1.The contributing factors of osteomalacia.
malabsorption due to gastrointestinal disorder which includes bariatric surgery .. IBS , hepatobiliary diseases
drugs including phenytoin,carbamazepin. 2.The clinical presentation and radiological findings of osteomalacia
clinical presentation
in severe cases can present as myalgia, muscle spasm, seizures, tetany.
Radiographic finding includes looser zones, or pseudo fractures which is a classic finding in osteomalacia. it also shows decreased distinctness of vertebral body trabeculae due to the inadequate mineralization of osteoid. 3.The bone changes in kidney transplant recipients
The reduction in FGF-23 levels is due to the increased phosphorus from the transplanted graft. There is a risk of tertiary hyperparathyroidism, which depends on the duration of ESKD, phosphorus control, and PTH levels. They are an also at risk of severe hypocalcemia post-parathyroidectomy due to hungry bone syndrome. As kidney disease further progresses, either in the native or transplanted kidney, phosphorus excretion declines, leading to hyperphosphatemia. This leads to the elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to elevation of PTH. Persistent elevation of PTH can lead to tertiary hyperparathyroidism and osteitis fibrosa cystica.
4.The effects of malabsorption on bone.
there are some GI conditions causes malabsorption absorptive osteomalacia , loss of bone density and fractures.
this malabsorption has direct effect on the skeletal and osteocytes of hormonal control and osteoid of its constituent calcium.
What are the bone changes in kidney transplant recipients?
if they had ckdmbd prior to tx it will take time to resolve assuming they get good graft function
post tx they have low phosphate due to FGF23 being high and takes time to go down
they can also become hypercalcaemic if they were on cinacalcet or have tertiary hyperparathyorid
assuming they have good graft function and it declines they will suffer the same consequences of ckd mbd as usual ckd population. worth bearing on mind that is they take might make it worse for them too.
Anticonvulsannts, (phenobarpitone, phenytoin, and carbamazepine).
Renal osteodystrophy.
Clinical manifestation of Osteomalacia
Asymptomatic.
Hypocalcemia (myalgia, muscle cramps, bone pain, seizure).
Long bone and limb angular deformities.
Radiologically osteomalacia appears as
Bone osteopenia.
Ground glass appearance and indistinct trabeculae.
Stress fractures with radiodense lines adjacent to regions of radiolucency (Milkman pseudofractures).
Bone changes in kidney transplantation
There is an adverse interaction between PTH, kidney, and bone, which leads to pathology in Ca, Pi, and bone.
These changes depend on the kidney function status, (mostly not shown in normal allograft function).
Allograft functioning normalizes phosphate levels and reduction of FGF23 and improved the risk of cardiovascular mortality.
there is a risk of tertiary hyperparathyroidism (may require parathyroidectomy) in transplant recipients due to the length of ESKD, previous Pi control, and PTH level.
ESKD before transplantation may cause a depletion of Ca and Pi bone store if there is an uncontrolled 2ndary hyperparathyroidism.
Effects of malabsorption on bone
Malabsorption cause nutrients and absorptive osteomalcia with decreased bone density, and fractures.
Has a profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of its constituent calcium.
Malabsorption can be considered in 2 forms
Pancreatic insufficiently, pancreatitis, cystic fibrosis, and hepatobiliary disease with reduce bile acid ssecretion with resultants deficient fat soluble vitamin which lead to vitamin D-deficiency osteomalcaia and low serum 25(OH)D.
Enteric malabsorption; loss of absorptive doudenum and jejunum (crohns, celiac, and sprue, surgical short bowel syndrome, or small interstinal bacterial overgrowth syndrome.
What are the contributing factors of osteomalacia?
Gastrointestinal disorders causing malabsorption (enteric, hepatobiliary, and pancreatic diseases, short bowel syndrome, and some bariatric procedures).
Medications including the anticonvulsants phenobarbital, phenytoin, and carbamazepine, which can alter hepatic vitamin D metabolism.
Renal osteodystrophy is a special case in which osteomalacia coexists with hyperparathyroidism.
renal tubular rickets and osteomalacia: proximal and distal tubular lesions.
Vitamin D, calcium, or phosphate deficiency.
What are the clinical presentation and radiological findings of osteomalacia ?
The clinical presentation: often asymptomatic but, when severe, mainly reflects symptoms of hypocalcemia (e.g. myalgias, muscle spasms,bone pain, tetany, and seizures).
