Scenario 2 - Part 1:
A 19-year-old male on regular hemodialysis for three years, presents for pre-transplant assessment. The patient reported recurrent attacks of severe bone and joint aches. The patient was taking sevelamer three times per day with meals and alfacalcidol 0.25 mcg three times a week.
Review of the patient’s laboratory investigations are shown in table 1:
|
Test |
Value |
|
S. Creatinine |
4.5 mg/dL |
|
Corrected s. Calcium |
7.4 mg/dL |
|
S. Phosphorus |
2.2 mg/dL |
|
25 (OH) Vit D |
10 ng/mL |
|
iPTH |
740 pg/mL |
|
Total alkaline phosphatase |
558 U/L |
X-ray of hip joints and iliac bones revealed rickets like rotting fence-post appearance with subchondral bone resorption at sacroiliac joints:
Computed tomography of the spine is shown in figure 1
A. Interpret the above laboratory investigations.
B. Interpret the abnormality in the above image.
C. What is the most likely cause beyond the patient’s spine abnormality?
D. How would you approach this case?
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A. Interpret the above laboratory investigations.
B. Interpret the abnormality in the above image Rugger jersey spine
C. What is the most likely cause beyond the patient’s spine abnormality?
It is diagnostic for osteosclerosis due to long-standing (untreated) hyperparathyroidism in ckd. It is caused by a difference in the density of normally mineralised bone and newly formed unmineralised bone (osteoid) at the vertebral endplates. In CKD with untreated hyperparathyroidism, osteoclasts increase bone resorption, which subsequently causes an increase in osteoblast activity. The osteoblasts form the new bone in the presence of low calcium levels and therefore the osteoid is low in hydroxyapatite and appears more opaque on radiographs. This difference in hydroxyapatite content between osteoid and normally mineralised bone causes the distinct striped pattern of the rugger-jersey spine.
D. How would you approach this case?
A. Interpret the above laboratory investigations.CKD patient with hypocalcemia, hypophosphatemia, Vit D def, Secondary hyperparathyroidism, and high TALP.
B. Interpret the abnormality in the above image.Rugger jersey spine is an alternating sclerotic-lucent-sclerotic appearance of vertebrae.
C. What is the most likely cause beyond the patient’s spine abnormality?Secondary hyperparathyroidism and osteomalacia
D. How would you approach this case
D. Improving vitamin D deficiency is the cornerstone in this patient’s management. Beside good dietary supplementations and sun exposure, patients with serum 25(OH)D <12 ng/mL (30 nmol/L), initial supplementation for 8 weeks with Vitamin D3 either 6,000 IU daily or 50,000 IU weekly can be considered. Once the serum 25-hydroxyvitamin D level exceeds 30 ng/mL, a daily maintenance dose of 1,000 to 2,000 IU is recommended. Stopping phosphate binders is required as the phosphorus level is on the lower side. Controlling the hyperparathyroidism with vitamin D receptor agonists will help to suppress the high bone resorption and improve the skeleton.
C. In chronic kidney disease with untreated hyperparathyroidism, there is an increased bone resorption by overactive osteoclasts, which subsequently causes an increase in osteoblasts activities. The osteoblasts form the new bone in the presence of low calcium levels and therefore the osteoid is low in hydroxyapatite and appears more opaque on radiographs. This difference in hydroxyapatite content between osteoid and normal mineralized bone causes the distinct striped pattern of the rugger-jersey spine
A. The patient presented with hypophosphatemia, hypocalcemia and high PTH level. Severe vitamin D deficiency in this case could contribute to these abnormalities. High alkaline phosphatase level reflects mostly high turnover bone disease.
B. The spines show alternating dense-lucent-dense appearance that is called rugger-jersey spine. It is commonly caused by osteosclerosis due to long standing untreated hyperparathyroidism.
Secondary hyperparathyroidism with high alkaline phosphatase , hypocalcemia and hypophosphatemia and hypovitaminosis D.
Rugger jersey
stop sevelamer
increase dose of alfacalcidol
add vitamin d
increase dialyse calcium
after improvement of serum calcium , add cinacalcet
A. Interpret the above laboratory investigations.
CKD-HD
Hypocalcemia-Low VD- Hypophospahtemia- High PTH and High ALP consistent with secondary hyperparathyroidism
B. Interpret the abnormality in the above image.
Collapsing of intervertebral discs with increased translucency in vertebral bodies seen in Rugger jersey spine
C. What is the most likely cause beyond the patient’s spine abnormality?
Secondary Hyperparathyroidism is most likely the cause
D. How would you approach this case?
Stop sevelamer
paricalcitol injectioncalcium supplements or use calcium dialysate solution
cinacalcet once serum calcium is normal
If the symptoms persist and iPTH continues to increase surgery is advised
A.Interpret the above laboratory investigations.secondary hyperparathyroidism, hypovitaminosis D , hypocalcemia and high level total alkaline phosphate.
