Mg balance is disrupted in CKD and dialysis patients. What are the possible mechanisms that could increase or decrease Mg in those patients?
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Marwa Alm
In CKD and dialysis pts, Mg balance is disturbed, possibly depending on pt status and disease severity
Reduced GFR-> limited Mg ultrafiltration -> Mg retention with resultant hypermagnesemia, but in early CKD: it is compensated due to an effective increase in FEMg.
T2DM(often present in CKD pts) has been associated with Mg wasting, hence hypomagnesemia. In diabetic nephropathy pt, hypomagnesemia is associated with progression to ESRD.
The use of diuretics-> disturbed Mg reabsorption in DCT, resulting in Mg wasting (since Mg can’t be reabsorbed downstream), consequently DCT-targeted diuretics e.g thiazide, are associated with hypomagnesemia. The use of loop diuretics in CKD pts indirectly reduces CTALH-Mg paracellular reabsorption.
Change in dietary intake
In dialysis pts, S.Mg is dependent on dialysis Mg concentration, a relatively low dialysis Mg of 0.5mmol/L (the most frequently used) renders hypomagnesemia common in dialysis pts
Use of some medications e.g PPI->decreases TRPM6 activity-> decreases GIT passive paracellular absorption.
the use of loop diuretics in CKD patients indirectly reduces paracellular reabsorption of Mg2þ in the thick ascending limb of Henle’s loop [40]. Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg2þ wasting [41, 42]. In more severe CKD, blood Mg2þ concentrations tend to increase, especially if the GFR drops to <10 mL/min/1.73 m2 [43]. In di- alysis patients, the blood concentration of Mg2þ is dependent on the dialysate Mg2þ concentrations [39]. The mean serum Mg2þ concentration was in the high–normal range of normal blood Mg2þ concentrations (0.98 mmol/L) in a European co- hort of haemodialysis patients [4]. However, on an individual level, hypomagnesaemia and hypomagnesaemia may be present depending on the patient’s status and disease severity, possibly depending on dietary intake [44].
Hypomagnesaemia is also common in dialysis patients. A relatively low dialysate Mg2þ concentration of 0.5 mmol/L is most frequently used [45]. In 34 Dutch haemodialysis patients, the mean plasma Mg2þ concentration was 0.88 mmol/L prior to dialysis, which declined post-dialysis to a mean value of 0.78 mmol/L when the dialysate Mg2þ was 0.5 mmol/L [46]. The Mg2þ concentration declined in most individuals. Obviously a dialysate concentration of 0.25mmol/L Mg2þ increases the risk for hypomagnesaemia even more [39]. In CKD, blood Mg2þ concentrations are further affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg2þ) and the presence of diabetes [47]. Monitoring and adjusting the blood Mg2þ concentration in CKD patients might be relevant, as hypomagnesaemia is associated with progression to end- stage renal disease in diabetic nephropathy patients [
The reabsorption of magnesium is dependent on the filtration rate. Fine-tuning occurs in the DCT. CKD patients usually use diuretics that interfere with renal handling. Disturbed Mg
In ESDR and dialysis, the magnesium level is primarily dependent on dialysate magnesium.
mainly due to limited ultrafiltration of this mineral. However, patients with early-stage CKD have normal blood Mg2þ concentrations due to an effective increase in fractional excretion of Mg2þ . Additionally, the use of loop diuretics in CKD patients indirectly reduces paracellular reabsorption ofMg2þ in the thick ascending limb of Henle’s loop .Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg2þ wasting. In more severe CKD, blood Mg2þ concentrations tend to increase, especially if the GFR drops to <10mL/min/1.73 m2 .In dialysis patients, the blood concentration of Mg2þ is dependent on the dialysate Mg2þ concentrations. The mean serum Mg2þ concentration was in the high–normal range of normal blood Mg2þ concentrations (0.98mmol/L) in a European cohort of haemodialysis patients. However, on an individual level, hypomagnesaemia and hypomagnesaemia may be present depending on the patient’s status and disease severity, possibly depending on dietary intake. Hypomagnesaemia is also common in dialysis patients.
A relatively low dialysate Mg2þ concentration of 0.5mmol/L is most frequently used. In 34 Dutch haemodialysis patients, the mean plasma Mg2þ concentration was 0.88mmol/L prior to dialysis, which declined post-dialysis to a mean value of 0.78mmol/L when the dialysate Mg2þ was 0.5mmol/L. The Mg2þ
concentration declined in most individuals.
Obviously a dialysate concentration of 0.25mmol/L Mg2þ increases the risk for hypomagnesaemia even more. In CKD, blood Mg2þ concentrations are further affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg2þ)and the presence of diabetes.
