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What is the impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markers?
What is the impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markers?
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38 Comments
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Both vitamin D analogs and calcimimetics decrease PTH while having the opposite effects on calcium. D vitamin analogs increase calcium. Thiazides, by lowering calcium in urine, increase calcium in the blood by this way, seems to have effect on the secretion of PTH (lowering effect)
Calcimimetics decrease FGF-23 but increase sclerostin while vitamin D analogs increase FGF-23 but also increase sclerostin
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Vitamin D analogues :
Decreases PTH and bone turnover marker, increase calcium phosphorus and FGF-23.
calcimimetics:
Decreases calcium, phosphorus, bone specific alkaline phosphatase, collagen 7 cross linked, PTH,FGF-23 PLUS cause small and transient decrease of klotho.
Thiazide diuretics ;
Decreases calcium excretion, ameliorate 2ry hyperparathyroidism. -
The impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markersvitamin D analogues can increase serum calcium and decrease the PTH and can also have impact on the rise of FGF23.
calcimimetics decreases the level of PTH and increase the FGF23
thiazide diuretics tight calciuria and have impact on increasing PTH levels -
Both vitamin D analogs and calcimimetics are able to decrease PTH. but they have opposite effects on FGF-23
Vit D analogues will rise serum Ca, P, CaP product, decrease PTH and bone specific alkaline phsphatase, increase FGF 23, increase Klotho and sclerostin
Calcimimetics decrease Ca (should be followed strictly) , decrease P, decrease PTH and bone specific Alkaline phsphatase, decrease FGF 23,may decrease klotho alittle and decrease sclerostin
Loop diuretic may decrease serum ca by calciuria, increase PTH calciuria reduces as renal function progresses, and whether this would interfere with these findings was not clear
Thiazide decrease ca wasting rising serum Ca and So decrease PTH
-
vtiamin d analogue: decreases PTH and bone turnover marker, increase calcium phosphorus and FGF-23.
calcimimetics: decreases calcium, phosphorus, bone specific alkaline phosphatase, collagen 7 cross linked, PTH,FGF-23 PLUS cause small and transient decrease of klotho. thiaize diuretics decreases calcium excretion, amoleriorate 2ry hyperparathyroidism -
The impact of vitamin D analogues, calcimimetics, and thiazide diuretics
EFFECT OF VITAMIN D ANALOGS:- Increase calcium
- Raise phosphate reabsorption
- Reduce PTH levels
- Increase FGF23, klotho, and sclerostin levels
Effect of calcimimitics
- Reduced calcium and phosphate
- Decrease FGF-23
- Increase the level of sclerostin.
- PTH can be reduced with calcimimetics.
Effect of diuretics :Diuretics are routinely used to treat hypertension and fluid overload in CKD patients.
Thiazide diuretics:
- Thiazides reduce urine calcium
- Thiazides reduces SHPT
- Thiazide can raise plasma Klotho and induces osteoblast differentiation.
Frusemide diuretics:
- Loop diuretics induce calcium waste.
- The usage of furosemide was linked to an increase in calciuria, an increase in PTH, resulting in an increased likelihood of developing SHPT.
- These diuretics’ effects may be linked to their indirect affect on calcium homeostasis.
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vitamin D analogues :Increase calcium and phosphour, decrease PTH, increase FGF-23, klotho and scerostin
calcimimetics: decrease( ca-ph-PTH) and also decreae FGF-23 but increase sclerostin
thiazide diuretics: increasae ca and klotho, decrease PTH, no effect on FGF-23
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Vitamin D analogues increase calcium, increase phosphate,increase fgf23,decrease PTH and increase klotho, increase sclerotin (How it will increase klotho and sclerotin ??)
Calcimemetic – decrease calcium, decrease phosphate, decrease PTH, decrease fgf23 and increase sclerotin. ( why does it increase sclerotin??)
