W2S2:

Two years later, the patient was seen in the bone clinic with low back pain. The patient underwent a plain X-ray on pelvis and lumbosacral spines that showed sacroiliac osteoarthritis (sacroiliitis). He had a GFR of 9 ml/min/1.73m2. His new labs are seen in table 2

Test

Value

S. Creatinine

6.9 mg/dL

Hgb

9.8 g/dL

S. Corrected Calcium 

8.5 mg/dL

S. Phosphorus

6.5 mg/dL

S. Potassium

5.4 mmol/L

D. Interpret the patient’s new labs.

E. Discuss the potential mechanisms leading to this clinical profile.

F. Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this.

45 Comments

  • KAMAL ELGORASHI


    Lab result

    • Stage 5 CKD should be planned for initiation dialysis.
    • Anemia.
    • Tend to be hypocalcemic compared with the previous calcium.
    • Hyperphosphatemia.
    • Hyperkalemia.

    The potential mechanism

    • Advanced CKD with reduced kidney function.
    • FGF23 activation.
    • PTH activation (secondary hyperparathyroidism)
    • Hyperphosphatemia and hypocalcemia.
    • Bone resorption (CKD-MBD).

    Bone fragility
    With progressive renal dysfunction, there is reduced vitD activation (hypocalcemia) with reduced Klotho, which activate FGF23 (hyperphosphatemia), and parathyroid gland, with resultant bone resorption and change in bone metabolism and bone osteoblast and osteoclast activity, with bone affection (mineralization, growth, and strength), which result in clinical syndrome CKD-MBD.

  • Rania Mahmoud


    D. Interpret the patient’s new labs.
    ESRD, sever anemia with secondary hyperparathyroidism ,hyperphosphatemia and hyperkalemia
    E. Discuss the potential mechanisms leading to this clinical profile.
    Renal function loss and loss of mass would result in a low level of klotho, resulting in a high FGF23 level and, finally, a low vit D3 level. As a result, Ca and PH intestine absorption would decrease, resulting in low Ca levels and high PTH. Because of the lack of renal excretion function, the PH level would rise. This alteration of metabolic factors in the bone profile would be deleterious to the bone.
    F. Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this.
    Bone fragility associated with CKD-MBD is one of the most complications of CKD. Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels.  
    All together, these factors contribute firstly to secondary hyperparathyroidism, and ultimately increased bone resorption that induces micro- and macrostructural bone changes and leads to low bone mineral density and an increased risk of fracture..

  • Nihal Bashir


    advanced CKD may be even ESRD, sever anemia with secondary hyperparathyroidism uncontrolled PO4
    low Vit D, unopposed PTH secretion, high FGF 23
    patients with bone fragility may have fractures as their first presentation, very high levels of PTH and low calcium levels with increased bone resorption with additive effects of age can cause osteoporotic like picture

  • HASSAN ALYAMMAHI


    D
    with progression from stage 4 to stage 5, patient has further reduction in his Hb, due to further reduction in iron absorption and Erythropoiesis

    The Ca and PO4 are typical of stage 5, with high PO4 because it cannot be excreted, and low Ca because of reduced vitamin D 1a hydroxylation and hence reduced absorption from GIT

    Potassium excretion is also failing because there are few nephron left to handle K load, so it increases in blood

    E
    As CKD progresses, FGF23 increase, Klotho decrease and PTH increase, all trying to get rid of accumulating PO4
    the increase in PTH enhances 1a hydroxylation of VitD, FGF23 does the opposite
    End result at this stage is that PO4 accumulate despite rise in FGF23 and PTH because of reduced nephron mass.
    Ca drops as absorption from GIT decreases due to decreasing 1a-hydroxylation, so hypocalcemia becomes evident
    Hyperkalemia is a manifestation of reduced nephron mass

    F
    High bone turnover causes Over resorption of bone that might start early and continue for long time, it results in under mineralization of bone and microfractures may occur culminating in a clinically evident fractures in late CKD
    Low bone turnover disease cause bone to reduce its repair mechanism, which usually result in a fragile bone, also prone to microfractures that culminates in a clinically evident fractures in late CKD.

