Mg through transcellular active transport by TRPM6 by the lumina potential provided by the apical K channel Kir1.1. Then the absorped Mg will be extruded via Mg/Na exchanger SLC41A1 across the basolateral membrane.
Renal Magnesium Control
A normal GFR kidney filters 2000–2400 mg of magnesium per day. This accounts for the fact that only 70% of serum magnesium (30% protein-bound) is accessible for glomerular filtration. Under normal settings, numerous coordinated transport mechanisms and magnesium transporters re-absorb 96% of filtered magnesium in the renal tubules.
The proximal tubule absorbs 10%–30% of filtered magnesium. While the processes are unknown, magnesium is assumed to be absorbed through a paracellular route facilitated by a chemical gradient formed by Na gradient–driven water transport that raises intraluminal magnesium and lumen-positive potential.
Thick ascending limb. A paracellular route in the thick ascending limb absorbs 40%–70% of filtered magnesium, primarily boosted by lumen-positive transepithelial voltage. Claudine 16 and 19 are important. NKCC2 transports Na, K, and Cl apically. The apical ROMK recycles K to the tubular lumen and generates lumen-positive voltage.
The distal portion of the convoluted tubule. The active transcellular transport mediated by TRPM6 is responsible for the majority of the remaining 5–10% of magnesium’s reabsorption in the distal convoluted tubule. Apical K channel, also known as Kv1.
kidney filters approximately 2000–2400 mg of magnesium per day.in normal GFR
Under normal conditions, 96% of filtered magnesium is reabsorbed in renal as following
1-Proximal Tubule. 10%–30% of the filtered magnesium is absorbed in the proximal tubule. magnesium absorbed via a paracellular pathway aided by a chemical gradient
2-Thick Ascending Limb. 40%–70% of filtered magnesium absorbed in thick ascending limb via paracellular pathway mostly enhanced by lumen-positive transepithelial voltage, in which claudin-16 and claudin-19 play an important role. and group of cotransporter
Distal Convoluted Tubule. 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6. The apical K channel Kv1.1 potentiates
2- Factors decrease magnesium absorption Hypermagnesemia Metabolic acidosis Hypercalcemia , Phosphate depletion . Potassium depletion Diuretics (loop and thiazide) Antibiotics (aminoglycosides) Antifungals (amphotericin B) Antivirals (foscarnet) Chemotherapy agents (cisplatin) Immunosuppressants (tacrolimus, cyclosporine, rapamycin) EGF receptor antagonists FHHNC caused by mutations in claudin-16 and claudin-19 HSH caused by mutations in TRPM6 Bartter’s syndrome caused by mutations in NKCC2 (type 1), ROMK (type II), ClC-Kb (type III), or CaSR (type V) Dominant hypomagnesemia caused by mutations of the FXYD2 gene, HNF1B, or CNNM2 Isolated dominant hypomagnesemia caused by mutations of Kv1.1 Isolated recessive hypomagnesemia caused by mutations of pro-EGF Gitelman’s syndrome caused by mutations of NCC EAST/SeSAME caused by mutations in Kir4.1
70% of Total Body Magnesium is filtered as 30% is protein bound
96% is reabsorbed
PCT- 10-30% Reabsorbed unknown mechanism
Thick Ascending Loop of Henle-( 40-70%) of Magnesium reabsorbed paracellularly by positive transluminal voltage caused Na/K/Cl and ROMK channel clckb and na/k/atpase
claudin 16/19 are tight junctions responsible for magnesium absorption
DCT -5-10% active transport by TMP6
Kidney dominate control of mg hemodtasis , freely filtered across glomerulus ;70% reabsorbed in TALH strongly negative paracellular protein paracellin-1 allow efficient absorption of mg under control of PTH . In DCT transmembrane trans cellular protein TRPM6 allow further uptake .
loss of paracellin 1 or TRPM6 lead to urinary mg wasting and hypoMG
30% of total serum Mg is protein bound, 70% is available for glomerular filtrate, assuming a normal GFR, the kidney filters ~2000-2400mg/d, 96% of which is reabsorbed as follows:
Renal Regulation of Magnesium:
Assuming a normal GFR, the kidney filters approximately2000–2400 mg of magnesium per day. This takes into account the fact that only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration. Under normal conditions, 96% of filtered magnesium is reabsorbed in the renal tubules.