Thiazide diuretic- increase calcium, decrease PTH, increase klotho (how it will increase klotho?)-
Good job. Thanks Dr. Alaa
Regarding your questions:
1- A close inter-relationship between 1,25(OH)2 VD and the sclerostin gene has been described in experimental models. In addition, there is a hypothesis that active vitamin D stimulates sclerostin synthesis and secretion.
2- There is controversial results regarding effect of calcimimetics on sclerostin levels. It would be reasonable to expect a decrease in sclerostin levels through attenuation of the severity of vascular calcification after appropriate therapy, e.g., calcimimetics. Intriguingly, Kuczera P et al. reported cinacalcet treatment in hemodialysis patients with severe SHPT decrease serum PTH concentration and increases plasma sclerostin concentration, reflecting the more robust suppression of high bone turnover status in the study. Compared with their study population receiving much higher therapeutic dose (maximal allowed dose of cinacalcet was 120 mg daily) for more advanced SHPT (mean iPTH level was 1138 pg/mL), other study subjects with a lower PTH level (748.6 pg/mL) were treated with a fixed low dose of oral Cinacalcet (25 mg/day), suggesting that different therapeutic strategies of cinacalcet result in different changes of circulating sclerostin. For further clarification, you can go through this article: Hung, K.C., Chang, J.F., Hsu, Y.H., Hsieh, C.Y., Wu, M.S., Wu, M.Y., Chiu, I.J., Syu, R.S., Wang, T.M., Wu, C.C. and Hung, L.Y., 2020. Therapeutic effect of calcimimetics on osteoclast–osteoblast crosslink in chronic kidney disease and mineral bone disease. International journal of molecular sciences, 21(22), p.8712.
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Vitamin D analog increase calcium , increase phosphate, decrease FGF23 decrease PTH and increase klotho, increase sclerostin
Calcimemetic – decrease calcium, decrease phosphate, decrease PTH, decrease fgf23 and increase sclerotin. ( why does it decrease ffg23?)
Thiazide diuretic- increase calcium, phosphate unsure? pth down klotho up
Loop diuretic effect of calcium is decreased what about phosphate and pth increases
is increase in sclerotin in vitamin d analog and calcimemetic good or bad?
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Good answer. Thanks Dr. Muhammad.
Regarding your question:
The clinical use of sclerostin remains controversial. In many studies, higher serum sclerostin levels are associated with fatal and nonfatal cardiovascular events. On the other side, increased serum sclerostin levels were associated with better short-term cardiovascular outcomes in a large cohort study of 673 dialysis patients. From these clues, it can be supposed that the calcified vascular cells will secrete more sclerostin to process autocrine or paracrine manners to inhibit Wnt signaling effects on osteogenic trans-differentiation of vascular smooth muscle cells, preventing further calcification of the vessel wall. Thus, circulating sclerostin levels should be interpreted according to clinical scenarios. In bone cases, osteocyte is the major source of sclerostin. The cross-sectional measurement of circulating sclerostin only reflects the dynamics of bone metabolism with particular reference to scenarios. Whether circulating the sclerostin level was bone-derived or vascular-derived in different bone turnover and vascular calcification status has yet to be elucidated.Regarding effect of cinacalcet on serum levels of sclerostin, it differs according to different therapeutic strategies of cinacalcet.
For more information, you can read this article: Hung, K.C., Chang, J.F., Hsu, Y.H., Hsieh, C.Y., Wu, M.S., Wu, M.Y., Chiu, I.J., Syu, R.S., Wang, T.M., Wu, C.C. and Hung, L.Y., 2020. Therapeutic effect of calcimimetics on osteoclast–osteoblast crosslink in chronic kidney disease and mineral bone disease. International journal of molecular sciences, 21(22), p.8712.
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What is the impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markers?
1- The impact of vitamin D analogues :
Increase ca
Increase p
Decrease PTH
Increase FGF-23
Increase klotho
Increase sclerostin
2-The impact of calcimimetics :
Decrease ca
Decrease p
Decrease PTH
Decrease FGF-23
Increase sclerostin
3-Impact of thiazide diuretics:
Increase ca
Decrease PTH
Increase klotho
No effect on FGF-23 and 25 vitamin D and sclerostin. -
Thiazid
- Increase Ca, and Klotho levels with suppression of PTH level
Loop Diuretics
-increase PTH.