B. Interpret the abnormality in the above image.osteomalacia (Rugger jersey spine)
renal osteodystrophy
C. What is the most likely cause beyond the patient’s spine abnormality?subperiosteal reabsorption due hyperparathyroidism , and hypophosphotemia
D. How would you approach this case?give vitamin d
calcium and iv phosphate
Secondary hyperparathyroidism with high alkaline phosphatase , hypocalcemia and hypophosphatemia and hypovitaminosis D.
Rugger jersey spine
Secondary hyperparathyroidism( high turnover bone disease)
stop sevelamer
increase dose of alfacalcidol
add vitamin d
increase dialyse calcium
after improvement of serum calcium , add cinacalcet
Laboratory investigations revealed
Sever 2HPTH and elevated ALP, with hypocalcemia and hypophosphatemia.
Bone image
Severe bone resorption, with bone loss and osteomalacia.
The cause of the abnormality
Severe uncontrolled 2HPTH
Approach
A. Interpret the above laboratory investigations.
B. Interpret the abnormality in the above image.
C. What is the most likely cause beyond the patient’s spine abnormality?Secondary Hyperparathyroidism
D. How would you approach this case?
Low Ca/P and vitamin D with high PTH and high ALP is consistent with high turnover bone disease. There is evidence of low bone density (osteomalacia?) of the spine. This patient may have mixed bone turnover. The PTH is also high because of vitamin D deficiency. We can perform a DEXA scan and manage this patient with calcium and vitamin D support in addition to Biphosphonate. I will check Ca/P/PTH later and then may try to increase the calcitriol minimally.
A. Interpret the above laboratory investigations. CKD with decreased levels of calcium , phosphorus , vit D and secondary hyperparathyroidism with elevated alkaline ph. levels denoting high turnover bone disease
B. Interpret the abnormality in the above image. collapse of intervertebral discs with increased translucency in vertebral bodies .
C. What is the most likely cause beyond the patient’s spine abnormality? Secondary Hyperparathyroidism
D. How would you approach this case? Stop the Sevelamer, calcium -containing phosphate binder and also increase his dose of vitamin D, vitamin D analogue .
A- renal impairment with decreased levels of calcium , phosphorus , vit D and secondary hyperparathyroidism with elevated alkaline ph. levels denoting high turnover bone disease
B – collapse of intervertebral discs with increased translucency in vertebral bodies
C – vit D deficiency induced osteoporosis
D – IV alpha hydroxylated vit D , calcium supplementation , IV phosphorus , cinacalcet if needed later after correction of serum calcium first
A)hypocalcemia ,hypophosphatemia,2ry hyperparathyroidism ,low VD with high bone turn over
B)Rugger jersey appearance and features of hyperparathyroidism
c)Secondary hyperparathyroidism
D)treat VD deficiency
add alfacalcidol and ca supplement
A. Has hypocalcimia, hypophosphamia, vitamin D deficiency, increase alkaline phosphotase, hyperparathyroidism
B. Rugger jersey appearance by ct scan and features of hyperparathyroidism in the x ray
C. Secondary hyperparathyroidism and osteomalacia
E. Add calcium supplements, give calcitriol
. Interpret the above laboratory investigations: Vitamin D deficiency which resulted in the patient developing hypercalcaemia and hypophosphataemia, Secondary Hyperparathyroidism
B. Interpret the abnormality in the above image: Rugger-Jersey appearance w
C. What is the most likely cause beyond the patient’s spine abnormality? Secondary Hyperparathyroidism
D. How would you approach this case? Stop the Sevelamer, calcium -containing phosphate binder and also increase his dose of vitamin D, vitamin D analogue
A. the patient has hypocalcemia due to low vitamin D and developed secondary hyperparathyreoidismus and high AP
B. Multiple radiolucent areas separated by radioopaque lines
C. Low vitamin D, low calcium and high PTH causes bone resorption
D. Vitamin D substitution with 25 OH Vitamin D Derivate and increasing active vitamin D receptor agonist (Calcitriol to daily) and the patient should take oral calcium (or calcium carbonate instead of sevelamer).
this patient has high turnover bone disease,as evident by high PTH and increase alk. phosphatase,x- ray showedsclerosis of upper and lower end plate and reduced density of the vetrebral body roger jersy spine. we could increase the dose of alfacalcidol to suppress PTH and correct hypocalcemia & hypophosphatemia
A. Interpret the above laboratory investigations.
CKD 5D
Hypocalcemia
Hypophosphatemia
Vitamin D deficiency
High PTH
High ALP
SHPT
High bone turnover
B. Interpret the abnormality in the above image.
There’s sclerotic bands in the vertebral bodies end plate goes with rugger jersey spine of osteosclerosis.