10%–30% of the filtered magnesium is absorbed in the proximal tubule via a paracellular pathway aided by a chemical gradient generated by Na gradient– driven water transport that increases intraluminal magnesium as well as lumen-positive potential.
Thick Ascending Limb: A paracellular pathway in the:thick ascending limb absorbs 40%–70% of filtered magnesium, mostly enhanced by lumen-positive transepithelial voltage, in which claudin-16 and claudin-19 play an important role.
Distal Convoluted Tubule: The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6.
How do the kidneys control Magnesium levels?Renal Regulation of Magnesium
Assuming a normal GFR, the kidney filters approximately 2000–2400 mg of magnesium per day. This takes into account the fact that only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration. Under normal conditions, 96% of filtered magnesium is reabsorbed in the renal tubules by several coordinated transport processes and magnesium transporters
Proximal Tubule 10%–30% of the filtered magnesium is absorbed in the proximal tubule.The exact mechanisms are not known, magnesium is believed to be absorbed via a paracellular pathway aided by a chemical gradient generated by Na gradient– driven water transport that increases intraluminal magnesium as well as lumen-positive potential.
Thick Ascending Limb. A paracellular pathway in the thick ascending limb absorbs 40%–70% of filtered magnesium, mostly enhanced by lumen-positive transepithelial voltage, in which claudin-16 and claudin-19 play an important role. The NKCC2 cotransporter mediates apical absorption of Na, K, and Cl. The apical ROMK mediates apical recycling of K back to the tubular lumen and generation of lumen-positive voltage. The Cl channel ClC-Kb mediates Cl exit through the basolateral membrane. Na, K,-ATPase also mediates Na exit through the basolateral membrane and generates the Na gradient for Na absorption. The tight junction proteins claudin-16 and claudin-19 play a prominent role in magnesium absorption. The CaSR has also been determined to regulate magnesium transport in this segment: upon stimulation, magnesium transport is decreased. Basolateral receptor activation inhibits apical K channels and possibly Na-2C1-K cotransport in the rat thick ascending limb
Distal Convoluted Tubule. The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6.
Bone. At least 50% of the total body magnesium content resides in bone as hydroxyapatite crystals. Dietary magnesium restriction causes decreased bone magnesium content
The filtered Mg is reabsorbed in the kidneys as follows:
increase absorption: Low Mg diet, PTH, glucagon, calcitonin, vasopressin, and mineralocorticoids, insulin, amiloride, metabolic alkalosis
Decrease absorption: High Mg, High Ca, low Pi, low K, Metabolic acidosis, Drugs e.g., diuretics, aminoglycosides, amphotericin B, CNIs, Genetic mutations e.g., Bartter’s syndrome
How do the kidneys control Magnesium levels?
Kidney filters 2g of Mg per day, 70% of total serum Mg is filtered by the glomeruli (30% are protein bound), 96% reabsorbed by the renal tubules, 10 to 30% by PCT presumably through paracelluar pathway, 40 to 70% thick ascending limb mediated by of claudin 16,19 & CaSR, 5 to 10% by the DCT, active transcelluar process mediated by TRPM6, basolateral K channel and Mg/Na exchanger (SLC41A1 family)
Factors that alter renal regulation of Mg
Increase absorption: Low Mg diet, Hormonal factors e.g., PTH, glucagon, calcitonin, vasopressin, and aldosterone, & insulin, Drugs e.g., amiloride, Metaboilc alkalosis
Decrease absorption: Electrolytes e.g., High Mg, High Ca, low Pi, low K, Metaboic acidosis, Drugs e.g., diuretics, aminoglycosides, ampho B, foscarnet, cisplatin, CNIs, Genetic mutations e.g., Bartter’s syndrome
Renal Regulation of Magnesium
Assuming a normal GFR, the kidney filters approximately 2000–2400 mg of magnesium per day. This takes into ac- count the fact that only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration.