Radiological findings: bones appear osteopenic on radiographs often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen. Milkman pseudofractures, looser lines, can be seen. Characteristic osteomalacic hip fractures resemble slipped femoral capital epiphyses. MRI and technetium bone scans might show stress fractures. Histologic characteristics of osteomalacia are trabeculae covered with long, wide osteoid seams due to the lack of mineralization. On bone biopsy with tetracycline labeling, smudged, indistinct tetracycline labels occur from the impaired mineralization.
What are the bone changes in kidney transplant recipients? There is reduction in FGF-23 levels due to enhanced phosphorus from functioning transplanted graft. There is a risk of tertiary hyperparathyroidism which is depending on the length of ESKD, previous phosphorus control, and PTH levels. They are also at risk of severe hypocalcemia post parathyroidectomy due to hungry bone syndrome. As kidney disease progresses, either in the native or transplanted kidney, phosphorus excretion declines leading to hyperphosphatemia. This leads to elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to increased elevation of PTH. Persistent, unregulated elevation of PTH can lead to tertiary hyperparathyroidism and osteitis fibrosa. Conversely, over-suppression of PTH via administration of calcitriol can also have negative consequences in the form of osteomalacia. Therefore, it is essential that patients regulate their phosphorus intake to prevent hyperparathyroidism and maintain good bone health
Explain the effects of malabsorption on bone.
Several gastrointestinal conditions can cause malabsorption of nutrients and absorptive osteomalacia, decreased bone density, and fractures.
Malabsorption of nutrients from GIT has profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of its constituent calcium.
Malabsorption is in two forms: (1) Pancreatic insufficiency, pancreatitis, cystic fibrosis, and hepatobiliary diseases, including cirrhosis and alcoholism, reduce the secretion of bile and pancreatic enzymes and impair the ability to digest and absorb fats including the fat-soluble vitamins, A, D, E, and K, contributing to an absorptive vitamin D-deficient osteomalacia and low serum 25(OH) D. (2) Enteric malabsorption is due to the loss of absorptive surfaces of the duodenum and proximal jejunum. Loss of absorptive villi can be due to inflammatory diseases such as Crohn’s disease, celiac disease, and sprue, surgical short bowel syndrome, or small intestinal bacterial overgrowth syndrome. Other forms of absorptive osteomalacia occur due to intestinal binding of calcium.
What are the contributing factors of osteomalacia?
Gastrointestinal disorders causing malabsorption (enteric, hepatobiliary, and pancreatic diseases, short bowel syndrome, and some bariatric procedures).
Medications including the anticonvulsants phenobarbital, phenytoin, and carbamazepine, which can alter hepatic vitamin D metabolism.
Renal osteodystrophy is a special case in which osteomalacia coexists with hyperparathyroidism.
renal tubular rickets and osteomalacia: proximal and distal tubular lesions.
Vitamin D, calcium, or phosphate deficiency.
What are the clinical presentation and radiological findings of osteomalacia?
The clinical presentation: often asymptomatic but, when severe, mainly reflects symptoms of hypocalcemia (e.g. myalgias, muscle spasms,bone pain, tetany, and seizures).
Radiological findings: bones appear osteopenic on radiographs often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen. Milkman pseudofractures, looser lines, can be seen. Characteristic osteomalacic hip fractures resemble slipped femoral capital epiphyses. MRI and technetium bone scans might show stress fractures. Histologic characteristics of osteomalacia are trabeculae covered with long, wide osteoid seams due to the lack of mineralization. On bone biopsy with tetracycline labeling, smudged, indistinct tetracycline labels occur from the impaired mineralization.
What are the bone changes in kidney transplant recipients?
There is reduction in FGF-23 levels due to enhanced phosphorus from functioning transplanted graft. There is a risk of tertiary hyperparathyroidism which is depending on the length of ESKD, previous phosphorus control, and PTH levels. They are also at risk of severe hypocalcemia post parathyroidectomy due to hungry bone syndrome. As kidney disease progresses, either in the native or transplanted kidney, phosphorus excretion declines leading to hyperphosphatemia. This leads to elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to increased elevation of PTH. Persistent, unregulated elevation of PTH can lead to tertiary hyperparathyroidism and osteitis fibrosa. Conversely, over-suppression of PTH via administration of calcitriol can also have negative consequences in the form of osteomalacia. Therefore, it is essential that patients regulate their phosphorus intake to prevent hyperparathyroidism and maintain good bone health.