2-decrease calcium.Calcimmitics like Cinacalcit
- Decrease Ca, and phosphate level with suppression of PTH level and FGF-23, while increasing the level of sclerostin.
i suggest writing the chemical name of each group to assess and revise each medicine and its action. like calcimmitic cinacalcite
VIT D analogue is it the paricalcetriol; or what ??? i am not sue
PLease PROF Amr if possible to show us the name of chemical name for each group ? -
*The impact of vitamin D analogs on
Calcium increase+. , phosphorous increase+ , Vitamin D -, PTH decrease – -, FGF23 increase ++, klotho increase +, sclerostin increase +
*Calcimimitic
Calcium decrease – , phos decrease -, PTH decrease – -, 25(OH) vitamin _, FGF23 decrease -, klotho? , sclerostin increase +
*thiazide diuretic
Calcium normal or increase + , phos _, PTH decrease – , vitamin D n/a., FGF23 n/a, klotho increase + sclerostin n/a
Thiazide diuretic decrease caciuria so prevent SHPT, it has direct effect on parathyroid gland regardless of caciuria, causes increase klotho and increase osteo last differentiation -
Impact of Diuretic on CKD-MBD:
- Loop diuretic associated with calcium wasting, with resultant aggravation SHPT.
- Thiazide diuretic associated with hypocalciuric, with resultant correcting SHPT.
- CRIC study shows that; the use of loop diuretic is associated with calcinuria and aggravating SHPT.
- CKD on furosemide has a 3.9 times higher risk of developing SHPT.
- Thiazide diuretics can induce osteoblast differentiation by interacting with Na,Cl cotransporter in bone, while furosemide influence bone by interacting with K-Cl transporter, but these roles are not clearly evident, so the action seems to be by an indirect effect on calcium hemostasis.
- Loop diuretics increase the risk of falls and fractures.
- Independently away from calcium level can directly affect PTH.
- Thiazide can increase Klotho level.
- Integrative approach has to follow in treating CKD-MBD as any change in one affects the other.
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The impact of medical therapy CKD-MBD biomarkers:
Vitamin D analogues:
- Increase Ca, and phosphate absorption from intestine leading to significant suppression of PTH. On the side they increase the levels of FGF-23, Klotho and sclerostin
Calcimemitics:
- Decrease Ca, phosphate level with suppression of PTH level and FGF-23, while increase the level of sclerostin.
Thiazide diuretics:
- Increase Ca, and Klotho levels with suppression of PTH level
-
the impact of vitamin D analogues, calcimimetics, and thiazide diuretics :
1- Vit D
increase Calcium, phosphate, FGF23 and klotho. and lower PTH.
2- Calcimimetic :
1-decrease calcium .
2-decrease phosphate.
3-suppression of PTH
3-decrease the expression of KLOTHO.
4- decrease FGF23.3-effect of diuretics
- Thiazides :
1- increase calcium and Klotho .
2- decrease of PTH.frusemide :
1-increase PTH.
2-decrease calcium. -
EFFECT OF VITAMIN D ANALOGS:
1-increase calcium reabsorption from GIT
2-increase phosphate reabsorption
3-decrease PTH level
4-increase FGF23 and klotho and sclerostin===============
effect of calcimimitics
1-reduce calcium and phosphate
2-marked suppression of PTH
3-reduce FGF23
4-increase sclerostin
effect of diuretics :
thiazide diuretics
1-suppress PTH
2-increase plasma klotho
mild increase calcium
unknown action on vit D ,FGF23 ,sclerostin
=========
frusemide
increase PTH
NO EFFECT ON CALCIUM OR PHOSPHATE
UNKNOWN ACTION ON VIT D ,FGF23,KLOTHO,SCLEROSTIN -
What is the impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markers?
- Vitamin D analogues :
1- Significant decrease of PTH.
2- No effect on 25- Hydroxy Vit. D.