  • Muhammad Soobadar


    D- CKD 5 high phosphate, Calcium lower end of normal, anaemia of CKD

    E With progressive CKD increased FGF23 and decreasing klotho there is reduction in 1& hydroxylase and decreased calcium absorption in gut and proximal tubule. there is also increased phosphate . it contributes to secondary hyperparathyroidism and increased PTH that leads to increased bone resorption that induces bone structure changes as well as mineralisation defect leading to increased fracture risk

    F Bone fragility in CKD is complex and no established standardised way of measuring it. Bone turnover, bone quality, bone volume and bone mineralisation are all contributing factors. Bone biopsy is definitive diagnosis and not done routinely and can also not be tolerated by patient. i think as result of above we act once patient have fractures. i am not sure if bone biopsy would have altered management

  • Asma Aljaberi


    D. Interpret the patient’s new labs.
    ESRD with low normal Ca, Hyperphosphatemia, hyperkalemia, and anemia.
    E. Discuss the potential mechanisms leading to this clinical profile.
    The natural process of renal function deterioration and loss of mass, would result in low level of klotho, causing high FGF23 level and eventually low vit D3 level. Therefor, Ca and PH intestinal absorption would decrease and result in low Ca level leading to high PTH. PH level would increase due to loss of renal excretion function. This disruption of bone profile biochemical parameters would negatively affect the bone.
    F. Bone fragility in CKD: frequently silent until advanced stage. Discuss your view Long standing of uncontrolled disrupted bone biochemical parameters, would result in CKD-MBD. Any type of CKD-MBD (osteitis fibrosa, Ostemalacia, or ABD) would have a serious impact on bone health and would increase the patient’s fracture risk leading to high morbidity and mortality. CKD-MBD is usually overlooked by physician and patient himself. Hence if it’s important to assess bone health early in the course of the disease. The following investigations should be done regularly; Bone profile, BTMs, and DXA with TBS to have a better idea about the bone quality. If the CKD-MBD is discovered and treated early, it would mitigate the risk of fragility fractures.

  • Amna Kununa


    Interpret the patient’s new labs

    • CKD V
    • hyperphosphatemia
    • s.Ca lower side of normal
    • anaemia

    Discuss the potential mechanisms leading to this clinical profile

    SHPT occurs in response to a series of mineral abnormalities that initiate and maintain increased PTH secretion:

    • Phosphate retention
    • Decreased Ca
    • Decreased calcitriol
    • Increased FGF23 and decreased klotho
    • The reduced expression of VDRs, CaSRs, fibroblast growth factor receptors, and klotho in the parathyroid glands.

    Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this
    
    These abnormalities result in increased bone resorption and subsequently lead to low bone mineral density and an increased risk of fracture.
    A vitamin D deficiency results in bone mineralization defects. severe Vit D deficiency results in osteomalacia.

  • Areij Alotaibi


    1-advance stage of with anemia, hyperphosphatemia

    2-mechanism: progressive loss of functioning kidney mass, klotho deficiency, increased FGF23, reduced vitamin D activation.
    lab finding with hyperparthyrodism all lead to increasing bone resorbtion and decreasing bone formation
    C. In CKD, low-bone turnover is associated with thin cortices with normal cortical porosity, while high bone-turnover diseases reveal high cancellous bone volume and normal cortical thickness (17). Accordingly, altered cortical bone structure contributes to bone fragility in CKD (36).

  • Rola Kotob


    Interpret the patient’s new labs.
    CKD5 in need to start dialysis, low GFR, anemic, low normal Ca, hyperphosphatemic, hyperkalemic

    Discuss the potential mechanisms leading to this clinical profile.
    As the ckd progresses result in decreasing activation of 1alpha hydroxylaze, low Ca both low calcitroil low ca stimulat PTH release by CaSR, VDRS acting on PTH release and degradation ,
    PTH and FGF 23 at the start increasing P04 excreasion, then with CKD progression FGF and klotho effect on kidney decrease result in increasing PO4, all has feedback axis togother

    Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this. All previous factors contribute firstly to secondary hyperparathyroidism, and ultimately, to micro- and macrostructural bone changes, which lead to low bone mineral density and fragility and an increased risk of fracture.

    As a result of these mechanisms, bone activity increases, osteoid formation is abnormal, immature and non-lamellar, and although this abnormal matrix formed is mineralized, it results in a bone with a lower strength and a greater fragility.