Explain the effects of malabsorption on bone.
Several gastrointestinal conditions can cause malabsorption of nutrients and absorptive osteomalacia, decreased bone density, and fractures.
Malabsorption of nutrients from GIT has profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of its constituent calcium.
Malabsorption is in two forms: (1) Pancreatic insufficiency, pancreatitis, cystic fibrosis, and hepatobiliary diseases, including cirrhosis and alcoholism, reduce the secretion of bile and pancreatic enzymes and impair the ability to digest and absorb fats including the fat-soluble vitamins, A, D, E, and K, contributing to an absorptive vitamin D-deficient osteomalacia and low serum 25(OH) D. (2) Enteric malabsorption is due to the loss of absorptive surfaces of the duodenum and proximal jejunum. Loss of absorptive villi can be due to inflammatory diseases such as Crohn’s disease, celiac disease, and sprue, surgical short bowel syndrome, or small intestinal bacterial overgrowth syndrome. Other forms of absorptive osteomalacia occur due to intestinal binding of calcium.
A range of gastrointestinal conditions can cause malabsorption of nutrients and absorptive osteomalacia, decreased bone density, and fractures. Malabsorption of nutrients from the gastrointestinal tract has profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of its constituent calcium.The subject of malabsorption is quite complex and, for our purposes, will be broadly considered in two forms.
(1) Pancreatic insufficiency, pancreatitis, cystic fibrosis, and hepatobiliary diseases, including cirrhosis and alcoholism, reduce the secretion of bile and pancreatic enzymes and impair the ability to digest and absorb fats including the fat-soluble vitamins, A, D, E, and K, contributing to an absorptive vitamin D-deficient osteomalacia and low serum 25(OH) D.
(2) Enteric malabsorption is due to the loss of absorptive surfaces of the duodenum and proximal jejunum. Loss of absorptive villi can be due to inflammatory diseases such as Crohn’s disease, celiac disease, and sprue, surgical short bowel syndrome, or small intestinal bacterial overgrowth syndrome.
Other forms of absorptive osteomalacia occur due to intestinal binding of calcium. Calcium absorption from the gastrointestinal tract is regulated by vitamin D and PTH. Vitamin D is fat-soluble and is dependent on bile salts for absorption, which primarily takes place in the proximal duodenum and proximal jejunum. Chelating agents such as oxalate (in spinach), phytate (in coarse cereals), or excessive concentrations of phosphate or free fatty acids make calcium more difficult to absorb as calcium can bind to these molecules creating materials that are insoluble in body fluids.
What are the bone changes in kidney transplant recipients?
Depending on the length of end-stage renal disease status, previous phosphorus control, and PTH levels, transplant patients are often at risk of tertiary hyperparathy- roidism requiring parathyroidectomy. They are also at risk of severe hypocalcemia post parathyroidectomy due to hungry bone syndrome. In end-stage renal disease patients, persistently elevated PTH levels deplete bone of calcium and phosphorus stores. Once the parathyroid gland is removed, calcium and phosphorus are aggressively taken up by bone. This leads to a precipitous drop in serum calcium and phosphorus concentration risking acute arrhythmia and respiratory failure if unaddressed.
As kidney disease advances, either in the native or transplanted kidney, phosphorous excretion declines leading to hyperphosphatemia. This leads to elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to increased elevation of PTH. Persistent, unregulated elevation of PTH can lead to ter- tiary hyperparathyroidism and osteitis fibrosa. Conversely, over-suppression of PTH via administration of calcitriol can also have negative consequences in the form of osteomalacia. Therefore, it is essential that patients regulate their phosphorus intake to prevent hyperparathyroidism and maintain good bone health.
What are the clinical presentation and radiological findings of osteomalacia?
The clinical presentation of osteomalacia is often asymptomatic but, when severe, mainly reflects symptoms of hypocalcemia, including myalgias, muscle spasms, and bone pain. More severe symptoms related to hypocalcemia include tetany and seizures; chronic vitamin D deficiency can lead to long bone and limb angular deformities.