C. What is the most likely cause beyond the patient’s spine abnormality?
SHPT
D. How would you approach this case?
First we should do US scan of the parathyroid gland , if < 1cm start medical treatment with cinacalcit, vitamin D and alfacalcidiol, calcium carbonate between meals , stop sevelamer, adequate sun exposure at the periphery of the mid day, regular monitoring of ca , po4 and PTH .
If no benefit after 3-6 months
OR
If the gland > 1cm
Then go for surgery/parathyroidectomy.
Localize the gland by SISTEMBI scan .
HYPOCALCIMIA , NORMAL PHOSPHOROUS , LOW VIT D WITH BONE RESORPTION .SO PATIENT HAS HIGH BONE TURNOVER , STOP PHOSPHATE BINDER , START ON CALCIUM , VIT D , VIT D ANALOG IV MAY IT WILL HELP , CAN ADD CINACALCET AFTER NORMALIZATION OF CALCIUM
A
this gentleman has SHPT with low PO4 (because of Sevelamer) with defeciency in VitD, High bone turn over
B
Rugger Jersey appearance typical of high bone turnover
C
SHPT
D
*VitD supplements
* stop sevelamer
*CaCO3
*Cinacalcet once serum Ca becomes normal
A- interpretation of lab
hypocalcemia low vit d level low normal po4 high pth mostly due secondary hyperparathyroidism high alkaline phosphatase those finding indicate high bone turn over.
B- image interpretation Rugger Jeresy spine disease. there is hypodensity of vertebral bodies with sclerotic bands at the ends.
C- the most likely cause dueto high bone turn over dueto secondary hyperparathyroidism.
D- stop sevelamer,correct hypovitaminosis d by giving patient 50000 / wk for 12 wk andca carbonate supplement and after correction of serum ca can we start cinacalcite for fear from hypocalcemia
A. Interpret the above laboratory investigations.lab . revealed
hypocalcemia
hypophosphatemia
vit deficiency
HPTH w high alkaline phosphatase
impression high turnover bone 2ry to HPTH
B. Interpret the abnormality in the above image.Osteolytic bone lesion
Rugger Jersey spine disease
C. What is the most likely cause beyond the patient’s spine abnormality?2ry HPTH
D. How would you approach this case?
alfacalcidole 0.25 od and cinacalcet added according the trend of PTH level
ca co3 2h after meal or before meal as calcium supplement
vit. D supplement
A. Interpret the above laboratory investigations.CKD 5D ,
SHPT with high bone turnover(elevated PTH ,high ALP ,hypocalcemia )
hypophosphatemia
hypovitaminosis D
B. Interpret the abnormality in the above image.Rugger Jeresy spine disease
C. What is the most likely cause beyond the patient’s spine abnormality?due to SHPT with high bone turnover
D. How would you approach this case?1-correct vitamin D deficiency
2-start calcium carbonate andincrease dose of alfacalcidol AND HOLD SEVELAMER
3-fu bone profile /2 weeks and PTH
A. Interpret the above laboratory investigations.
B. Interpret the abnormality in the above image.
C. What is the most likely cause beyond the patient’s spine abnormality?
D. How would you approach this case?
A. Interpret the above laboratory investigations.
B. Interpret the abnormality in the above image.
C. What is the most likely cause beyond the patient’s spine abnormality?
D. How would you approach this case?
A. Interpret the above laboratory investigations.Insufficient amounts of vitamin D, lead to hypocalcemia and hypophosphatemia.
iPTH and ALP levels that are high are suggestive of secondary hyperparathyroidism.B. Interpret the abnormality in the above image.
rugger-jersey spine(subperiosteal resorption with loss of bone density with sclerotic band
C. What is the most likely cause beyond the patient’s spine abnormality?
secondary hyperparathyroidism
D. How would you approach this case?
I will increase the vitamin D dose or give an analogous vitamin D.
add calcium carbonate.
-stop sevelamer
A.Interpret the above laboratory investigations.
B. Interpret the abnormality in the above image.
C. What is the most likely cause beyond the patient’s spine abnormality?
D. How would you approach this case
Note: sevelamer must be stop, because Pi is now below the target according to KDIGO guidelines. Hypophosphatemia can also results from vitamin D deficiency but this is rare in CKD5D
Interpret the above laboratory investigations.
B. Interpret the abnormality in the above image. .thoracolumbar spine with dense end- plates produce rugger-jersey spine diagnostic for osteosclerosis.
C. What is the most likely cause beyond the patient’s spine abnormality?secondary hyperparathyroidism with high bone turnover.
D. How would you approach this case?
start vitamin D.3000 iu daily
follow up Alk ph .PTH.s.Ca .ph
parathyroidectomy.