  • Mohamed Abdulahi Hassan


    CKD stage 5 . anemia , hyperphosphatemia and hypocalcemia .
    progressive loss of renal function and mass again goes back to the long precess of pathology FGF23 ,klotho, hypocalcemia .
    ckd-mbd startes in stage 3 onwards

  • Marwa Alm


    A. Labs: CKD G5 for RRT, anemia, hyper-phosphatemia, lower normal Ca.
    B: mechanism: progressive loss of functioning kidney mass, klotho deficiency, increased FGF23, reduced vitamin D activation, with lab abnormalities (hypo-calcemia, hyper-phosphatemia), PTHR hyporesponsiveness, all share increasing bone resorbtion and decreasing bone formation (RANK stimulation, Wnt inhibition)
    C. Bone fragility starts early in CKD G2 (which may be due to renal osteodystrophy or age related osteoprosis), characterized by low bone mineral density and microarchitectural deterioration leading to low bone strength hence increased fracture risk, both can occurs with high/ low turn over bone disease. Fragility increases as CKD progress up to fragility fractures. So follow up should be started early as CKD G 3a for early management & primary/ secondary prevention

  • Rihab Elidrisi


    Interpret the patient’s new labs.
    The patient progress rapidly to CKD stage 5 for HD
    Hyperphosphatemia 
    Hypocalcemia 
    Hyperkalemia 
    Anemia

     Discuss the potential mechanisms leading to this clinical profile.

    This patient has advanced CKD 5 with loss of renal mass, and this will lead to an increase in the FGF23 and a decrease in Klotho. All these with associated with hyperphosphatemia and hypocalcemia, and all changes will increase the PTH level and lead to SHPTH .

    Bone fragility in CKD: frequently silent until the advanced stage. Discuss your view on this.
    As CKD progresses the long high PTH level will affect the Bone mineralisation and osteoid bone formation,and this action will be on both type of bone the cortical, which is 85% of the body bone and the trabecula, which is 15% of the total body bone .

    The CKD-MBD starts ear in ckd through the low-level calcitriol when the eGFR 70 t0 80 , then as the CKD progress, the high level of PTH continues the mineralization effect on the bone (two type of bone) and this will end up with a fragile non lamellar bone .

    Although DEXA scan is not optimal to detect the bone quality but it is still used
    on the other hand we have HR bone quality bone scan which can more precise indetecting the quality of the bone

  • Riaan Flooks


    D: Chronic Kidney Disease – Stage 5, with anemia, hypocalcemia, hyperphosphatemia – hyperparathyroidism

    E: CKD results in nephron loss which results in hyperphosphatemia, form a dietary origin. Associated with an increase in FGF23, and a reduction in Klotho – resulting in hypocalcemia. The aforementioned and the latter results in Vitamin D deficiency and the subsequent development of Hyperparathyroidism.

    F: Bone Fragility:
    This is associated with increased morbidity and mortality
    Associated with the development of secondary hyperparathyroidism

  • MOHAMMED HAJI HASSAN


    D. Interpret the patient’s new labs.

    CKD5, Anemia, Hyperphosphatemia

    E. Discuss the potential mechanisms leading to this clinical profile.

    Low renal mass causes low renal output and increases FGF23 and low clotho with low vitamin leading to Hypocalcemia and Hyperphosphatemia with high PTH causing secondary Hyperparathyroidism.

    Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this:

    Bone fragility associated with CKD-MBD is very complex, High PTH,increase FGF23, Hypocalcemia and Hyperphosphatemia associated with bone resorption that induces micro- and macrostructural bone changes and leads to low bone mineral density and an increased risk of fracture.

  • Elsayed Ghorab


    a- pt. progressing to CKD stag 5 anemia hyper hyperphosphatemia
    b- the potential mechanism in this pt. complicated CKD-MBD
    increasing FGF23 to compensate hyperphosphatemia . decrease klotho
    decrease 1-alfa calcidiol – hyperphosphatemia – decrease erythropoietin-H
    increase uremic toxins
    all these factor lead to high turn over bone disease and increase bone fragility and bony ache

  • Rabab ALaa Eldin keshk Rabab


    D- investigation interpretation s5 ckd anemia hyperphosphatemia.
    E-the potential mech.loss if renal tissue decrease in koltho and increase in fgf23 and decrease of active vit d so leading to increase in pth and increase bone resorption
    F- yes with progression of ckd the secondary hyperparathyroidism occur leading to high bone turn over causing increase bone fragility

