A 56-year-old male who has been on maintenance hemodialysis for two years, complains of increasing bony pains.
Review of the patient’s laboratory investigations are shown in table 1
Test |
Value |
S. Creatinine |
4.5 mg/dL |
S. Corrected Calcium |
7.9 mg/dL |
S. Phosphorus |
6.9 mg/dL |
iPTH |
978 pg/mL |
A. Interpret the above laboratory investigations.
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
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Lab result
Severe secondary hyperparathyroidism, with hypocalcemia and hyperphosphatemia.
Pathogenic mechanism
CKD-MBD, renal osteodystrophy, high bone turnover disease.
Advanced CKD and HD have a failing regulatory mechanism, so the FGF23 level raises and induces hyperphosphatemia (although the patient is on dialysis), this will activate the parathyroid gland to compensate for hypocalcemia, via bone resorption which leads to clinical syndrome and symptoms.
Calcium vs non-calcium Pi binder
Calcium based
Non-calcium Pi binder
A. Interpret the above laboratory investigations.
ESRD with secondary hyperparathyroidism due to hypocalcemia and hyperphosphatemia
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
Individuals with CKD have low levels of klotho but high FGF 23 levels. Elevated FGF23 levels inhibit the 1–hydroxylase enzyme and lower the level of calcitriol. Decreased calcitriol levels cause impaired calcium reabsorption and hypocalcemia, which stimulates the synthesis and release of PTH. Phosphorus homeostasis is lost due to receptor resistance to FGF 23, which results in a loss of its phosphaturic activity in chronic renal disease, leading in hyperphosphatemia.
C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting
– Reducing dietary phosphate intake, using phosphate binding agents, and increasing phosphate removal by increasing dialysis duration
– Calcium- containing phosphate binders (especially calcium carbonate) are effective in reducing serum phosphorus and PTH
– Therapy may need to monitored to keep calcium, PO4 within normal range and iPTH between 150 to 300
– Despite the the fact that he had low calcium in the blood, this may not reflect his total body calcium and he may actually have positive calcium balance
– Non calcium containing phosphate binders can decrease phosphate and PTH level without correction of serum calcium.
– Calcium-based phosphate binders can exacerbate vascular calcifications
scenarion 1
A secondary hyperparathyroidism
B reduced active Vit D with reduction in ca absorption, and parthyroid glang over secrets the PTH trying to increase the ca level
C calcium based phosphate binders will cause more vascular calcification, but it should increase the level of serum calcium, non calcium binders will reduce the absorption of PO4 in the gut with no effect on calcium, which leads to less tissue calcification
A
The level of iPTH is too high representing a likely high bone turnover disease. the low Ca is indicative of failing 1a-hydroxylation, and the high phosphate is expected in this setting of high turnover and a failing kidney to excrete PO4
B
High iPTH leads to bone resorption releasing Ca and PO4 to the blood.
since PO4 cannot exit because failing kidney, it tends to accumulate.
Ca reabsorption from intestine is reduced by reduced amounts of active Vitamin D
C
Calcium and non-calcium based can reduced PO4 reabsorption from intestine.
The problem with Ca based is that Ca will be reabsorbed but will not be used in the bones because of hyperparathyroidism, so soft tissue calcification will be enhanced.
A. Interpret the above laboratory investigations.
ESRD with secondary hyperparathyroidism resulted from hypocalcemia and hyperphosphatemia.
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
With loss of renal mass, there is a decrease in Klotho, FGF23 cofactor. That would result in an increase in FGF23 level. Phosphate level will start to creep up, Calcium level will decrease due to low level of active form Vit D that attributed to inactivation of conversion of vit D2 to D3 by inhibition of 1-alpha hydrolxylase by FGF23. Low level of Ca and high level of PH will stimulate PTH secretion, which overtime would lead to secondary hyperparathyroidism.
C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
Ca and non Ca phosphate binders have almost the same effect in controlling serum PH and PTH levels. They differ in their effect on Ca level. So as this patient has hypocalacemia and hyperphosphatemia, I would recommend starting calcium acetate with food, to help increasing Ca level, and decreasing PH level as a PH binder.