Mg balance is disrupted in CKD and dialysis patients. What are the possible mechanisms that could increase or decrease Mg in those patients?
In patients with CKD, Mg balance is disturbed, initially mainly due to limited ultrafiltration of this mineral. However,patients with early-stage CKD have normal blood Mg concentrations due to an effective increase in fractional excretionof Mg
Additionally, the use of loop diuretics in CKD patients indirectly reduces paracellular reabsorption of Mg2þ in the thick ascending limb of Henle’s loop
Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg wasting
In more severe CKD, blood Mg concentrations tend to increase, especially if the GFR drops to <10 mL/min/1.73 m2 In dialysis patients, the blood concentration of Mg is dependent on the dialysate Mg concentrations. The mean serum Mg concentration was in the high–normal range of normal blood Mg concentrations (0.98 mmol/L)
On an individual level, hypomagnesaemia may be present depending on the patient’s status and disease severity, possibly depending on dietary intake
A dialysate concentration of 0.25 mmol/L Mg increases the risk for hypomagnesaemia even more
In CKD, blood Mg concentrations are further affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg2þ) and the presence of diabetes
Hypomagnesaemia is associated with progression to endstage renal disease in diabetic nephropathy patients
In CKD, Mg balance is disturbed due to: Limited ultrafiltration, Use of loop diuretics, Diabetes, Dietary restriction. In Dialysis: dialysate Mg concentration, Dietary restriction, Diabetes.
Mg balance is disrupted in CKD and dialysis patients. What are the possible mechanisms that could increase or decrease Mg in those patients? factor disturbance of Mg re-absorption are:
diuretic ( eg thiazides ) Associated with hypomagnesemia by reduce paracellular reabsorption of Mg DM type 2 associated with hypomagnesaemia . medication used in CKD as proton pump. loop diuretics, cisplatin
In Dialysis
Mg concentration depends on dialysate Mg concentration.
decrease intake.
Hypomagnesemia is associated with low dialysate Mg .
The possible mechanisms to disrupt the mg level were
Use of loop diuretics in Ckd decrease paracellular transport in thick loop of henle interfere with paracellular transport and lead to hypomagnesemia.
Type 2 Diabetes causes hypomagnesemia.
In dialysis patients blood level depend on the Mg level in dialysate.
Other factors like medication as Proton pump inhibitor, diuretics, use of low potassium diet, and DM affect level of mg also the kidney is the main way with excretion of mg and may cause hypermagnisimia in diaylisis patients if increase mg level in diaylisate or when taken in supplement
In patients with CKD, Mg balance is disturbed, initially mainly due to limited ultrafiltration of this mineral. However, patients with early-stage CKD have normal blood Mg con- centrations due to an effective increase in fractional excretion of Mg2þ. Additionally, the use of loop diuretics in CKD patients cause hypomagnesemia. Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg wasting. In more severe CKD, blood Mg concentrations tend to increase, especially if the GFR drops to <10 mL/min/1.73 m2.
In dialysis patients, the blood concentration of Mgis dependent on the dialysate Mg2þ concentrations. THowever, on an individual level, hypomagnesaemia and hypomagnesaemia may be present depending on the patient’s status and disease severity, possibly depending on dietary intake .
Hypomagnesaemia is also common in dialysis patients.
In CKD, blood Mg concentrations are further affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg2þ) and the presence of diabetes .
Monitoring and adjusting the blood Mg2þ concentration in CKD patients might be relevant, as hypomagnesaemia is associated with progression to end- stage renal disease in diabetic nephropathy patients
magnesium level can be both decreased or increased
decreased level occurs predialysis or post intiation of dialysis.
predialysis hypomagnesemia is mainly related ot DM which is the main cause of CKD and frequent use of loop diuretics
post dialysis hypomagnesemia is related to use of low magnesium dialysate.
hypermagnesemia occurs predialysis due to decreased filteration of magnesium
The main regulator of Mg level is the kidney and to lesser extent intestine and bone.
90%of filtered Mg reabsorped in the proximal tubule and thick ascending loop of henle through paracellular transport.
Fine tuning occurred in Distal CTin which disturbed reabsorption lead to Mg wasting, like use of thiazide diuretics causes hypoMg.
Use of loop diuretics in Ckd decrease paracellular transport in thick loop of henle interfere with paracellular transport and lead to hypoMg.
Type 2 Diabetes causes hypoMg.
In dialysis patients blood level depend on the Mg level in dialysate.