  • Hagar Ali


    D-the case progress and become CKD stage 5,hyperphosphatemia ,ca decreased ,anemia
    E-loss of renal mass increase FGF 23 ,decrease klotho and decreased 1 alpha hydroxylase lead to hypocalcemia ,hyperphosphatemia and secondary hyperparathyroidism.
    F-yes ,hyperparathyroidism lead to high bone turn over which lead to fragility this is apart from bone mineralization defect and mixed type

    • Rabab Elrefaey


      Thankyou dr Hagar.
      Bone fragility associated with CKD-MBD is one of the most devastating complications of CKD. Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels. All together, these factors contribute firstly to secondary hyperparathyroidism, and ultimately increased bone resorption that induces micro- and macrostructural bone changes and leads to low bone mineral density and an increased risk of fracture. A vitamin D deficiency is common in CKD patients, and low circulating 25(OH)D levels are invariably associated with high serum PTH levels and rarely mineralization defects, such as osteomalacia in case of severe forms of vit D deficiencies.

  • Asmaa Salih KHUDHUR


    Interpret the patient’s new labs.
    The patient progress rapidly to CKD stage 5 for HD
    Hyperphosphatemia 
    Hypocalcemia 
    Hyperkalemia 
    Anemia

    Discuss the potential mechanisms leading to this clinical profile.

     As the kidney function decreased due to loss renal mass with reduced urine output , the increased FGF23 become not functioning as phosphaturic action .decrease klotho with impaired kidney activation of vitamin D3 due to decreased 1 & hydroxylase , this lead to impaired intestinal absorption of Calcium with the resultant hypocalcemia, which in edition to hyperphosphatemia cause secondary hyperparathyroidisim 
    To maintain blood level of calcium and lead to high bone turn over with bone resorption and decrease bone density.

    Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this.

    CKD patients present a more fragile bone with a higher risk of fractures. Unfortunately, the measurement of bone mineral density (BMD) by bone densitometry (DXA) does not capture the quality of bone (cortical and trabecular microarchi- tecture), but it can be assessed using high-resolution quantitative peripheral computed tomography (HR-pQCT).

    High serum PTH levels accelerates bone turnover, PTH stimulates bone cell proliferation and the activity of each remodeling unit, and also increases the recruitment of new bone remodeling units .As a result of these two mechanisms, bone activity increases, osteoid formation is abnormal, immature and non-lamellar, and although this abnormal matrix formed is mineralized, it results in a bone with a lower strength and a greater fragility.

  • Ahmed Altalawy


    D. Interpret the patient’s new labs.

    • ESRD for hd.
    • Anemia 
    • Hyperphosphatemia
    • Low normal s.ca.
    • high S. K.

    E. Discuss the potential mechanisms leading to this clinical profile.

    With progression of his CKD and loss of kidney mass FGF23 will increase to very high levels also klotho deficiency both lead to low calcitriol level due to inhibition of alfa hydroxylase enzyme lead to hypocalcemia and high Po4. Which enrolled secretion of more PTH, down regulation of calcium sensing receptor on parathyroid gland, and decrease PTH degradation with consequence bone morphological and architecture changes.

    F. Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this.

    With progression of CKD , compensatory mechanisms protect against rapid biochemical changes on expense of bone quality till severe affection of bone .

    • Rabab Elrefaey


      Thank you dr Ahmed.
      Bone fragility associated with CKD-MBD is one of the most devastating complications of CKD. Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels. All together, these factors contribute firstly to secondary hyperparathyroidism, and ultimately increased bone resorption that induces micro- and macrostructural bone changes and leads to low bone mineral density and an increased risk of fracture. A vitamin D deficiency is common in CKD patients, and low circulating 25(OH)D levels are invariably associated with high serum PTH levels and rarely mineralization defects, such as osteomalacia in case of severe forms of vit D deficiencies.