3- Increase in all other markers.- Calcimimetics :
1- Decrease in serum calcium, FGF-23, and PTH.
2- Increase sclerostin and phosphate.
3- No effect on 25-Hydroxy Vit. D.
4- Unknown effect on Klotho.- Thiazides :
1- mild increase in serum calcium and Klotho levels.
2- mild decrease of PTH.
3- No effect on Phosphate.
4- Unknown effect on 25-hydroxy Vit. D, FGF-23, and sclerostin levels. -
the impact of classical drugs in ttt of ckd mbd is useful to decrease level of pth but unfortunately there was no or little effect on FGF23or even increase in most of cases.
the use of thiazide diuretcs useful than loop diurtics in patient with ckd mbd by indircet action to prevent ca loss in urine to promote ca absorption and decrease level of pth
also thiazide has direct action on oesteoblast in bone -
Vitamin D will increase in Serum Calcium, phosphate, FGF and klotho. But lower PTH.
Calcimimetics lower PTH, calcium, phosphate , and FGF.
Thiazide diuretic will increase calcium and decrease PTH. It increase also clotho factor.
So these medicine are preventing mineral bone disease through lowering secondary hyperparathyroidism but in diffrent mechanism.Loop diuretics will induce calcuria ( opposite to thiazide) and will decrease calcium in Serum
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CKD-MBD therapy:
Drugs that decease PTH level:
- Vitamin D analogs
- Nutritional vit D
- Cacimimetics
- Thiazide diuretics ?
Hyperphosphatemia:
- Dietary phosphate restrictions
- Phosphate binders
Notes
- In advance CKD-MBD the above therapy may not work due significant down regulation of the VDR and CaSR. In such cases the patient will be a surgical candidate but it is better prevent such kind of suituation due to high morbidity and mortality.
- The current therapy of CKD-MBD may not necessarily prevent CV events and CV mortality (i.e not effect oh hard outcomes)
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Thanks Dr. Ben.
Vitamin D analogues increase serum calcium, phosphorus, and FGF23 while they decrease PTH.
Calcimimetics decrease serum calcium, phosphorus, FGF23 and PTH.
Thiazide diuretics decrease urinary calcium loss and thus suppress PTH.
-
PTH levels may be lowered using a combination of vitamin D analogs and calcimimetics. On the other hand, these factors have the opposite impact on FGF-23.
Thiazides can lower the amount of calcium that is lost in the urine. They can also lower PTH levels.
By interacting with a sodium chloride cotransporter found in bones, thiazide diuretics have the potential to stimulate osteoblast development.
as the diuretic medicines induce or reduce calciuria. decreases the risk of SHPT in the case of thiazide diuretics, whereas loop diuretics increase the risk of SHPT.
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Both vitamin D analogs and calcimimetics decrease PTH while having the opposite effects on calcium. D vitamin analogs increase calcium. Thiazides, by lowering calcium in urine, increase calcium in the blood by this way, seems to have effect on the secretion of PTH (lowering effect)
Calcimimetics decrease FGF-23 but increase sclerostin while vitamin D analogs increase FGF-23 but also increase sclerostin
Vitamin D analogues :
Decreases PTH and bone turnover marker, increase calcium phosphorus and FGF-23.
calcimimetics:
Decreases calcium, phosphorus, bone specific alkaline phosphatase, collagen 7 cross linked, PTH,FGF-23 PLUS cause small and transient decrease of klotho.
Thiazide diuretics ;
Decreases calcium excretion, ameliorate 2ry hyperparathyroidism.
The impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markersvitamin D analogues can increase serum calcium and decrease the PTH and can also have impact on the rise of FGF23.
calcimimetics decreases the level of PTH and increase the FGF23
thiazide diuretics tight calciuria and have impact on increasing PTH levels
Both vitamin D analogs and calcimimetics are able to decrease PTH. but they have opposite effects on FGF-23
Vit D analogues will rise serum Ca, P, CaP product, decrease PTH and bone specific alkaline phsphatase, increase FGF 23, increase Klotho and sclerostin
Calcimimetics decrease Ca (should be followed strictly) , decrease P, decrease PTH and bone specific Alkaline phsphatase, decrease FGF 23,may decrease klotho alittle and decrease sclerostin
Loop diuretic may decrease serum ca by calciuria, increase PTH calciuria reduces as renal function progresses, and whether this would interfere with these findings was not clear
Thiazide decrease ca wasting rising serum Ca and So decrease PTH
vtiamin d analogue: decreases PTH and bone turnover marker, increase calcium phosphorus and FGF-23.
calcimimetics: decreases calcium, phosphorus, bone specific alkaline phosphatase, collagen 7 cross linked, PTH,FGF-23 PLUS cause small and transient decrease of klotho. thiaize diuretics decreases calcium excretion, amoleriorate 2ry hyperparathyroidism
Great answer. Thanks Dr. Ahmed
The impact of vitamin D analogues, calcimimetics, and thiazide diuretics
EFFECT OF VITAMIN D ANALOGS:
Effect of calcimimitics
Effect of diuretics :Diuretics are routinely used to treat hypertension and fluid overload in CKD patients.
Thiazide diuretics:
Frusemide diuretics:
Well done. Thanks Dr. Rania
vitamin D analogues :Increase calcium and phosphour, decrease PTH, increase FGF-23, klotho and scerostin
calcimimetics: decrease( ca-ph-PTH) and also decreae FGF-23 but increase sclerostin
thiazide diuretics: increasae ca and klotho, decrease PTH, no effect on FGF-23
Good job. Thanks Dr. Mahmoud
Vitamin D analogues increase calcium, increase phosphate,increase fgf23,decrease PTH and increase klotho, increase sclerotin (How it will increase klotho and sclerotin ??)
Calcimemetic – decrease calcium, decrease phosphate, decrease PTH, decrease fgf23 and increase sclerotin. ( why does it increase sclerotin??)
Thiazide diuretic- increase calcium, decrease PTH, increase klotho (how it will increase klotho?)
Good job. Thanks Dr. Alaa
Regarding your questions:
1- A close inter-relationship between 1,25(OH)2 VD and the sclerostin gene has been described in experimental models. In addition, there is a hypothesis that active vitamin D stimulates sclerostin synthesis and secretion.
2- There is controversial results regarding effect of calcimimetics on sclerostin levels. It would be reasonable to expect a decrease in sclerostin levels through attenuation of the severity of vascular calcification after appropriate therapy, e.g., calcimimetics. Intriguingly, Kuczera P et al. reported cinacalcet treatment in hemodialysis patients with severe SHPT decrease serum PTH concentration and increases plasma sclerostin concentration, reflecting the more robust suppression of high bone turnover status in the study. Compared with their study population receiving much higher therapeutic dose (maximal allowed dose of cinacalcet was 120 mg daily) for more advanced SHPT (mean iPTH level was 1138 pg/mL), other study subjects with a lower PTH level (748.6 pg/mL) were treated with a fixed low dose of oral Cinacalcet (25 mg/day), suggesting that different therapeutic strategies of cinacalcet result in different changes of circulating sclerostin. For further clarification, you can go through this article: Hung, K.C., Chang, J.F., Hsu, Y.H., Hsieh, C.Y., Wu, M.S., Wu, M.Y., Chiu, I.J., Syu, R.S., Wang, T.M., Wu, C.C. and Hung, L.Y., 2020. Therapeutic effect of calcimimetics on osteoclast–osteoblast crosslink in chronic kidney disease and mineral bone disease. International journal of molecular sciences, 21(22), p.8712.
Vitamin D analog increase calcium , increase phosphate, decrease FGF23 decrease PTH and increase klotho, increase sclerostin
Calcimemetic – decrease calcium, decrease phosphate, decrease PTH, decrease fgf23 and increase sclerotin. ( why does it decrease ffg23?)
Thiazide diuretic- increase calcium, phosphate unsure? pth down klotho up
Loop diuretic effect of calcium is decreased what about phosphate and pth increases
is increase in sclerotin in vitamin d analog and calcimemetic good or bad?
