A 36-year-old female with ESKD, maintained on HD for three years presented with persistent dry cough for 2 months. Medication review included calcium carbonate 2000 mg orally, and alfacalcidol 0.5 mcg orally per day. Â
Review of her routine laboratory work-up revealed:
Test
Value
S. Creatinine
3.9 mg/dL
S. corrected CalciumÂ
11.52 mg/dL
S. Phosphorus
5.7 mg/dL
iPTH
127 pg/mL
Hemoglobin (Hgb)
10.5 g/dL
A. Interpret the above laboratory investigation.
B. What would be your next management plan?
Â
47 Comments
Radwa Ellisy
this patient with ESRD has mild anemia, positive calcium balance, and iPTH below the target according to KDIGO guidelines
mild hyperphosphatemia and hypercalcemia
restriction of calcium supplementation and use of non-calcium-based binders
use of low calcium dialysate, and follow up
if no improvement: investigation for hypercalcemia espicially in the presence of dry cough
A. Interpret the above laboratory investigation. ESRD with hypercalcemia and hyperphosphatemia. B. What would be your next management plan? stop calcium-containing binders
So: hyperCa, hyperP and PTH is below the target with mild anaemia
B. What would be your next management plan?
She is on calcium carbonate 2000 mg per day (800mg elemental Ca).
Of note, one gram of calcium carbonate equals 400mg of elemental calcium.
Daily elemental Ca intake (dietary and Ca-based phosphate binders) recommendations in CKD IIIa through CKD5 HD/PD vary; KDOQI 2003 recommends not exceeding 2000 mg/day.
So do not exceed 3,750 mg/day Ca carbonate (1,500 mg/day elemental calcium).
index case has hypercalcemia may be a result of:
High dietary calcium source
medication related/ dialysate
pathological disease
Young female with an unclear underline cause of her ESKD and persistent dry cough, I would like to exclude granulomatous disease (Sarcoidosis, TB and lymphoma).
My approach:
Ensure adequate HD with low Ca dialysate
Dietitian review
D/C Calcium Carbonate
Consider non-calcium-based phosphate binder
Workup for hyperCa:
Hx (drug Hx very important ) and clinical examination
Rule out sarcoid, lymphoma and TB (CXR,1,25 vit D and 25 vit D, Sputum AAFB, ACE level, blood film, lymph node bx if exist, etc.).
Interpret the above laboratory investigation. ESRF with hypercalcemi and hyperphosphatemia, with low PTH FOR DIALYSIS MIDDLE AGE FEMALE
What would be your next management plan? REVIEW ALL HISTORY AGAIN, DRUG HISTORY
stop any drug us or interact with ckd mbd drugs
ask fo full updated Lab results add PTH , bon specific ALK, 2hydroxy vit D level
x ray for the skull, pelviabd us ,HRCT,
ESRD pt, hypercalcemia, hyperphosphatemia, low PTH, possible low turnover bone ds
next step: stop calcium and alfacalcidol supplements, dialyse against low calcium dialysate, check for 25OH vitamin D, HRCT chest
Hypercalcaemia, hyperphosphatemia, PTH below optimal level
Stop Ca based binders
Stop active vit D
Use non Ca based binders
Work up for HYPERCALCEMIA with low PTH
A. Interpret the above laboratory investigation. ESKD , hypercalcimia , hyperphosphatemia, low PTH, mild anemia. B. What would be your next management plan? stop calcium and start non calcium phosphate binders stop one Alfa use low dialysate calcium.
CXR and CT chest
TB screen
follow up of ca ,ph , PTH .
A)case of hypercalcemia ,hyperphosphatemia and low pTH
B)stop ca supplement and alfacalcido if high ca not improved give non ca containing phosphate binder dialysis with low ca dialysate(1.25) can improve ca and pth level measure PSALP chest Xray for her chest problem
A. Interpret the above laboratory investigation. ESRD- Hpercalcemia- Hyperphosphatemia – Low PTH B. What would be your next management plan? 1-Stop calcium carbonate and alphacalcidol 2-Start non calcium containing phosphate binders. 3- Low calcium dialysate. 4- chest X ray. 5- Measure Vitamin D level and ACI level .