  • Israa Hammoodi


    D. The patient progress to stage 5, increase anemia, hypocalcimia, hyperphosphatemia, hyperkalemia
    E. As GFR decrease lead to decrease urinary excretion of potassium and phosphorus, vitamin D synthesis decrease due to decrease activity and secretion of 1 alfa hydrxylase from reduced kidney mass and increase FGF23, decrease intestinal absorption of calcium lead to hypocalcimia which will cause stimulation of PT gland to secrete PTH which causes increase bone turnover, increase osteoblast and osteoclast activity and stimulate secretion of 1 alfa hydrxylase to increase calcitriol level
    F. Yes it become evident in advanced stage so indicate the importance of evaluate not only laboratory but also use of DXA scan to assess the patient for fragility risk and use of FRAX scores.

  • Khaldon Rashed Ahmed Moqbil


    D-ESRD ,anemia , mild hyperkalmia and hyperphosphatemia (Renalosteodystrophy)

    E- ⬇️ eGFR lead
    ⬆️po4
    ⬇️ FGF23
    ⬇️ Acive form vid d

    F-
    yes totaly agree
    2nd PTH ➡️ increase bone turnover lead yo abnormal osteoid formation

  • Mahmoud Elsheikh


    1-

    • ESKD for RRT.
    • anemia 
    • hyperphosphatemia
    • normal s.ca.
    • highS. K.

    2
    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.
    .
    3
    kidney function decrease 
    s. calcium level with decreased phosphate excretion leading to hyperphosphatemia and secondary hyperparathyroidism
    THE
    PTH RESISTANCE. with increase bone resorption.

  • Ben Lomatayo


    D. Interpret the patient’s new labs?

    • Unfortunately, this patient had rapidly progressed to CKD-5G in a span of only two years (eGFRwas ~24 ml/min/1.73m2)
    • There is something wrong with this patient because he just progressed awkwardly.
    • So we need to look for factors associated with rapid progression of CKD e.g., acidosis, severe secondary hyperparathyroidism, proteinuria ..etc.
    • Comparing with the previous two years, now he had more anemia, developed low normal Ca, hyperphosphatemia and rising K levels
    • The drop in Ca, and increase in PO4 at this stage of CKD5G are suggestive of secondary hyperparathyroidism

    E. Discuss the potential mechanisms leading to this clinical profile?

    • Bone pain in advanced CKD or kidney failure is highly suggestive of CKD-MBD
    • Here is the story; High iPTH or severe secondary hyperparathyroidism leads to high turn over bone disease, which ultimately contribute tolow bone strength , bone pain & fragility fracture.
    • This goes beyond the bone and results in vascular calcification which is important cause of CVD morbidity & mortality in these cohorts of patents.
    • Other factors include: osteoporosis, vitamin D deficiency or osteomalacia, and aluminum bone disease

    F. Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this.

    Yes, agree with the above statements due the following factors in advanced CKD:

    • High iPH : accelerate bone turn over, stimulate bone cell proliferation and activity of each remodeling unit and recruit new remodeling unit
    • Bone activity increases
    • Osteoid formation is abnormal (but mineralized), immature and non-lamellar
    • Low bone strength
    • Greater fragility
  • Alaa Abdel Nasser


    New lab shows more progressive deterioration of renal function eGFR 9ml/min/1.73m2 (CKD stage 5),anaemia becomes more evident,normal serum calcium,hyperphosphatemia and high normal serum potassium.

     In the early stages of CKD, high levels of FGF23 attenuate hyperphosphatemia(it 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) at the expense of 1,25(OH)2vitamin D suppression, thus initiating the development of secondary hyperparathyroidism.
    With CKD progression, with reduction of klotho expression and renal mass,FGF23 cannot decrease serum phosphate level leading to hyperphophatemia.

    Frequently silent until advanced stages, bone fragility associated with chronic kidney disease-mineral and bone disease (CKD-MBD) is one of the most devastating complications of CKD.
    Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels.
    Altogether, these factors contribute firstly to secondary hyperparathyroidism, and ultimately, to micro- and macrostructural bone changes, which lead to low bone mineral density and an increased risk of fracture.
    A vitamin D deficiency is common in CKD patients, and low circulating 25(OH)D levels are invariably associated with high serum parathyroid hormone (PTH) levels as well as with bone mineralization defects, such as osteomalacia in case of severe forms.

  • ahmed bhnassi


    Interpret the patient’s new labs.

    • More deterioration of his kidney function and more loss of kidney mass which is clear in progression of his CKD stage, Low Hb and hyperphosphatemia, normal serum calcium, his K at upper normal level.