On radiographs, bones appear osteopenic often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen on the concave sides of bones. These are termed Looser lines, also called Milkman pseudofractures, after the aptly named radiologist, Louis Milkman, who described the radiological appearance of pseudofractures in osteomalacia .
Characteristic osteomalacic hip fractures resemble slipped femoral capital epiphyses and may occur over time with minimal symptoms. Stress fractures are common and may be seen by MRI and technetium bone scans; they may not be apparent radiographically until a healing callus is present. Histologic characteristics of osteomalacia are trabeculae covered with long, wide osteoid seams due to the lack of mineralization, contributing to the ground glass radiologic appearance of trabeculae .On bone biopsy with tetracycline labeling, smudged, indistinct tetracycline labels occur from the impaired mineralization.
What are the contributing factors of osteomalacia?
Etiological Classification of Rickets and Osteomalacia I.Deficiency Rickets and Osteomalacia
A. Vitamin D deficiency
B. Calcium deficiency
C. Phosphorus deficiency
D. Chelators in diet II.Absorptive Rickets and Osteomalacia
A. Gastric abnormalities
B. Biliary disease
C. Enteric absorptive defects III.Renal Tubular Rickets and Osteomalacia
A. Proximal tubular lesions
B. Proximal and distal tubular lesions
C. Distal tubular lesions (renal tubular acidosis)
1. Primary
2. Secondary IV.Renal Osteodystrophy
What are the clinical presentation and radiological findings of osteomalacia? it could be asymptomatic or with severe cases may leads to muscle and bone pain patient may have tetany or seizures.
contribution factors for osteomalacia include the following ; vit D deficiency low Ca and po4 RTA proximal and distal type
What are the bone changes in kidney transplant recipients?
Usually after RTX the level of FGF23 will decrease as it is secreted through the kidney because of that eraly post-operative period complicated with hypophatemia. and this will reduce the CV risk .
Allograft dysfunction can lead to reduced renal mass, hyperphosphatemia, increase FGF23, low calcitriol, low Ca and secondary hyperparathroidism
Explain the effects of malabsorption on bone.
malabsorption can lead to severe Ca and PO4 deficiency which will be resulting in reduced bone density and finally cause fractures, Malabsorption can result in depriving osteocytes of hormonal control and osteoid of calcium.
1. Сontributing factors of osteomalacia are:
Deficiency of vitamin D, calcium and phosphate deficiency. Chelation in diets.
Absorption problem like gastric, biliary or enteropathy.
Renal problems like proximal and distal tubular lesions (RTA) and ROD.
2.Clinical findigs are a wide range from asymptomatic till severe with symptoms of myalgias, muscle spasms and bone pain. More severe symptoms related to hypocalcemia are tetany and seizure. Chronic Vitamin D Deficencies can lead to long bones and limb angular deficincies.
Radiologic findigs are :
osteopenic with ground glass appearance and indistinct trabecula
stress fracture with radiodence lines adjacent to region of radiolucency may be seen on concave side of bone(also termed looser line, or named Milkmann pseudofracture).
Characteristic osteomalacic fracture include slipped femoral capital epiphyses.
3 Bone Changes in Kidney transplant patient are related to kidney transplant function. Studies shows that Hypophosphatemia lead to improved allograft function and improvement in cardiovascular calcification. This improvement is due to enhanced phophorus secretion and lowering FGF23 after Transplantation.
Depending on the length on CKD , patients may be at risk of tretiary hyperparathyreoidismus requiring parathyreoidectomy.
After parathyreoidectomy , transplant patient are at risk of hypocalcemia due to Hungry bone syndrome.This may lead in severe cases to acutre respiratory failure and acute arrythmias.
4. Malabsorption can have dramatic effects on bones leading to osteomalacia.
Pancreatic insufficiency , pancreatitis, cystic fibrosis, hepatobiliary diseases, Crohn , celiac disease and sprue and loss of enteric absorptive surface in duodenum and proximal jejunum can reduce absorption of fat and fat soluble vitamins contributing to osteomalacia and low vitamin D.
Bariatric surgeries can lead also to osteomacia and icreased risk of fracture especially hip fracture with 6-10 % risk of bone loss 1year after surgery. The risk of fractures include fragility fracture at the hip, spine and wrist after bariatric surgery. Management of malnutrition especially after bariatric procedures are important are can be done using high dose of calcium, vitamin D analogs like ergocalciferol and monitoring 25(OH) D, PTH , serum and urine calcium and using DEXA scan.