CKD patient with elevated creatinine,2ndary hyperparathyroidism ,hyperphosphatemia and hypocalcemia.
increase in FGF 23 and decrease of klotho leads to decrease in renal mass,decrease calcitorial level.
hypocalcemia leads the release of PTH.
non calcium phosphate binders to avoid calcification
1- 2ndry hyperparathyroidisn with hyperpo4 and vitamin d deficiency
2-fgf23 increased as GFr decreased so lead to suppressing 1a hydroxlayse and 1,25(OH)3 D production .
PTH stimulated by hypocalcemia , and decrease 1,25(OH)2H and hyper phosphatemia
3- non calcium phosphate binder better avoid vascular calcification from calcium phosphate binder
A. Labs showed SHPT (2ry to hypo-calcemia and hyper-phospatemia along with hypo-vitaminosis D) probably occurs after inadequate dialysis (low creatinine indicating reduced muscle mass in relation to pt age)
B. Expected pathogenesis:
ESRD (decreased functioning kidney mass hence klotho deficiency and increased FGF23 expression- aiming to normalize high S.phosphorus-), decreased calcidiol activation (-> decreased calcium absorbtion) along with inadequate removal of retained S.phosphorus by dialysis,, all leads to persistent stimulation of parathyroid gland (persistent low Ca, low vit D, high phosph and resistant gland to feedback inhibition)
C. In this setting check 25 hydroxy vit D3, replenish stores for inactive vit D & calcium (better with calcium based phosphate binders- after exclusion of +ve calcium balance and soft tissue calcification- otherwise non Ca based binders with the advantage of FGF23 reduction will be preferable), add active vit D, improve dialysis adequacy, prolong dialysis time, phosph restriction especially inorganic form.
a-the lab. investigation revealed hypocalcemia and hyper phosphatemia and associated with 2nry hyperparathyroidism
b-the pathogenic mechanism expected in this situation increase ,suppress FGF-23R and VDR with 2ry HPTH associated with high turn over bone disease
c- the non calcium phosphate binder better than ca phosphate to avoid suppression of parathyroid gland and avoid vascular calcification
A- interpretation Hypocalcemia as ca level 7.9 hyperphosphatemia as po4 6.9
Secondary Hyperparathyroidism as pth 978.
B- pathogenic mechanisms
Decrease level of koltho and vit d leading increase level of fgf23 and pth to compansate hyperphosphatimia and hypocalcemia .
C- role of ca and non ca phosphate binder
Recently we prefare non ca phosphate binder to avoid metastatic calcification
Interpret the above laboratory investigations.
56y old male ESRFon HD with hypocalcemia, hyperphosphatemia and secondary hyperparathyroidism
Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
as hes in end stage renal disease with low 1-α-hydroxylase so low calcitriol , low calcium resulting in stimulation of PTH release decreasing degradation, with high FGF23 and lower klotho expression all cant act on late severe diseased kidney so cant excrete phosphate phosphate remain high, beside all act togother in different feedback mechanisms
Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
recently we discoverred that renal patient in positive ca balance so for high phosphate
decrese diat phosphate
check dialysis adequacy and extend dialysis
check patient medication example if patient taking vit D analogues (hold)
better to give non Ca containing phosphate binder and to avoid any vascular or tissue calcification as CaP product is high, also avoid aluminum containing binders
A- hypocalcemia, hyperphosphatemia and secondary Hyperparathyroidism
B- po4 retention .high FGF23 and decrease klotho factor
decrease active form of V.D lead to hypocalcemia
C- ca containing phosphate binder can lead to more calcification but we can use in this case and follow up
very good dr Hagar.
Patients with CKD have low levels of klotho and high FGF 23 levels. Increased FGF23 levels inhibit 1-α-hydroxylase enzyme and decrease calcitriol level. Low levels of calcitriol cause decreased calcium reabsorption and produce hypocalcemia which in turn acts as a stimulus for the synthesis and release of PTH. Loss of phosphorus homeostasis occurs due to resistance to FGF 23 at the receptor level which leads to loss of its phosphaturic action in chronic kidney disease resulting in hyperphosphatemia
A.Interpret the above laboratory investigations:
CKD-HD, Hypocalcemia, Hyperphosphatemia, and High PTH are correlated with secondary Hyperparathyroidism
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
An increase of FGF23 and reduction of its cofactor Clotho combined with ESRD findings lead to hyperphosphatemia.
decrease of 1-α-hydroxylase in the kidney leads to low levels of calcitriol and hypocalcemia which stimulate PTH release. The increase in PTH favors bone turnover and resorption and stimulates the production of 1-α-hydroxylase.