    Discuss the potential mechanisms leading to this clinical profile.
    With progression of his CKD and loss of kidney mass FGF23 will increase to very high levels also klotho deficiency both lead to low calcitriol level due to inhibition of alfa hydroxylase enzyme lead to hypocalcemia and high Po4. Which enrolled secretion of more PTH, down regulation of calcium sensing receptor on parathyroid gland, and decrease PTH degradation with consequence bone morphological and architecture changes.
     Bone fragility in CKD: frequently silent until advanced stage. Discuss your view.
    loss of the ability to maintain mineral hemostasis, hyperphosphatemia and secondary hyperparathyroidism with PTH hypo responsiveness all lead to bone resorption, and abnormal bone turnover.
    PTH increased in early CKD stages with subsequent activate on bone remodeling exert bone changes in early disease and may be silent process, The bone turnover rate affects both the cancellous (trabecular) and the compact (cortical) bone, and it depends on the activity of the bone remodeling units regulated by multiple factors, including PTH, which plays a key role in the remodeling process.
    High serum PTH levels accelerates bone turnover, PTH stimulates bone cell proliferation and the activity of each remodeling unit, and also increases the recruitment of new bone remodeling units As a result bone activity increases, osteoid formation is abnormal, immature and non-lamellar, and although this abnormal
    matrix formed is mineralized, results in a bone with a lower strength and a greater fragility. serum PTH and bone alkaline phosphatase, are most widely used biochemical parameters to evaluate non-invasively bone activity. serum PTH levels, usually greater than 450 pg/ml, have a reasonable good histological predictive value of accelerated bone turnover, but moderately high PTH values (300–450 pg/ml) do not have good correlation with bone turnover

  • Mahmud ISLAM


    It seems that the patient is now in the end stage but this is unexpected according to the yearly expected deterioration. Of course, it depends, but apart from that we have CKD stage 5 now with doubled creatinine and uncontrolled phosphorus, calcification and sclerosis. this correlates with coronary and aortic calcification. Pelvis score (1+1+1+1) = 4 .
    with advancing of kidney failure, hypocalcemia, vitamin d and calcitriol resistance, hyperphosphatemia and secondary hyperparathyroidism there is a high metabolic bone disease (probably). This can be checked with a DEXA scan despite the limitations. QCT may be preferred if available



    • Great dr Mahmud.
      Bone fragility associated with CKD-MBD is one of the most devastating complications of CKD. Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels. All together, these factors contribute firstly to secondary hyperparathyroidism, and ultimately increased bone resorption that induces micro- and macrostructural bone changes and leads to low bone mineral density and an increased risk of fracture. A vitamin D deficiency is common in CKD patients, and low circulating 25(OH)D levels are invariably associated with high serum PTH levels and rarely mineralization defects, such as osteomalacia in case of severe forms of vit D deficiencies.

  • Nour Al Natout


    D. ESKD , condier dialysis or at least AV fistula if patient still not uremic. Stop ACE inhibitor (Lisinopril).
    Hyperphosphatemia because of progression of renal function deterioration.

    E.the Potential mechanism are increassing PTH for years and then because of increased pth hyporesponsivness, decreased renal phosphate excretion by ESRD , decreased klotho in kidney it come to decompensation and hyperphosphatemia.
    High pth especially above 450 is associated with high turnover bone disease.

    F. Yes, because of high PTH there is increased turnover in cortical bone, abnormal osteoid formation, osteoid is immature and non lamellar and this lead to greater bone fragility.
    Low vitamin D, the formation of calcium phosphate complex on the setting of hyperphosphatemia will aggrevate his bone disease.

  • Ashraf Ahmed Mahmoud


    Interpret the patient’s new labs.

    • ESKD for RRT.
    • anemia and hyperphosphatemia
    • normal s.ca.
    • high normal K.

    . Discuss the potential mechanisms leading to this clinical profile.

    decrease renal mass increase FGF23 causes hyperphosphatemia low vit D low Ca absorption .
    .
    Bone fragility in CKD: frequently silent until advanced stage. Discuss your view .

    with deterioration of kidney function decrease s. calcium level with decreased phosphate excretion leading to hyperphosphatemia and secondary hyperparathyroidism .
    with PTH hypo responsiveness. with increase bone resorption.