Good answer. Thanks Dr. Muhammad.
Regarding your question:
The clinical use of sclerostin remains controversial. In many studies, higher serum sclerostin levels are associated with fatal and nonfatal cardiovascular events. On the other side, increased serum sclerostin levels were associated with better short-term cardiovascular outcomes in a large cohort study of 673 dialysis patients. From these clues, it can be supposed that the calcified vascular cells will secrete more sclerostin to process autocrine or paracrine manners to inhibit Wnt signaling effects on osteogenic trans-differentiation of vascular smooth muscle cells, preventing further calcification of the vessel wall. Thus, circulating sclerostin levels should be interpreted according to clinical scenarios. In bone cases, osteocyte is the major source of sclerostin. The cross-sectional measurement of circulating sclerostin only reflects the dynamics of bone metabolism with particular reference to scenarios. Whether circulating the sclerostin level was bone-derived or vascular-derived in different bone turnover and vascular calcification status has yet to be elucidated.
Regarding effect of cinacalcet on serum levels of sclerostin, it differs according to different therapeutic strategies of cinacalcet.
For more information, you can read this article: Hung, K.C., Chang, J.F., Hsu, Y.H., Hsieh, C.Y., Wu, M.S., Wu, M.Y., Chiu, I.J., Syu, R.S., Wang, T.M., Wu, C.C. and Hung, L.Y., 2020. Therapeutic effect of calcimimetics on osteoclast–osteoblast crosslink in chronic kidney disease and mineral bone disease. International journal of molecular sciences, 21(22), p.8712.
What is the impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markers?
1- The impact of vitamin D analogues :
Increase ca
Increase p
Decrease PTH
Increase FGF-23
Increase klotho
Increase sclerostin
2-The impact of calcimimetics :
Decrease ca
Decrease p
Decrease PTH
Decrease FGF-23
Increase sclerostin
3-Impact of thiazide diuretics:
Increase ca
Decrease PTH
Increase klotho
No effect on FGF-23 and 25 vitamin D and sclerostin.
Great job. Thanks Dr. Asmaa
Thiazid
Loop Diuretics
-increase PTH.
2-decrease calcium.
Calcimmitics like Cinacalcit
i suggest writing the chemical name of each group to assess and revise each medicine and its action. like calcimmitic cinacalcite
VIT D analogue is it the paricalcetriol; or what ??? i am not sue
PLease PROF Amr if possible to show us the name of chemical name for each group ?
Thank you Dr. Rihab for your answer.
Regarding your question:
Calcimimetics: Cinacalcet and Etelcalcetide
Vitamin D analogues: Calcitriol, Paricalcitol, Doxercalciferol, Alfacalcidol
Loop diuretics: Bumetanide, Ethacrynic acid, Furosemide
*The impact of vitamin D analogs on
Calcium increase+. , phosphorous increase+ , Vitamin D -, PTH decrease – -, FGF23 increase ++, klotho increase +, sclerostin increase +
*Calcimimitic
Calcium decrease – , phos decrease -, PTH decrease – -, 25(OH) vitamin _, FGF23 decrease -, klotho? , sclerostin increase +
*thiazide diuretic
Calcium normal or increase + , phos _, PTH decrease – , vitamin D n/a., FGF23 n/a, klotho increase + sclerostin n/a
Thiazide diuretic decrease caciuria so prevent SHPT, it has direct effect on parathyroid gland regardless of caciuria, causes increase klotho and increase osteo last differentiation
Good answer Dr. Israa. Thanks
Impact of Diuretic on CKD-MBD:
Thanks Dr. Kamal. However, what is the effect of vitamin d analogues and calcimimetics on CKD-MBD markers?
The impact of medical therapy CKD-MBD biomarkers:
Vitamin D analogues:
Calcimemitics:
Thiazide diuretics:
Great job. Thanks Dr. Asmaa
the impact of vitamin D analogues, calcimimetics, and thiazide diuretics :
1- Vit D
increase Calcium, phosphate, FGF23 and klotho. and lower PTH.