C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
Reduction of dietary phosphate intake, use of phosphate binding agents, and increase phosphate removal by adding more hours or days of dialysis.
All available phosphate binders are effective in reducing serum phosphate, although it must be taken into account that calcium-based phosphate binders can increase vascular calcifications and those containing aluminum have shown to be dangerous
Great dr Mohammed
Interpret the above laboratory investigations:
-CKD stage 5D
-mild hypocalcemia
-hyperphosphatemia
-secondary hyperparathyroidism.
Explain the expected pathogenetic mechanisms beyond these lab abnormalities:
the increase in FGF23, the decrease of Klotho, and the reduction of renal mass are possibly the earliest events in the pathogenesis of CKD-MBD. These changes favor the reduction of 1-α-hydroxylase in the kidney, which results in low levels of calcitriol, the most active natural activator of VDR, a fact that reduces the absorption of calcium in the intestine and favors the decrease in serum calcium, which in turn acts as a stimulus for the synthesis and release of PTH. The increase in PTH favors bone turnover and resorption and stimulates the production of 1-α-hydroxylase. All of these mechanisms translate into compensatory increases to normalize serum calcium.
Evaluate the potential role of calcium vs non-calcium phosphate binders in this setting:
All available phosphate binders are effective in reducing serum phosphate, although it must be taken into account that calcium-based phosphate binders can increase vascular calcifications and those containing aluminum have shown to be dangerous and they are the only type of phosphate binding agents not associated with survival benefits .
Thank you dr Asmaa
A- Hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism
B –
⬇️po4 excretion
⬆️ FGF23
⬇️Klotho.
decrease active firm vit d
c- non ca binder to be use
and use vit d analogues with correct vit d deficiency and follow phos ca and PTH if not response calcimimetic agents
Thankyou drKhaldon.
Patients with CKD have low levels of klotho and high FGF 23 levels. Increased FGF23 levels inhibit 1-α-hydroxylase enzyme and decrease calcitriol level. Low levels of calcitriol cause decreased calcium reabsorption and produce hypocalcemia which in turn acts as a stimulus for the synthesis and release of PTH. Loss of phosphorus homeostasis occurs due to resistance to FGF 23 at the receptor level which leads to loss of its phosphaturic action in chronic kidney disease resulting in hyperphosphatemia
A. Interpret the above laboratory investigations:
Hypocalcemia, hyperphosphatemia, and high iPTH are most likely signs of secondary hyperparathyroidism.
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
Reduced po4 excretion
increases FGF23
decreases Klotho.
Decrease kidney 1-α-hydroxylase, which lowers calcitriol, the most potent natural activator of VDR, which decreases intestinal calcium absorption and serum calcium, which stimulates PTH production.
C. Evaluate the potential role of calcium vs. non-calcium phosphate binders in this setting.
a Non-calcium phosphate binder,
If no response, cinacalcet in addition to Vit-D
Thanks dr Mahmoud.
Calcium- containing phosphate binders (especially calcium carbonate than calcium acetate) are effective in reducing serum phosphorus and PTH. However, positive calcium balance and risk of cardiovascular calcification are more common with these groups than non-calcium-based phosphate binders. Moreover, serum calcium level is not a good indicator of the calcium balance.
A. Interpret the above laboratory investigations.
ESRD on regular HD , Hypercalcemia , Hyperphosphatemia and High PTH ,complaining of bony pains mostly due to secondary Hyperparathyroidism .
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
Hypercalcemia mostly as a result of calcitriol deficiency
Hyperphosphatemia in this patient how most probably anuric or oliguric with loss of phosphaturic effect of FGF-23 and PTH with accumulation of ingested P and also as a consequence of bone resorption .
C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
in this patient we can use calcium containing phosphate binders in addition to non calcium containing phosphate binder , CA P product is acceptable with less possibility of vascular calcification ,
Thank you dr Ahmed.