Other factors like medication as Proton pump inhibitor, diuretics, use of low potassium diet, and DM affect level of Mg
there are several factors that can affect magnesium homeostasis in CKD patients, including restricted ultrafiltration, loop diuretics, and diabetes. In early-stage CKD, fractional Mg2 excretion increases, which can help maintain normal blood Mg2 concentrations.
However, as CKD progresses, hypomagnesemia may occur, particularly in dialysis patients whose blood Mg2 concentrations depend on dialysate concentrations.
Hypomagnesemia is also more likely to occur in CKD patients who take certain drugs, diuretics or follow low-potassium diets.
Initially, restricted ultrafiltration of Mg2 disrupts Mg2 homeostasis in CKD patients. Nevertheless, fractional Mg2 excretion increases in early-stage CKD patients, resulting in normal blood Mg2 concentrations.
Nevertheless, fractional Mg2 excretion increases in early-stage CKD patients, resulting in normal blood Mg2 concentrations. Loop diuretics indirectly diminish paracellular Mg2 reabsorption in the thick ascending limb of Henle’s loop in CKD patients.
Loop diuretics indirectly diminish paracellular Mg2 reabsorption in the thick ascending limb of Henle’s loop in CKD patients.
Hypomagnesaemia and renal Mg2 squandering are also linked to type 2 diabetes in CKD patients. Mg2+ concentrations rise in severe CKD, particularly if GFR decreases below 10 mL/min/1.73 m2.
Dialysis patients’ blood Mg2 concentrations depend on dialysate concentrations. In a European cohort of hemodialysis patients, the mean serum Mg2+ concentration (0.98 mmol/L) was high-normal. Nevertheless, depending on the patient’s condition, illness severity, and nutrition, hypomagnesemia may occur.
Dialysis patients often have hypomagnesemia.
Most dialysates employ 0.5 mmol/L Mg2+. In 34 Dutch hemodialysis patients, the mean plasma Mg2+ concentration was 0.88 mmol/L before dialysis and 0.78 mmol/L after dialysis when the dialysate Mg2+ was 0.5.
Most people lost Mg2+.
Hypomagnesaemia is significantly more likely with a dialysate concentration of 0.25 mmol/L Mg2.
Drugs including proton pump inhibitors, thiazides, and loop diuretics, low-potassium diets, and diabetes all impact blood Mg2+ levels in CKD. Hypomagnesaemia is linked to end-stage renal disease in diabetic nephropathy patients, hence CKD patients may benefit from monitoring and modifying their blood Mg2 concentration.
The kidney is the central organ for maintaining Mg balance 90% of the filtered load of Mg is reabsorbed paracellular in the proximal tubule and thick ascending limb of Henle’s
Many factor disturbance of Mg re-absorption as ## diuretic ( eg thiazides ) Associated with hypomagnesemia by reduce paracellular reabsorption of Mg
##Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg2þ wasting
## In more severe CKD, blood Mg concentrations tend to increase, especially if the GFR drops to <10ml/min/1.73m2
##In dialysis patients, the blood concentration of Mg is dependent on the dialysate Mg concentrations
Also Mg concentration , affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg and the presence of diabetes
Mg balance is disrupted in CKD and dialysis patients. What are the possible mechanisms that could increase or decrease Mg in those patients? A. Mechanisms that increase Mg
In CKD and dialysis pts, Mg balance is disturbed, possibly depending on pt status and disease severity
CKD /HD patient have reduced effective nephrons or anephric for ulltrafiltration and that could increase Magnesium
Patient with CKD usually are on diuretic for fluid control and that could lead to low magnesium due to decreased paracellular absorption
Renal Diet could have less Magnesium and reduce mg level
In HD pt their mg level is based on dialysate level could be normal/high to low
the use of loop diuretics in CKD patients indirectly reduces paracellular reabsorption of Mg2þ in the thick ascending limb of Henle’s loop [40]. Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg2þ wasting [41, 42]. In more severe CKD, blood Mg2þ concentrations tend to increase, especially if the GFR drops to <10 mL/min/1.73 m2 [43]. In di- alysis patients, the blood concentration of Mg2þ is dependent on the dialysate Mg2þ concentrations [39]. The mean serum Mg2þ concentration was in the high–normal range of normal blood Mg2þ concentrations (0.98 mmol/L) in a European co- hort of haemodialysis patients [4]. However, on an individual level, hypomagnesaemia and hypomagnesaemia may be present depending on the patient’s status and disease severity, possibly depending on dietary intake [44].