Lab investigations show hypercalcemia and hyperphosphatemia, the iPTH is within the recommended range, Hb is slightly lower than recommended
Since he has hypercalcemia, I would look for causes of hypercalcemia, and since he is coughing then he may have TB or Sarcoid (contributing to hypercalcemia)
so CXR / HRCT / Sputum culture and AFB / and serum ACE
I will have to stop his CaCO3 and VitD3
Lab investigations show:hypercalcemia,hyperphosphatemia,accepted PTH level(2 times more than the normal range) and anaemia(HB level accepted for patient on CHD)
What would be your next management plan?
1-Stop calcium carbonate and alphacalcidol
2-if serum phosphorus is not improving, start non calcium containing phosphate binders(sevelamer)
3- Check drugs that cause cough like ACEI, ARBS and omperazole.
4- chest radiology to exclude any chest radiology .
5- Measure Vitamin D level
6-Follow up serum ca ,po4, and PTH.
Cough: rule out TB and sarcoidosis by CXR, sputum AFBx3, and sputum C/S, and ACE level. Stop the Calcium and Vitamin D Monitor PTH , calcium and vitamin D level
A. Interpret the above laboratory investigation. ESRD with Hypercalcemia, hyperphosphatemia, hyperparathyroidism, and anemia. B. What would be your next management plan? As I don’t have much info about the reason for ESRD in this young patient, and in view of hx of persistent cough for 2 months, and taking into consideration the biochemical parameters results, I would investigate for granulomatous disease in such patient. I would explain my thought process, young female with ESRD and chronic cough, could be sarcoidosis. Sarcoidosis might started years back, with hypercalcemia, she might had long standing nephrolithiasis, leading to nephrocalcinosis, with/or without interstational nephritis, which eventually resulted in ESRD. If I continue to believe in Sarcoidosis as a primary disease, that means her 1-25 Vit D is high, due to increase activation of 1-alpha hydroxylase in the abundant macrophages. High 1-25 vit D, increases intestinal absorption of Ca, and PH. Other cause of granulomatous disease, TB. It could be that this patient is having TB due to her immunocompromised status. Since TB is granulomatous disease too, and has high number of macrophages. The 1-25 VitD would increase and Ca, and PH would increase too due to high intestinal absorption. I would stop Ca, and alfacalcidol. I would order CXR, sputum AFBx3, and sputum C/S, and ACE level. I would check if the patient has any skin lesion, or lymph node which could be biopised as sometimes if would be difficult to reach such diagnosis.
A: The patient is having CKD – Stage 5 (on RRT), with Hypercalcemia, Hyperphosphatemia, Anemia and an elevated PTH
B: Cough:
Enquire about constitutional symptoms ( night sweats, hemoptysis, LOA, LOW,
dyspnoea, PND, orthopnoea, etc)
Enquire about smoking – possible risk factor for Ca lung
Enquire about any other meds that patient is using, esp ACE-inhibitors
Investigations:
CXR + CT Chest: evaluate lung fields and mediastinum
Echocardiogram: exclude any cardiac causes for coughing
Serum ACE for Sarcoidosis
Biochemical abnormalities:
The abnormalities seen with the Calcium and Phosphate is most probably driven
by her current meds: Vitamin D and Calcium-containing phosphate binder – STOP
the meds, and change onto a Non-Calcium containing phosphate binder.
Improve/educate patient on low phosphate containing foods
Monitor the Ca, PO4 and PTH – in order to restart the Vit D
A- interpretation of investigation hypercalcimia, hyperphosphatemia,high pth level and anemia.
B- management plane stop vit d and ca and follow up and do chest x-ray to detect the cause of cough
Ca load from phosphorus binding Ca Carbonate together with active vitamin D plays a role in hypercalcemia. Stopping calÅŸcitriol and shifting to sevelamer or low-dose Lantanum will help decrease calcium load and phosphorus absorption minimally increase with active vitamin D. After PTH returns to around 300, we may restart the lower dose of Calcitriol.
female pt. 36y/o esrd on regular HD since 3y on caco3 200mg and alfacalcidiol 0.5 mic lab investigation revealed :-
anemia
hypercalcemia
hyperphosphatemia
suppressed iPTH Action plan :-
should be stop ca phosphat binder ca carbonate and shifting to non ca phosphate binder
and stop alfacalcdiol
and search about dry cough review the medication exclude ACEI
investigate pt. for dry cough and 2ry hypercalcemia
chest x-ray to rule out TB
Follow up and observation
Interpret the above laboratory investigation. This patient is having ESRD on HD with new onset of chronic cough along with hypercalcemia and hyperphosphatemia and low iPTH .