  • Weam El Nazer


    D. Interpret the patient’s new labs.
    progressive loss of GFR (CKD stage 5 now), with hyperphosphatemia and S. calcium levels in the lower normal range. there are early signs of secondary hyperparathyroidism

    E. Discuss the potential mechanisms leading to this clinical profile.

    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

    F. Bone fragility in CKD: frequently silent until an advanced stage Discuss your view on this.

    Damaged kidneys can’t change vitamin D to its active form, and this can lead to bone weakness. In kidney disease, too much parathyroid hormone is released to keep calcium levels in the blood balanced. By taking calcium from the bones, the bones become weaker. With the progressive loss of the GFR, the Vit-D level will be low and more resistant to the action of PTH on the bones.

  • Mark Nagy Zaki Amin Mark


    D- as compared to previous labs :
    A progressive decrease in GFR , decrease HGB levels , decreased calcium levels with hyperphosphatemia and upper normal potassium levels
    E- with progression of renal function there is associated decrease in calcium levels with decreased po4 excretion leading to hyperphosphatemia and secondary hyperparathyroidism leading to bone marrow fibrosis and contribute to more progressive course of HGB drop as well as increased potassium levels
    PTH assays and vit D levels need to be checked in this patient



    • Great dr Mark.
      Bone fragility associated with CKD-MBD is one of the most devastating complications of CKD. Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels. All together, these factors contribute firstly to secondary hyperparathyroidism, and ultimately increased bone resorption that induces micro- and macrostructural bone changes and leads to low bone mineral density and an increased risk of fracture. A vitamin D deficiency is common in CKD patients, and low circulating 25(OH)D levels are invariably associated with high serum PTH levels and rarely mineralization defects, such as osteomalacia in case of severe forms of vit D deficiencies.

  • Emad mohamed mokbel Salem


    D-
    CKD G5 ND
    anaemia
    Hyperphosphatemia
    Mild hyperkalemia
    Serum calcium within normal range
    Sacroiliac OA

    E-
    Progression of CKD and loss of nephron mass and dietary phosphate
    And loss of action of FGF23 because decrease klotho
    Elevated parathyroid level

    F-
    In early ckd
    There compensatory mechanism to maintaining mineral bone haemostasis

    As the kidney function decline there is progressive loss of the ability to maintain mineral haemostasis and normal bone turnover



    • Good job dr Emad.
      Bone fragility associated with CKD-MBD is one of the most devastating complications of CKD. Its pathophysiology includes the reduction of active vitamin D metabolites, phosphate accumulation, decreased intestinal calcium absorption, renal alpha klotho production, and elevated fibroblast growth factor 23 (FGF23) levels. All together, these factors contribute firstly to secondary hyperparathyroidism, and ultimately increased bone resorption that induces micro- and macrostructural bone changes and leads to low bone mineral density and an increased risk of fracture. A vitamin D deficiency is common in CKD patients, and low circulating 25(OH)D levels are invariably associated with high serum PTH levels and rarely mineralization defects, such as osteomalacia in case of severe forms of vit D deficiencies.

  • Abdulrahman Almutawakel


    STAGE 5 CKD , HYPERKALEMIA , HYPERPHOSPHATEMIA , INDICATED FRO INITIATION OF DIALYSIS , PHOSPHATE BINDERS NON CALCIUM BASED , ESA , FURTHER INVESTIGATION NEEDED



    • Thanks dr Abdulrahman.
      please can you answer these questions also.
      E. Discuss the potential mechanisms leading to this clinical profile.
      F. Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this.

  • Ibrahim Omar


    D. Interpret the patient’s new labs.

    • advanced CKD with ESRD.
    • moderate anemia and hyperphosphatemia.

    E. Discuss the potential mechanisms leading to this clinical profile.

    • rapid decline in GFR due to the progression of a serious underlying disease rather than a usual progression of CKD by GFR loss of 5-10 ml/min/year.
    • there may be additional risk factors such as uncontrolled HTN, hyperuricemia, NSAIDs for bony pains, superimposed obstructive uropathy due to BPH,… etc

    F. Bone fragility in CKD: frequently silent until advanced stage. Discuss your view on this.

    • a degree of compensation is maintained until late stages of CKD
    • related symptoms are usually attributed to the underlying CKD or aging.
    • chronic symptoms are usually tolerated until late stages.

Leave a Reply