Calcium- containing phosphate binders (especially calcium carbonate than calcium acetate) are effective in reducing serum phosphorus and PTH. However, positive calcium balance and risk of cardiovascular calcification are more common with these groups than non-calcium-based phosphate binders. Moreover, serum calcium level is not a good indicator of the calcium balance.
This patient is having the typical metabolic finding od advanced CKD 5D along with hyperSHPTH.
pathogenetic mechanisms beyond these lab abnormalities.
This metabolic changes is strted with severe reanal loss mass ,with increasing of FGF23 and hyperphophatemia and the former will need to decrease the 1,25,Vd (calciferol) and as per the study thids deficency of the active form of Vitamin D is started very early when the eGFR is 70 to 80 ml/mint .Then the FGF23 attenuate the effect on hyperphophatemia at the expense of calcitriol .
After that low cacitrol will reduce Ca reabsorbtion from intestin an d lead to hypocalcemia .and then the low Ca will stimulate PTH secretion and the PTH will affect the bone mibneralization with increase bone fragility and loss of bone volum .
Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
With this laboratory finding we need to treat first the hyperphophatemia with Phophate binder line sevelamer as the Ca binder base will increase the total Ca in the body and this will increase the risk of vascular calcification.
The level of PTH is more than 9 times the normal level,and i think at this level we will not depends on the trend of rising as it is sky high figuer .,we need to treate it through paricalcitrole as the calcimmometic will worsen the CA level .
A.Interpret the above laboratory investigations?
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities?
C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting?
56 year old patient with ESKD on CHD(for 2 years), stage 5D
Lab investigations: show hypocalcemia, hyperphosphatemia and secondary hyperparathyroidism.
Pathogenetic mechanisms beyond these lab abnormalities:
Plasma FGF23 enhances phosphate excretion in the proximal renal tubule by decreasing the expression of luminal sodium-dependent phosphate transporters and may also decrease intestinal phosphate absorption by inhibiting NaPi cotransporter activity.
In addition, it reduces the synthesis of 1,25-dihydroxyvitamin D [1,25(OH)2D3] by down-regulating the activity of 1α-hydroxylase and accentuating the activity of 24-hydroxylase.
In the early stages of CKD, high levels of FGF23 attenuate hyperphosphatemia at the expense of 1,25(OH)2vitamin D suppression, thus initiating the development of secondary hyperparathyroidism.
The decrease in serum 1,25(OH)2D3 leads to decreased intestinal calcium absorption.
The triad of low levels of calcium, calcitriol and hyperphosphatemia further enhances excessive PTH secretion. This excess PTH leads to mobilization of calcium from the bone and osteitis fibrosa.
Other consequences of progressive worsening of kidney function include hypo-responsiveness of the vitamin D receptor (VDR) on the parathyroid gland with further enhancement of production of PTH and reduced expression of the calcium-sensing receptor on the parathyroid gland leading to parathyroid gland hyperplasia. In some subsets of patients, the parathyroid gland undergoes hypertrophy and becomes autonomous.
Evaluate the potential role of calcium vs non calcium phosphate binders in this setting:
Although calcium containing phosphate binders can correct hypocalcemia, hyperphosphatemia and secondary hyperparathyroidism, They are associated with the risk of vascular and valvular calcification as well as arterial stiffness (as ckd patients are on positive calcium balance despite being hypocalcemic.)
Non calcium containing phosphate binders can decrease phosphate and PTH level without correction of serum calcium.
A: The patient is already on dialysis, thus CKD Stage 5D
The blood picture is in keeping with Secondary Hyperparathyroidism:
Reduced Calcium
Elevated PTH
Elevated Phosp
B: The reduced renal mass, results in the development of Hyperphosphatemia, resulting
in the following:
Skeletal resistance – causing Hypocalcemia
Reduced 1,25 (OH)s D3
Calcitriol resistance
Parathyroid cell growth
Reduced renal mass also causes an increase in FGF-23 and reduced Klotho levels
C: Non-calcium containing phosphate binders is preferred because of the risk of vascular and metatstatic calcifications.
Our case has hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism outside targets. I suppose this patient already used calcitriol or paricalcitol before. We are limited by high phosphorus and hypocalcemia. Hypocalcemia limits us regarding cinacalcet.