Proximal Tubule:
10%–30% of the filtered magnesium is absorbed in the proximal tubule. via a paracellular pathway aided by a chemical gradient generated by Na gradient– driven water transport that increases intraluminal magnesium as well as lumen-positive potential.
Thick Ascending Limb :
A paracellular pathway in the thick ascending limb absorbs 40%–70% of filtered magnesium.
The CaSR has also been determined to regulate magnesium transport in this segment: upon stimulation, magnesium transport is decreased.
Distal Convoluted Tubule:
The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6.
Bone:
At least 50% of the total body magnesium content resides in bone as hydroxyapatite crystals .Dietary magnesium restriction causes decreased bone magnesium content .
The kidney filters approximately 2000–2400 mg of magnesium per day. Only 70% of total serum magnesium (30% is protein-bound) is available for glomerular filtration. Under normal conditions, 96% of filtered magnesium is reabsorbed in the renal tubules.
Proximal Tubule: 10%–30% of the filtered magnesium is absorbed in the proximal tubule. magnesium is believed to be absorbed via a paracellular pathway aided by a chemical gradient generated by Na gradient–driven water transport that increases intraluminal magnesium as well as lumen-positive potential.
Thick Ascending Limb: A paracellular pathway in the thick ascending limb absorbs 40%–70% of filtered magnesium, mostly enhanced by lumen-positive transepithelial voltage, in which claudin-16 and claudin-19 play an im- portant role. The CaSR has also been determined to regulate magnesium transport in this segment: upon stimulation, magnesium transport is decreased.
Distal Convoluted Tubule. The remaining 5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6.
The kidneys control Magnesium levels through
The important segment for Mg2+ reabsorption is the cortical thick ascending limb of Henle’s loop. In this segment, about 40–70% of Mg2+ is reabsorbed active and passive process .
In The proximal tubule reabsorbs about 20% of the filtered Mg2+ passive .
In the distal convoluted tubule reabsorbs 5–10% of the filtered Mg2+,which active transport .very little reabsorption occurs in the collecting duct. Under steady state conditions, the urinary excretion of Mg2+ is about 5% of the filtered load
How do the kidneys control Magnesium levels?
important segment for Mg2+ reabsorption is the cortical thick ascending limb of Henle’s loop. In this segment, about 40–70% of Mg2+ is reabsorbed .
The transport of Mg2+ in the cortical TALH is both passive and active. Passive transport is dependent on the lumen-positive voltage difference secondary to Na/K/2Cl cotransporter activity and back-leak of K+ into the lumen via ROMK.
This positive voltage difference facilitates paracellular movement of Mg2+
in The proximal tubule reabsorbs about 20% of the filtered Mg2+ (passive ).
in The distal convoluted tubule reabsorbs 5–10% of the filtered Mg2+,which transport from the lumen to the cell occurs via an epithelial Mg2+ channel called the TRPM6.
very little reabsorption occurs in the collecting duct. Under steady state conditions, the urinary excretion of Mg2+ is about 5% of the filtered load.
Renal regulation of Magnesium
via a paracellular pathway.
2. Thick ascending loop of Henle
3. DCC
The kidneys filter magnesium every day and reabsorb most of it(96%). Different parts of the renal tubules work together to achieve this. The proximal tubule (10-30%)and the thick ascending limb absorb (40-70%)a large amount of magnesium through a paracellular route, helped by receptors such as Claudine 16, Claudine 19, and NKCC2. The distal convoluted tubule absorbs the remaining magnesium through active transport mediated by TRPM6 and the Kv1 receptor.
Renal Regulation of Mg
In normal GFR, the kidney filter 2000-2400mg /day, 96% reabsorped bt renal tubule
Proximal tubule : 10-30% reabsorped in Proximal CT through a paracellular transport induced by chemical gradient by Na gradient driven water transport.
