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.
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Lab result
The potential mechanism
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.
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..
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
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.
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
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.
Interpret the patient’s new labs
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:
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.
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).
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.
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
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
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
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
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.
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
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
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
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.
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.
Very good dr Asmaa
D. Interpret the patient’s new labs.
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 .
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.
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.
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
1-
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.
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.
Yes, agree with the above statements due the following factors in advanced CKD:
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.
Interpret the patient’s new labs.
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
Excellent dr Ahmed.
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.
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.
You are doing very well dr Nour.
Interpret the patient’s new labs.
. 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.
Thank you very much dr Ashraf.
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.
Excellent dr Weam.
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.
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.
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.
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.
The early rise of FGF23 and decreased klotho with reduction of the functioning renal mass are recognized key pathogenetic mechanisms leading to this clinical profile.