2- Calcimimetic :
1-decrease calcium .
2-decrease phosphate.
3-suppression of PTH
3-decrease the expression of KLOTHO.
4- decrease FGF23.
3-effect of diuretics
1- increase calcium and Klotho .
2- decrease of PTH.
frusemide :
1-increase PTH.
2-decrease calcium.
Well done Dr. Ashraf.
EFFECT OF VITAMIN D ANALOGS:
1-increase calcium reabsorption from GIT
2-increase phosphate reabsorption
3-decrease PTH level
4-increase FGF23 and klotho and sclerostin
===============
effect of calcimimitics
1-reduce calcium and phosphate
2-marked suppression of PTH
3-reduce FGF23
4-increase sclerostin
effect of diuretics :
thiazide diuretics
1-suppress PTH
2-increase plasma klotho
mild increase calcium
unknown action on vit D ,FGF23 ,sclerostin
=========
frusemide
increase PTH
NO EFFECT ON CALCIUM OR PHOSPHATE
UNKNOWN ACTION ON VIT D ,FGF23,KLOTHO,SCLEROSTIN
Thank you Dr. Emad for you comprehensive answer.
Loop diuretics increase urinary calcium, thus increasing risk of developing secondary hyperparathyroidism.
What is the impact of vitamin D analogues, calcimimetics, and thiazide diuretics on the CKD-MBD markers?
1- Significant decrease of PTH.
2- No effect on 25- Hydroxy Vit. D.
3- Increase in all other markers.
1- Decrease in serum calcium, FGF-23, and PTH.
2- Increase sclerostin and phosphate.
3- No effect on 25-Hydroxy Vit. D.
4- Unknown effect on Klotho.
1- mild increase in serum calcium and Klotho levels.
2- mild decrease of PTH.
3- No effect on Phosphate.
4- Unknown effect on 25-hydroxy Vit. D, FGF-23, and sclerostin levels.
the impact of classical drugs in ttt of ckd mbd is useful to decrease level of pth but unfortunately there was no or little effect on FGF23or even increase in most of cases.
the use of thiazide diuretcs useful than loop diurtics in patient with ckd mbd by indircet action to prevent ca loss in urine to promote ca absorption and decrease level of pth
also thiazide has direct action on oesteoblast in bone
Thanks Dr. Rabab
Vitamin D analogues increase serum calcium, phosphorus, and FGF23 while they decrease PTH.
Calcimimetics decrease serum calcium, phosphorus, FGF23 and PTH.
Vitamin D will increase in Serum Calcium, phosphate, FGF and klotho. But lower PTH.
Calcimimetics lower PTH, calcium, phosphate , and FGF.
Thiazide diuretic will increase calcium and decrease PTH. It increase also clotho factor.
So these medicine are preventing mineral bone disease through lowering secondary hyperparathyroidism but in diffrent mechanism.
Loop diuretics will induce calcuria ( opposite to thiazide) and will decrease calcium in Serum
Well done. Thanks Dr. Nour
CKD-MBD therapy:
Drugs that decease PTH level:
Hyperphosphatemia:
Notes
Thanks Dr. Ben.
Vitamin D analogues increase serum calcium, phosphorus, and FGF23 while they decrease PTH.
Calcimimetics decrease serum calcium, phosphorus, FGF23 and PTH.
Thiazide diuretics decrease urinary calcium loss and thus suppress PTH.
Yes, Eman
PTH levels may be lowered using a combination of vitamin D analogs and calcimimetics. On the other hand, these factors have the opposite impact on FGF-23.
Thiazides can lower the amount of calcium that is lost in the urine. They can also lower PTH levels.
By interacting with a sodium chloride cotransporter found in bones, thiazide diuretics have the potential to stimulate osteoblast development.
as the diuretic medicines induce or reduce calciuria. decreases the risk of SHPT in the case of thiazide diuretics, whereas loop diuretics increase the risk of SHPT.
Thanks Dr.Weam. Please try to answer in your own way the next times.