Her Hb is low compared to her age (non-menopausal age)
The cause of High Ca is the use of Ca supplements along with the use of Vita AND both of them will lead to high Ca and high Phosphorous and this will lead to suppressing the PTH level. This patient is most likely having a low turnover bone disease.
What would be your next management plan?
I would stop the Ca supplement and Vitamin. D and will start non-Ca binder phosphates on the same time I will start to work her up for her dry cough by doing full investigation which includes chest x ray and further chest assessment to rule out secondary causes for hypercalcemia.
PATIENT IS ESKD ON HD MOSTLIKLY HE HAS ADEQUATE DIALYSIS , MILDY ANEMIC , SHE HAS HYPERCALEMIA AND HYPERPHOSPHATEMIA MOSTLY DUE TO OVER TREATMENT , NEEDS TO STOP CALCIUM AND ALFACALCIDOL ADD PHOSPHATE BINDER NONCALCIUM CONTAINING . DIALYSIS WITH LOW CALCIUM DIALYSATE 1.5-2.0 OR EVEN LOWER BUT FOR SHORT PERIOD , TO AVOID BONE DEMINERALIZATION. DETAILED HISTORY AND MEDICATION HISTORY , THEN GO FOR FURTHER INVESTIGATION FOR HER COUGH STARTNIG WITH MEDICATION HISTORY , CXR , PULMONOLOGY CONSULTATION AND
interpret above laboratory investigation?
CKD 5D
anaemia of ckd likely
hypercalcaemia on calcium carbonate and alfacalcidol
pth 127 ( Possibly suppressed)
In context of chronic cough need to rule out tb/sarcoid
A- A case of ESRD with average s.cr with hypercalcemia ,hyperphosphatemia with suppressed iPTH ( mostly low turnover bone disease) caused by over treatment with calcium and active vit D in addition to normal Hgb as compared to the target value for this population .
B- management plan
1-stop calcium supplemention immediately
2-use of non calcium containing po4 binders instead of calcium containing
3- stop vit D to increase iPTH and decrease hyperphosphatemia
4- Dietary phosphate restriction with the help of po4 pyramid
5- use the least ca dialysate concentration (1.25 mmol)
6- use of nocturnal prolonged daily HD if still persistant high po4
Well done! however, the best dialysis regimen for controlling hyperphosphatemia needs further exploration. It is likely that short frequent rather than prolonged sessions is more effective. Ofcourse, longer dialysis can remove more but at slower rate.
A. CKD stage 5, hypercalcimia, hyperphosphatemia, low PTH, anemia
B. need the following investigation
Bone specific alkaline phosphotase, 1,25 vitD, 25 vit D, iron study, chest x-ray
Patient need to stop calcium tab. And alfa calcidol and give him non calcium containing phosphate binders
ESRD on HD with mild hypercalcemia and mild hyperphosphatemia and low normal iPTH
the impression is an adynamic bone disease(iatrogenic)
B. What would be your next management plan?
stop calcium and one alfa
follow-up the level of Ca, po4,iPTH,25-OHvit-D, and ALK.phosphatase(bone-specific)
Lateral ABD-XR and Echo
If persistent hypercalcemia, dialysis against low path Ca. and start workup for hypercalcemia.
mild hyperphosphatemia and hypercalcemia
use of low calcium dialysate, and follow up
if no improvement: investigation for hypercalcemia espicially in the presence of dry cough
ACE level, Vit D level
A. Interpret the above laboratory investigation.
ESRD with hypercalcemia and hyperphosphatemia.
B. What would be your next management plan?
stop calcium-containing binders
A. Interpret the above laboratory investigation
Treatment goals in CKD5D:
So: hyperCa, hyperP and PTH is below the target with mild anaemia
B. What would be your next management plan?
She is on calcium carbonate 2000 mg per day (800mg elemental Ca).
index case has hypercalcemia may be a result of:
Young female with an unclear underline cause of her ESKD and persistent dry cough, I would like to exclude granulomatous disease (Sarcoidosis, TB and lymphoma).