What are the contributing factors of osteomalacia?
vitamin D deficiency ,malabsorption .drugs ,renal osteodystrophy
What are the clinical presentation and radiological findings of osteomalacia?
clinical presentation is bone pain and proximal myopathy
radiological:
On radiographs, bones appear osteopenic often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen on the concave sides of bones. These are termed Looser lines, also called Milkman pseudofractures,
1. Сontributing factors of osteomalacia are:
Deficiency of vitamin D, calcium and phosphate deficiency. Chelation in diets.
Absorption problem like gastric, biliary or enteropathy.
Renal problems like proximal and distal tubular lesions (RTA) and ROD.
1-What are the contributing factors of osteomalacia?
Mostly due to deficiency in vitamin D, Calcium and Phosphate,Gastrointestinal disorders interfere with absorption of calcium and phosphorus
Renal Tubular disorders and renal osteodystrophy
2-What are the clinical presentation and radiological findings of osteomalacia?
Clinical: mostly asymptomatic but maybe bone pain, muscle spasm, and myalgia.
Radiological:Osteopenia, ground glass in the bone, and unclear trabeculae; radiodense area close to radiolucency known as looser zone or milkman microfracture.Hip fractures manifest as slipping capital femoral epiphysis; MRI and technesium scan show asymptomatic microfractures.
3-What are the bone changes in kidney transplant recipients?
Changes in bone mineral abnormality as in serum calcium, phosphate can occur in patients with renal transplant depends on:
the functioning of the transplanted kidney ,hypophosphatemia leads to improved transplant graft survival,
length of ESRD
pre-transplant phosphate control and degree of hyperparathyroidism
4-Explain the effects of malabsorption on bone.
Different cause of git disease can cause malabsorption of nutrients essential of bone health resulting in reduced bone density and finally causing fractures,Malabsorption can result in depriving osteocytes from hormonal control and osteoid of calcium.
What are the clinical presentation and radiological findings of osteomalacia? Clinical presentation: Mostly asymptomatic disease, Symptoms of hypocalcemia in severe disease e.g.,malyagias, muscle spasm, bone pain and deformities, tetany, & seizures Radiological findings: Looser line or Milkman pseuodofracture on the concave side of bone, Cupping,flaring, and metaphyseal widening in the distal radius
Explain the effects of malabsorption on bone.
Depriving osteocytes of its hormonal control, Depriving osteoid of its constituent calcium, decrease bone density and fracture
Important causes are pancreatic/liver dysfuction, celiac disease, Chron’s disease,short bowel syndrome,and instestinal
What are the contributing factors of osteomalacia?
Deficiency of vitamin D, CA, PO4, & chelators in the diet
What are the contributing factors of osteomalacia?
*Lack of vitamin D, and consequently low Ca and PO4 *GIT absorptive disorders *Tubular Acidosis *Renal Osteodystrophy
What are the clinical presentation and radiological findings of osteomalacia?
Clinical:bone pain, spasm, and myalgia, or severe symptoms such as tetany, convulsion, obtundation, and coma, or chronic vitamin D limb and long bone angular deformity. Osteopenia, ground glass look in the bone, and unclear trabeculae; radiodense area close to radiolucency known as looser zone or milkman microfracture. Hip fractures manifest as slipping capital femoral epiphysis; MRI and technesium scan show asymptomatic microfractures.
What are the bone changes in kidney transplant recipients?
Long-standing ESKD patients have hyperphosphatemia, hypocalcemia, an increase in FGF23, hyperparathyroidism, and a low vitamin D level. In Kidney Transplant recipient when graft function, Hungry bone disease happen where high PTH leads to phosphaturia and hypophosphatemia ensues, serum Ca also becomes low because Ca get deposited in bones.
Explain the effects of malabsorption on bone.
profound effects on the skeleton due to the hormonal control loss in osteocytes and calcium deprivation in osteoid. this leads to lower bone density, higher risk of fractures, and a spectrum of bone illnesses including osteomalacia, renal osteodystrophy, and osteoporosis. Hyperparathyroidism, a lack of osteoid mineralization, and bone resorption are symptoms of renal osteodystrophy. It is caused by an imbalance between calcium and phosphorus levels, leading to an increase in parathyroid hormone production and consequent bone loss. Malabsorption can lead to decreased calcium absorption, leading in decreased bone density and increased risk of fractures. Nutrient malabsorption can have negative effects on the skeleton, increasing the risk of fractures and causing a variety of bone disorders.