Thick ascending limb of loop of henle :
40-70%of filtered Mg through paracellular transport enhanced by lumen positive Trans epithelial voltage in which Claudine 16 and claudin 19 in the tight junction play an important role in Mg absorption.
The lumen positive voltage provided by the NKCC2, ROMK and ClC/Kb which enhance absorption.
Stimulation of CaSR will decrease Mg transport
Caudin 10 determines paracellular Na permeability and if lost lead to hyperMg an NC.
Distal convoluted tubule :
Cause absorption of 5-10% of Mg through transcellular active transport by TRPM6 by the lumina potential provided by the apical K channel Kir1.1. Then the absorped Mg will be extruded via Mg/Na exchanger SLC41A1 across the basolateral membrane.
Renal Magnesium Control
A normal GFR kidney filters 2000–2400 mg of magnesium per day. This accounts for the fact that only 70% of serum magnesium (30% protein-bound) is accessible for glomerular filtration. Under normal settings, numerous coordinated transport mechanisms and magnesium transporters re-absorb 96% of filtered magnesium in the renal tubules.
The proximal tubule absorbs 10%–30% of filtered magnesium. While the processes are unknown, magnesium is assumed to be absorbed through a paracellular route facilitated by a chemical gradient formed by Na gradient–driven water transport that raises intraluminal magnesium and lumen-positive potential.
Thick ascending limb. A paracellular route in the thick ascending limb absorbs 40%–70% of filtered magnesium, primarily boosted by lumen-positive transepithelial voltage. Claudine 16 and 19 are important. NKCC2 transports Na, K, and Cl apically. The apical ROMK recycles K to the tubular lumen and generates lumen-positive voltage.
The distal portion of the convoluted tubule. The active transcellular transport mediated by TRPM6 is responsible for the majority of the remaining 5–10% of magnesium’s reabsorption in the distal convoluted tubule. Apical K channel, also known as Kv1.
Renal Regulation of Magnesium
kidney filters approximately 2000–2400 mg of magnesium per day.in normal GFR
Under normal conditions, 96% of filtered magnesium is reabsorbed in renal as following
1-Proximal Tubule.
10%–30% of the filtered magnesium is absorbed in the proximal tubule.
magnesium absorbed via a paracellular pathway aided by a chemical gradient
2-Thick Ascending Limb.
40%–70% of filtered magnesium absorbed in thick ascending limb via paracellular pathway mostly enhanced by lumen-positive transepithelial voltage,
in which claudin-16 and claudin-19 play an important role. and group of cotransporter
Distal Convoluted Tubule.
5%–10% of magnesium is reabsorbed in the distal convoluted tubule mainly by active transcellular transport mediated by TRPM6. The apical K channel Kv1.1 potentiates
1- Factors increase Magnesium Absorption
Dietary magnesium restriction
Parathyroid hormone
Glucagon
Calcitonin
Vasopressin
Aldosterone
Insulin
Amiloride
Metabolic alkalosis
2- Factors decrease magnesium absorption
Hypermagnesemia
Metabolic acidosis
Hypercalcemia , Phosphate depletion . Potassium depletion
Diuretics (loop and thiazide)
Antibiotics (aminoglycosides)
Antifungals (amphotericin B)
Antivirals (foscarnet)
Chemotherapy agents (cisplatin)
Immunosuppressants (tacrolimus, cyclosporine, rapamycin)
EGF receptor antagonists
FHHNC caused by mutations in claudin-16 and claudin-19
HSH caused by mutations in TRPM6
Bartter’s syndrome caused by mutations in NKCC2 (type 1), ROMK (type II), ClC-Kb (type III), or CaSR (type V)
Dominant hypomagnesemia caused by mutations of the FXYD2 gene, HNF1B, or CNNM2 Isolated dominant hypomagnesemia caused by mutations of Kv1.1
Isolated recessive hypomagnesemia caused by mutations of pro-EGF
Gitelman’s syndrome caused by mutations of NCC
EAST/SeSAME caused by mutations in Kir4.1
How do the kidneys control Magnesium levels?
Factors that alter renal regulation of Mg
A.Increase absorption
B.Decrease absorption