My approach:
Ensure adequate HD with low Ca dialysate
Dietitian review
D/C Calcium Carbonate
Consider non-calcium-based phosphate binder
Workup for hyperCa:
Hx (drug Hx very important ) and clinical examination
Rule out sarcoid, lymphoma and TB (CXR,1,25 vit D and 25 vit D, Sputum AAFB, ACE level, blood film, lymph node bx if exist, etc.).
A-ESRD , hyper Ca hyper phos, low PTH, mild anemia
low turn over MBD
B- stop calcium
stop one Alfa
use low dialysate calcium.
CXR
CT chest
TB screen
repate after 3 months PTh and ca phos within 1 month .
Interpret the above laboratory investigation.
ESRF with hypercalcemi and hyperphosphatemia, with low PTH FOR DIALYSIS MIDDLE AGE FEMALE
What would be your next management plan?
REVIEW ALL HISTORY AGAIN, DRUG HISTORY
stop any drug us or interact with ckd mbd drugs
ask fo full updated Lab results add PTH , bon specific ALK, 2hydroxy vit D level
x ray for the skull, pelviabd us ,HRCT,
ESRD pt, hypercalcemia, hyperphosphatemia, low PTH, possible low turnover bone ds
next step: stop calcium and alfacalcidol supplements, dialyse against low calcium dialysate, check for 25OH vitamin D, HRCT chest
ESKD with hypercalcemia and hyperphosphatemia.
Next management plan
stop calcium-containing binders
Cxray
AFB
Hypercalcaemia, hyperphosphatemia, PTH below optimal level
Stop Ca based binders
Stop active vit D
Use non Ca based binders
Work up for HYPERCALCEMIA with low PTH
A. Interpret the above laboratory investigation.
ESKD , hypercalcimia , hyperphosphatemia, low PTH, mild anemia.
B. What would be your next management plan?
stop calcium and start non calcium phosphate binders
stop one Alfa
use low dialysate calcium.
CXR and CT chest
TB screen
follow up of ca ,ph , PTH .
A)case of hypercalcemia ,hyperphosphatemia and low pTH
B)stop ca supplement and alfacalcido
if high ca not improved give non ca containing phosphate binder
dialysis with low ca dialysate(1.25) can improve ca and pth level
measure PSALP
chest Xray for her chest problem
A. Interpret the above laboratory investigation.
ESRD- Hpercalcemia- Hyperphosphatemia – Low PTH
B. What would be your next management plan?
1-Stop calcium carbonate and alphacalcidol
2-Start non calcium containing phosphate binders.
3- Low calcium dialysate.
4- chest X ray.
5- Measure Vitamin D level and ACI level .
Lab investigations show hypercalcemia and hyperphosphatemia, the iPTH is within the recommended range, Hb is slightly lower than recommended
Since he has hypercalcemia, I would look for causes of hypercalcemia, and since he is coughing then he may have TB or Sarcoid (contributing to hypercalcemia)
so CXR / HRCT / Sputum culture and AFB / and serum ACE
I will have to stop his CaCO3 and VitD3
Lab investigations show:hypercalcemia,hyperphosphatemia,accepted PTH level(2 times more than the normal range) and anaemia(HB level accepted for patient on CHD)
What would be your next management plan?
1-Stop calcium carbonate and alphacalcidol
2-if serum phosphorus is not improving, start non calcium containing phosphate binders(sevelamer)
3- Check drugs that cause cough like ACEI, ARBS and omperazole.
4- chest radiology to exclude any chest radiology .
5- Measure Vitamin D level
6-Follow up serum ca ,po4, and PTH.
Interpret the above laboratory investigation.
ESRD- Hpercalcemia- Hyperphosphatemia- Anemia
What would be your next management plan?
Cough: rule out TB and sarcoidosis by CXR, sputum AFBx3, and sputum C/S, and ACE level.
Stop the Calcium and Vitamin D
Monitor PTH , calcium and vitamin D level
…
A. Interpret the above laboratory investigation.
ESRD with Hypercalcemia, hyperphosphatemia, hyperparathyroidism, and anemia.
B. What would be your next management plan?
As I don’t have much info about the reason for ESRD in this young patient, and in view of hx of persistent cough for 2 months, and taking into consideration the biochemical parameters results, I would investigate for granulomatous disease in such patient.