**What are the contributing factors of osteomalacia?
1.Deficiency ricket and osteomalacia :calcium deficiency, phosphorous Def., vitamin D deficiency, chelators agent
2. Absorptive ricket and osteomalacia :gastric abnormalities, biliary problem, enteric malabsorption
3.renal cause:proximal renal tubular disease, distal and proximal tubular disease, distal renal tubular disease include primary and secondary
4.renal osteodystrophy
**What are the clinical presentation and radiological findings of osteomalacia?
Clinical :features of hypocalcimia bone pain, spasm and myalgia or severe symptoms in the form of tetany, convulsion obtundation and coma or chronic vitamin D limb and long bone angular deformaty
Radiological :osteopenia, ground glass appearance in the bone and indistinct trabeculae, radiodense area adjacent to radiolucency called looser zone or milkman microfracture
Hip fractures appear as slipped capital femoral epiphysis, MRI detect microfracture also technesium scan which is asymptomatic
**What are the bone changes in kidney transplant recipients?
Patients in ESKD specially long standing has hyperphosphatemia, hypocalcimia, increase FGF23, hyperparathyroidism and low vitamin D level.
In Kidney Transplant recipient when graft function this lead to excretion of phosphorous lead to hypophosphametic and decrease FGF23 which has effect on cardiovascular disease, some time patient my need for parathyroidectomy this lead to shifting of the calcium and phosphorus to the bone this is called hungry bone disease
**Explain the effects of malabsorption on bone
The malabsorption has profound effect on the bone by deprivation of the osteocyte of hormonal control and osteoid of its constitute Ca, lead to a decrease bone density and liable to fracture
What are the contributing factors of osteomalacia?
Gastrointestinal disorders causing Malabsorption such as enteric, hepato-biliary, and pancreatic diseases, short bowel syndrome, and some bariatric procedures
Inadequate intake of vitamin D and diminished renal synthesis of vitamin D
Renal insufficiency and over suppression of the parathyroid gland
What are the clinical presentation and radiological findings of osteomalacia?
The clinical presentation of osteomalacia is often asymptomatic, but when severe it mainly is symptoms of hypocalcemia such as myalgias, muscle spasms, and bone pain.
Radiologically, osteomalacia is characterized by bones that appear osteopenic, often with a ground glass appearance and indistinct trabeculae. On radiographs, bones may also demonstrate Looser lines (also called Milkman pseudofractures), which are characteristic of osteomalacia and resemble slipped capital femoral epiphyses. The epiphyseal plate can demonstrate cupping, flaring, and metaphyseal widening associated with deficient mineralization.
What are the bone changes in kidney transplant recipients?
Kidney transplant recipients may experience calcium, phosphorus, and bone pathology due to adverse interactions among the parathyroid gland, kidney, and bone. This can manifest as renal osteodystrophy, which is a condition characterized by hyperparathyroidism, lack of osteoid mineralization (osteomalacia), and bone resorption. Patients with advanced kidney disease are also at risk of bone disorders that range from osteitis fibrosa to adynamic bone disease (osteomalacia). Additionally, bone loss can occur after bariatric surgery due to metabolic bone changes. Special considerations must be taken into account when assessing the bone health of patients fitting these criteria, such as reduced calcium absorption, increased bone resorption, and increased risk of fractures. To attenuate bone loss, dietary restrictions, and bone health management strategies must be implemented.
Explain the effects of malabsorption on bone.
Malabsorption of nutrients from the GI tract can have profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of their constituent calcium. this leads to decreased bone density, increased risk of fractures, and a range of bone disorders including osteomalacia, renal osteodystrophy, and osteoporosis. Renal osteodystrophy is a condition characterized by hyperparathyroidism, lack of osteoid mineralization, and bone resorption. It is caused by an imbalance between calcium and phosphorus levels, leading to an increase in parathyroid hormone production and consequent bone loss.
Malabsorption can lead to decreased calcium absorption, resulting in decreased bone density and increased risk of fractures.
Malabsorption of nutrients can have serious effects on the skeleton, leading to a range of bone disorders and increased risk of fractures.
What are the contributing factors of osteomalacia?