What I will plan:
strict diet
maximizing P-lowering agents. I prefer Lantanum here but after 3×1000 mg I may need to add Ca acetate. I will plan paricalcitol plus cinacalcet to superss PTH. meanwhile, this will balance the Ca (target >8.4-<10.4 mg/dl). Phosphorus is a key target (4.5-5.5 max) and should be my target not influence my treatments (cinacalcet and paricalcitol); drug doses are modified later
With ESRD as my colleagues said, the klotho deprivation, resistance to FGF-23 effect and in addition anuric patients will not benefit from phosphaturic effect if minimally peresent, wee need to control diet and do effective HD, maximize anti-P treatment
A. The patient has CKD5D, hypocalcimia, hyperphosphatemia and hyperparathyroidism
B. Hypocalcimia caused by decrease activity and secretion of 1 alfa hydrxylase which lead to decrease calcitriol and decrease intestinal absorption of calcium and subsequently hypocalcimia
Hyperphosphatemia caused by decrease in renal mass and decrease in urinary excretion of phosphate in addition to food containing phosphorous
Hyperparathyroidism caused by stimulation of calcium sensing Receptor by hypocalcimia and decrease in calcitriol so stimulation of VDR in parathyroid gland.
C. The use of calcium containing phosphate binder will improve calcium level but increase risk of vascular calcification and risk of a dynamic bone disease, and some times better to use combination of calcium and non calcium containing phosphate binder.
C. Sorry regarding calcium containing pho binder increase risk of vascular and soft tissue calcification not a dynamic bone disease
Very good dr Israa.
Patients with CKD have low levels of klotho and high FGF 23 levels. Increased FGF23 levels inhibit 1-α-hydroxylase enzyme and decrease calcitriol level. Low levels of calcitriol cause decreased calcium reabsorption and produce hypocalcemia which in turn acts as a stimulus for the synthesis and release of PTH. Loss of phosphorus homeostasis occurs due to resistance to FGF 23 at the receptor level which leads to loss of its phosphaturic action in chronic kidney disease resulting in hyperphosphatemia.
A.CKD5D, hyperphophatemia, hypocalcemia, secondary hyperparathyroidism .
B.Decreased calcium bcause of vitamin D deficiency .
High phosphat because with deterioration of renal function there is decreased secretion
High ipth because parathyroid gland try to compensate the low calcium and high phosphate. Actually these level will stimulate CaSR and VDR cause increased secretion and post transcriptional increase in iPTH
C.calcium containing phosphate Binders will decrease phosphate and increase calcium level (but may increase vascular calcification).
Non calcium containing phosphate Binders have lower risk to cause vascular calcification. Aluminum containing phosphate Binders have not mortality benefits.
Good job dr Nour.
Patients with CKD have low levels of klotho and high FGF 23 levels. Increased FGF23 levels inhibit 1-α-hydroxylase enzyme and decrease calcitriol level. Low levels of calcitriol cause decreased calcium reabsorption and produce hypocalcemia which in turn acts as a stimulus for the synthesis and release of PTH. Loss of phosphorus homeostasis occurs due to resistance to FGF 23 at the receptor level which leads to loss of its phosphaturic action in chronic kidney disease resulting in hyperphosphatemia.
QA . Interpret the above laboratory investigations.
ESKD on hemodialysis.
hypocalcemia.
hyperphosphatemia.
secondary hyperparathyroidism.
Q2 . Explain the expected pathogenetic mechanisms beyond these lab abnormality ies.
1- decrease 1-α-hydroxylase causing low Vit D so decrease intestinal absorption of calcium so low s.Ca .
2-with decrease renal mass decrease the phosphate excretion causing hyperphosphatemia.
3- -with decrease renal mass there is PTH hypo responsiveness .
Q3- C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
1- follow up with dietitian .
2-start ca supplement tab. before meal .
3- use non ca phosphate binder with meal.
Thank you dr Ashraf.
A. Interpret the above laboratory investigations.
Hypocalcemia, hyperphosphatemia, and high iPTH are most likely signs of secondary hyperparathyroidism.