I would explain my thought process, young female with ESRD and chronic cough, could be sarcoidosis. Sarcoidosis might started years back, with hypercalcemia, she might had long standing nephrolithiasis, leading to nephrocalcinosis, with/or without interstational nephritis, which eventually resulted in ESRD. If I continue to believe in Sarcoidosis as a primary disease, that means her 1-25 Vit D is high, due to increase activation of 1-alpha hydroxylase in the abundant macrophages. High 1-25 vit D, increases intestinal absorption of Ca, and PH.
Other cause of granulomatous disease, TB. It could be that this patient is having TB due to her immunocompromised status. Since TB is granulomatous disease too, and has high number of macrophages. The 1-25 VitD would increase and Ca, and PH would increase too due to high intestinal absorption.
I would stop Ca, and alfacalcidol.
I would order CXR, sputum AFBx3, and sputum C/S, and ACE level.
I would check if the patient has any skin lesion, or lymph node which could be biopised as sometimes if would be difficult to reach such diagnosis.
Interpretation of the result
Plan
D/C alfacacidol
A: The patient is having CKD – Stage 5 (on RRT), with Hypercalcemia, Hyperphosphatemia, Anemia and an elevated PTH
B: Cough:
Enquire about constitutional symptoms ( night sweats, hemoptysis, LOA, LOW,
dyspnoea, PND, orthopnoea, etc)
Enquire about smoking – possible risk factor for Ca lung
Enquire about any other meds that patient is using, esp ACE-inhibitors
Investigations:
CXR + CT Chest: evaluate lung fields and mediastinum
Echocardiogram: exclude any cardiac causes for coughing
Serum ACE for Sarcoidosis
Biochemical abnormalities:
The abnormalities seen with the Calcium and Phosphate is most probably driven
by her current meds: Vitamin D and Calcium-containing phosphate binder – STOP
the meds, and change onto a Non-Calcium containing phosphate binder.
Improve/educate patient on low phosphate containing foods
Monitor the Ca, PO4 and PTH – in order to restart the Vit D
A- interpretation of investigation hypercalcimia, hyperphosphatemia,high pth level and anemia.
B- management plane stop vit d and ca and follow up and do chest x-ray to detect the cause of cough
Ca load from phosphorus binding Ca Carbonate together with active vitamin D plays a role in hypercalcemia. Stopping calÅŸcitriol and shifting to sevelamer or low-dose Lantanum will help decrease calcium load and phosphorus absorption minimally increase with active vitamin D. After PTH returns to around 300, we may restart the lower dose of Calcitriol.
female pt. 36y/o esrd on regular HD since 3y on caco3 200mg and alfacalcidiol 0.5 mic
lab investigation revealed :-
anemia
hypercalcemia
hyperphosphatemia
suppressed iPTH
Action plan :-
should be stop ca phosphat binder ca carbonate and shifting to non ca phosphate binder
and stop alfacalcdiol
and search about dry cough review the medication exclude ACEI
investigate pt. for dry cough and 2ry hypercalcemia
chest x-ray to rule out TB
Follow up and observation
Interpret the above laboratory investigation.
This patient is having ESRD on HD with new onset of chronic cough along with hypercalcemia and hyperphosphatemia and low iPTH .
Her Hb is low compared to her age (non-menopausal age)
The cause of High Ca is the use of Ca supplements along with the use of Vita AND both of them will lead to high Ca and high Phosphorous and this will lead to suppressing the PTH level. This patient is most likely having a low turnover bone disease.
What would be your next management plan?
I would stop the Ca supplement and Vitamin. D and will start non-Ca binder phosphates on the same time I will start to work her up for her dry cough by doing full investigation which includes chest x ray and further chest assessment to rule out secondary causes for hypercalcemia.
PATIENT IS ESKD ON HD MOSTLIKLY HE HAS ADEQUATE DIALYSIS , MILDY ANEMIC , SHE HAS HYPERCALEMIA AND HYPERPHOSPHATEMIA MOSTLY DUE TO OVER TREATMENT , NEEDS TO STOP CALCIUM AND ALFACALCIDOL ADD PHOSPHATE BINDER NONCALCIUM CONTAINING . DIALYSIS WITH LOW CALCIUM DIALYSATE 1.5-2.0 OR EVEN LOWER BUT FOR SHORT PERIOD , TO AVOID BONE DEMINERALIZATION. DETAILED HISTORY AND MEDICATION HISTORY , THEN GO FOR FURTHER INVESTIGATION FOR HER COUGH STARTNIG WITH MEDICATION HISTORY , CXR , PULMONOLOGY CONSULTATION AND
Great! furthermore, PTH level is below the target which should be 2-9 folds of the upper limit in patients with ESKD on HD
management plan
stop caco32- and alfacalcidol for some time and review with repeat bloods
cxr
1-25 oh levels
ace levels
ca dialysate 1.25
Agree, but the patient will be still in a need of non-calcium containing phosphate binder
A non-calcium containing phosphate binder is needed as well.
interpret above laboratory investigation?