Hypomagnesaemia is also common in dialysis patients. A relatively low dialysate Mg2þ concentration of 0.5 mmol/L is most frequently used [45]. In 34 Dutch haemodialysis patients, the mean plasma Mg2þ concentration was 0.88 mmol/L prior to dialysis, which declined post-dialysis to a mean value of 0.78 mmol/L when the dialysate Mg2þ was 0.5 mmol/L [46]. The Mg2þ concentration declined in most individuals. Obviously a dialysate concentration of 0.25mmol/L Mg2þ increases the risk for hypomagnesaemia even more [39]. In CKD, blood Mg2þ concentrations are further affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg2þ) and the presence of diabetes [47]. Monitoring and adjusting the blood Mg2þ concentration in CKD patients might be relevant, as hypomagnesaemia is associated with progression to end- stage renal disease in diabetic nephropathy patients [
The reabsorption of magnesium is dependent on the filtration rate. Fine-tuning occurs in the DCT. CKD patients usually use diuretics that interfere with renal handling. Disturbed Mg
In ESDR and dialysis, the magnesium level is primarily dependent on dialysate magnesium.
mainly due to limited ultrafiltration of this mineral. However, patients with early-stage CKD have normal blood Mg2þ concentrations due to an effective increase in fractional excretion of Mg2þ . Additionally, the use of loop diuretics in CKD patients indirectly reduces paracellular reabsorption ofMg2þ in the thick ascending limb of Henle’s loop .Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg2þ wasting. In more severe CKD, blood Mg2þ concentrations tend to increase, especially if the GFR drops to <10mL/min/1.73 m2 .In dialysis patients, the blood concentration of Mg2þ is dependent on the dialysate Mg2þ concentrations. The mean serum Mg2þ concentration was in the high–normal range of normal blood Mg2þ concentrations (0.98mmol/L) in a European cohort of haemodialysis patients. However, on an individual level, hypomagnesaemia and hypomagnesaemia may be present depending on the patient’s status and disease severity, possibly depending on dietary intake. Hypomagnesaemia is also common in dialysis patients.
A relatively low dialysate Mg2þ concentration of 0.5mmol/L is most frequently used. In 34 Dutch haemodialysis patients, the mean plasma Mg2þ concentration was 0.88mmol/L prior to dialysis, which declined post-dialysis to a mean value of 0.78mmol/L when the dialysate Mg2þ was 0.5mmol/L. The Mg2þ
concentration declined in most individuals.
Obviously a dialysate concentration of 0.25mmol/L Mg2þ increases the risk for hypomagnesaemia even more. In CKD, blood Mg2þ concentrations are further affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg2þ)and the presence of diabetes.
Mg balance is disrupted in CKD and dialysis patients. What are the possible mechanisms that could increase or decrease Mg in those patients?
In CKD, Mg balance is disturbed due to: Limited ultrafiltration, Use of loop diuretics, Diabetes, Dietary restriction.
In Dialysis: dialysate Mg concentration, Dietary restriction, Diabetes.
Mg balance is disrupted in CKD and dialysis patients. What are the possible mechanisms that could increase or decrease Mg in those patients?
factor disturbance of Mg re-absorption are:
diuretic ( eg thiazides ) Associated with hypomagnesemia by reduce paracellular reabsorption of Mg
DM type 2 associated with hypomagnesaemia .
medication used in CKD as proton pump. loop diuretics, cisplatin
The possible mechanisms to disrupt the mg level were
Use of loop diuretics in Ckd decrease paracellular transport in thick loop of henle interfere with paracellular transport and lead to hypomagnesemia.
Type 2 Diabetes causes hypomagnesemia.
In dialysis patients blood level depend on the Mg level in dialysate.
Other factors like medication as Proton pump inhibitor, diuretics, use of low potassium diet, and DM affect level of mg also the kidney is the main way with excretion of mg and may cause hypermagnisimia in diaylisis patients if increase mg level in diaylisate or when taken in supplement
In patients with CKD, Mg balance is disturbed, initially mainly due to limited ultrafiltration of this mineral. However, patients with early-stage CKD have normal blood Mg con- centrations due to an effective increase in fractional excretion of Mg2þ. Additionally, the use of loop diuretics in CKD patients cause hypomagnesemia. Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg wasting. In more severe CKD, blood Mg concentrations tend to increase, especially if the GFR drops to <10 mL/min/1.73 m2.
In dialysis patients, the blood concentration of Mgis dependent on the dialysate Mg2þ concentrations. THowever, on an individual level, hypomagnesaemia and hypomagnesaemia may be present depending on the patient’s status and disease severity, possibly depending on dietary intake .
Hypomagnesaemia is also common in dialysis patients.
In CKD, blood Mg concentrations are further affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg2þ) and the presence of diabetes .