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
Reduced po4 excretion by the kidney increases FGF23 and decreases Klotho. These modifications limit kidney 1-α-hydroxylase, which lowers calcitriol, the most potent natural activator of VDR, which decreases intestinal calcium absorption and serum calcium, which stimulates PTH production
C. Evaluate the potential role of calcium vs. non-calcium phosphate binders in this setting.
According to the guideline: In adult patients with CKD G3a–5D receiving phosphate-lowering treatment, we suggest restricting the dose of calcium-based phosphate binders
so I will start with a Non-calcium phosphate binder, If no response, I will add cinacalcet in addition to Vit-D
Excellent dr Weam.
A- Interpretation of lab results :
it is a case of hypocalcemia , hyperphosphatemia and hyperparathyroidism ( mostly secondary type ).
B- it is mostly a case of high turnover bone disease ( previously known as osteitis fibrosa cystica ) caused by hypocalcemia and hyperphosphatemia which are both stimulants for secondary hyperparathyroidism as evidenced by high PTH level above the normal target ( 2-9 fold of normal level).
C- in this case, it is preferred to use calcium containing po4 binders over non calcium types to make a triple benefit of correcting calcium levels , decrease po4 levels as well as suppresion of PTH to decrease progression to tertiary hyperparathyroidism which may need surgical treatment later as calcimimetics as cinaclet cannot be used in the setting of hypocalcemia .
Great dr Mark.
let me please add some information:
A-
CKD G5D
Mild hypocalcemia
Hyperphospatemia
Elevated PTH level
SHPT
‐——————-
B-
Non adherence to diet and medicine
Review medication containing phosphate
Inadequate hemodialysis
Hypovitaminosis D
————–‐———————-
C-
According to KDIGO guidelines >>>>suggest restricting the dose of calcium based phosphate binders
The excess exposure to calcium either by diet or medications increase the risk hypercalcemia ,arterial calcification ,ABD,low PTH
Good dr Emad.
THIS PATIENT HAS ESRD ON REGULLAR DIALYSIS WITH 2RY HYPERPARATHYROIEDISM , HYPOCALCEMIA AND HYPERPHOSPHATEMIA , I WILL ADVISE HIME FOR DIET CONTROL AND I WILL CHECK FOR ADEQUACY OF DIALYSIS START HIM ON CALCIUM BASED PHOSPHATE BINDER VITAMIN D LIKE PARICALCITOL , KEPPING EYE ON HIS PHOSPHOROUS AND CALCIUM IF NEEDED CINACALCIT MAY BE ADDED LATER ON
Thanks dr Abdulrahman.
IF you could please answer every question separately so that you will not miss any of them.
What about the pathogenesis beyond these lab abnormalities especially the role of FGF 23?
A- Secondary hyperparathyroid( increased phosphate and low calcium and increased phosphate)
B- increased phosphate due to inadequate dialysis or non compliance with diet or binders .
C- it would be be better to check vitamin d and correct vitamin D deficiency. Then use non calcium based binder to decrease PTH
Thanks dr Muhammad.
Can you explain the role of FGF 23 in the pathogenesis of CKD MBD?
And what about the role of calcimimetics in this case?
Interpret the above laboratory investigations:
Explain the expected pathogenetic mechanisms beyond these lab abnormalities:
SHPT occurs in response to a series of events:
Evaluate the potential role of calcium vs non-calcium phosphate binders in this setting:
A combination of increased calcium (ingestion+ calcium phosphate binder) and decreased calcium excretion could lead to a positive calcium balance, even in the absence of hypercalcemia.
very good dr Amna.
Patients with CKD have low levels of klotho and high FGF 23 levels. Increased FGF23 levels inhibit 1-α-hydroxylase enzyme and decrease calcitriol level. Low levels of calcitriol cause decreased calcium reabsorption and produce hypocalcemia which in turn acts as a stimulus for the synthesis and release of PTH. Loss of phosphorus homeostasis occurs due to resistance to FGF 23 at the receptor level which leads to loss of its phosphaturic action in chronic kidney disease resulting in hyperphosphatemia.
A. Interpret the above laboratory investigations.
B. Explain the expected pathogenetic mechanisms beyond these lab abnormalities.
C. Evaluate the potential role of calcium vs non calcium phosphate binders in this setting.
Great! FGF23 per se plays a fundamental role in the pathogenesis of CKD-MBD. We may consider this point in addressing the pathogenetic background