CKD 5D
anaemia of ckd likely
hypercalcaemia on calcium carbonate and alfacalcidol
pth 127 ( Possibly suppressed)
In context of chronic cough need to rule out tb/sarcoid
Agree that PTH level is below the target which should be 2-9 folds of the upper limit in patients with ESKD on HD
A. Interpret the above laboratory investigation.
B. What would be your next management plan?
*Differential diagosis of cough in this patient
Further investigations
Interventions
Put her a transplant list
Thank you for your comprehensive answer!
wlcm
A- A case of ESRD with average s.cr with hypercalcemia ,hyperphosphatemia with suppressed iPTH ( mostly low turnover bone disease) caused by over treatment with calcium and active vit D in addition to normal Hgb as compared to the target value for this population .
B- management plan
1-stop calcium supplemention immediately
2-use of non calcium containing po4 binders instead of calcium containing
3- stop vit D to increase iPTH and decrease hyperphosphatemia
4- Dietary phosphate restriction with the help of po4 pyramid
5- use the least ca dialysate concentration (1.25 mmol)
6- use of nocturnal prolonged daily HD if still persistant high po4
Well done! however, the best dialysis regimen for controlling hyperphosphatemia needs further exploration. It is likely that short frequent rather than prolonged sessions is more effective. Ofcourse, longer dialysis can remove more but at slower rate.
A. CKD stage 5, hypercalcimia, hyperphosphatemia, low PTH, anemia
B. need the following investigation
Bone specific alkaline phosphotase, 1,25 vitD, 25 vit D, iron study, chest x-ray
Patient need to stop calcium tab. And alfa calcidol and give him non calcium containing phosphate binders
Thanks!
Interpret the above laboratory investigation.
B. What would be your next management plan?
Thanks Dr Asharaf! we will need to add non-calcium containing phosphate binder as well.
A. Hypercalcemia , hyperphosphatemia , secondary hyperparathyroidism.
B.switch calcium carbonate to non calcium containing phosphate Binders( like sevelamer or lanthanum) .
Stop calcitriol.
Measure 1,25 OH vitamin D and 25 OH vitamin D.
HD with Dialysate 1,25 Ca
CXR(lymphadenopathy?) , AP, LDH ,if possible rPTH, serum electrophoresis.
Thank you! but PTH level is below the target which should be 2-9 folds of the upper limit in patients with ESKD on HD
A. Interpret the above laboratory investigation.
ESRD on HD with mild hypercalcemia and mild hyperphosphatemia and low normal iPTH
the impression is an adynamic bone disease(iatrogenic)
B. What would be your next management plan?
stop calcium and one alfa
follow-up the level of Ca, po4,iPTH,25-OHvit-D, and ALK.phosphatase(bone-specific)
Lateral ABD-XR and Echo
If persistent hypercalcemia, dialysis against low path Ca. and start workup for hypercalcemia.
Thanks! I think we are adding non-calcium containing phosphate binder to the patient.
A-
CKD G5D
mild hypercalcemia
hyperphosphatemia
inappropriately low PTH(target on dialysis 150–450 pg/l)
hemoglobin level within target
==========================
B:
1-HOLD CALCIUM AND ALFACALCIDOL
2-DIALYSIS WITH DIALYSATE CALCIUM 1.25 MMOL/L
3-FULL HISTORY AND EXAMINATION TO R/O MALIGNANCY ,SARCOIDOSIS ,
4- LAB
1-rPTHpALKALINE PHOSPHATASE
2-1,25(OH)D3
3-CXR ,HRCT,ACE
4-TFT
===========
Thanks Dr.Emad, starting with non-calcium containing phosphate binder and frequent dialysis may help reduce the phosphorus load.
A. Interpret the above laboratory investigation.
B. What would be your next management plan?
Thanks Dr. Ibrahim, starting with non-calcium containing phosphate binder and frequent dialysis may help reduce the phosphorus load as well.