Monitoring and adjusting the blood Mg2þ concentration in CKD patients might be relevant, as hypomagnesaemia is associated with progression to end- stage renal disease in diabetic nephropathy patients
magnesium level can be both decreased or increased
decreased level occurs predialysis or post intiation of dialysis.
predialysis hypomagnesemia is mainly related ot DM which is the main cause of CKD and frequent use of loop diuretics
post dialysis hypomagnesemia is related to use of low magnesium dialysate.
hypermagnesemia occurs predialysis due to decreased filteration of magnesium
The main regulator of Mg level is the kidney and to lesser extent intestine and bone.
90%of filtered Mg reabsorped in the proximal tubule and thick ascending loop of henle through paracellular transport.
Fine tuning occurred in Distal CTin which disturbed reabsorption lead to Mg wasting, like use of thiazide diuretics causes hypoMg.
Use of loop diuretics in Ckd decrease paracellular transport in thick loop of henle interfere with paracellular transport and lead to hypoMg.
Type 2 Diabetes causes hypoMg.
In dialysis patients blood level depend on the Mg level in dialysate.
Other factors like medication as Proton pump inhibitor, diuretics, use of low potassium diet, and DM affect level of Mg
there are several factors that can affect magnesium homeostasis in CKD patients, including restricted ultrafiltration, loop diuretics, and diabetes. In early-stage CKD, fractional Mg2 excretion increases, which can help maintain normal blood Mg2 concentrations.
However, as CKD progresses, hypomagnesemia may occur, particularly in dialysis patients whose blood Mg2 concentrations depend on dialysate concentrations.
Hypomagnesemia is also more likely to occur in CKD patients who take certain drugs, diuretics or follow low-potassium diets.
Mg imbalance in CKD and Dialysis patients
Initially, restricted ultrafiltration of Mg2 disrupts Mg2 homeostasis in CKD patients. Nevertheless, fractional Mg2 excretion increases in early-stage CKD patients, resulting in normal blood Mg2 concentrations.
Nevertheless, fractional Mg2 excretion increases in early-stage CKD patients, resulting in normal blood Mg2 concentrations. Loop diuretics indirectly diminish paracellular Mg2 reabsorption in the thick ascending limb of Henle’s loop in CKD patients.
Loop diuretics indirectly diminish paracellular Mg2 reabsorption in the thick ascending limb of Henle’s loop in CKD patients.
Hypomagnesaemia and renal Mg2 squandering are also linked to type 2 diabetes in CKD patients. Mg2+ concentrations rise in severe CKD, particularly if GFR decreases below 10 mL/min/1.73 m2.
Dialysis patients’ blood Mg2 concentrations depend on dialysate concentrations. In a European cohort of hemodialysis patients, the mean serum Mg2+ concentration (0.98 mmol/L) was high-normal. Nevertheless, depending on the patient’s condition, illness severity, and nutrition, hypomagnesemia may occur.
Dialysis patients often have hypomagnesemia.
Most dialysates employ 0.5 mmol/L Mg2+. In 34 Dutch hemodialysis patients, the mean plasma Mg2+ concentration was 0.88 mmol/L before dialysis and 0.78 mmol/L after dialysis when the dialysate Mg2+ was 0.5.
Most people lost Mg2+.
Hypomagnesaemia is significantly more likely with a dialysate concentration of 0.25 mmol/L Mg2.
Drugs including proton pump inhibitors, thiazides, and loop diuretics, low-potassium diets, and diabetes all impact blood Mg2+ levels in CKD. Hypomagnesaemia is linked to end-stage renal disease in diabetic nephropathy patients, hence CKD patients may benefit from monitoring and modifying their blood Mg2 concentration.
The kidney is the central organ for maintaining Mg balance
90% of the filtered load of Mg is reabsorbed paracellular in the proximal tubule and thick ascending limb of Henle’s
Many factor disturbance of Mg re-absorption as
## diuretic ( eg thiazides ) Associated with hypomagnesemia by reduce paracellular reabsorption of Mg
##Type 2 diabetes, often present in CKD patients, has also been associated with hypomagnesaemia and renal Mg2þ wasting
## In more severe CKD, blood Mg concentrations tend to increase, especially if the GFR drops to
<10ml/min/1.73m2
##In dialysis patients, the blood concentration of Mg is dependent on the dialysate Mg concentrations
Also Mg concentration , affected by the use of medication (e.g. proton pump inhibitors, thiazides and loop diuretics), the prescription of diets low in potassium (food products rich in potassium are generally also rich in Mg and the presence of diabetes
Mg balance is disrupted in CKD and dialysis patients. What are the possible mechanisms that could increase or decrease Mg in those patients?
A. Mechanisms that increase Mg
B. Mechanisms that decrease Mg