I. Deficiency Rickets and Osteomalacia
A. Vitamin D deficiency, B. Calcium deficiency, C. Phosphorus deficiency, D. Chelators in diet
II. Absorptive Rickets and Osteomalacia
A. Gastric abnormalities, B. Biliary disease, C. Enteric absorptive defects
III. Renal Tubular Rickets and Osteomalacia
A. Proximal tubular lesions, B. Proximal and distal tubular lesions, C. Distal tubular lesions (renal tubular acidosis) 1. Primary 2. Secondary
IV. Renal Osteodystrophy
What are the clinical presentation and radiological findings of osteomalacia?
Osteomalacia is frequently asymptomatic, but when severe, it causes hypocalcemia-related myalgias, muscular spasms, and bone pain. Chronic vitamin D insufficiency may cause lengthy bone and limb angular deformities, tetany, and seizures from hypocalcemia.
Rickets, the juvenile variant of osteomalacia, is characterized by under mineralized freshly produced bone. Radiographs show osteopenic bones with ground-glass trabeculae. Bones with concave sides may have stress fractures with radiodense lines near radiolucency. Looser lines, often called Milkman pseudofractures after the appropriately named radiologist Louis Milkman, characterize the radiological appearance of pseudofractures in osteomalacia.
What are the bone changes in kidney transplant recipients?
Most transplant patients with a functional transplanted kidney do not encounter these pathologic interactions, although they may need to change their diet and phosphorus consumption. Hypophosphatemia improves cardiovascular and transplant graft survival. The working transplanted graft increases phosphorus, lowering FGF-23, which is connected to cardiovascular mortality. 24,25 Depending on end-stage renal disease duration, phosphorus management, and PTH levels, transplant patients may need parathyroidectomy for tertiary hyperparathyroidism. The hungry bone syndrome may cause severe hypocalcemia after parathyroidectomy.
Explain the effects of malabsorption on bone.
removing osteocytes from the hormonal control they normally have, and removing the calcium, which is an essential component of osteoid.
The final outcome is a lower bone density and an increased risk of fracture.
Key reasons include pancreas and liver dysfunction, celiac disease, Chron’s disease, short bowel syndrome, and intestinal blindness to calcium caused by chelating drugs. Other possible causes include short bowel syndrome and Chron’s disease
the contributing factors of osteomalacia are I. Deficiency Rickets and Osteomalacia
A. Vitamin D deficiency
B. Calcium deficiency
C. Phosphorus deficiency
D. Chelators in diet II. Absorptive Rickets and Osteomalacia
A. Gastric abnormalities
B. Biliary disease
C. Enteric absorptive defects III. Renal Tubular Rickets and Osteomalacia
A. Proximal tubular lesions
B. Proximal and distal tubular lesions
C. Distal tubular lesions (renal tubular acidosis) 1. Primary 2. Secondary IV. Renal Osteodystrophy the clinical presentationof osteomalacia
is often asymptomatic but, presented with , myalgias, muscle spasms, and bone pain. Due to hypocalcemia More severe hypocalcemia presented with tetany and seizures;
chronic vitamin D deficiency can lead to long bone and limb angular deformities
Undermineralized newly formed bone is the hallmark of both osteomalacia and rickets, the juvenile form of osteomalacia radiological findings of osteomalacia . On radiographs, bones appear osteopenic often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen on the concave sides of bones.
What are the contributing factors of osteomalacia?
Osteomalacia is demineralisation due to deficincy of calcium, phosphorus, or vitamin D.
factors of osteomalacia include
nutritional deficiency,
diminished absorptive capabilities (often due to gastrointestinal disorders),
renal insufficiency.
What are the clinical presentation and radiological findings of osteomalacia? A.Clinical presentation
Mostly asymptomatic disease
Symptoms of hypocalcemia in severe disease e.g muscle spasm, bone pain and deformities, tetany, & seizuresreduced bone denisity B.Radiological findings
reduced bone denisity
Looser line or Milkman pseuodofracture on the concave side of bone
metaphyseal widening in the distal radius.
What are the bone changes in kidney transplant recipients?
depends mainly on pre transplant status.
tertiary hyperparathyroidism and high possibility of hungry bone syndrome after parathroidectomy .
Hypophosphatemia, low FGF23 with improved allograft function.
Hungry bone syndrome due to parathroidectomy.
Allograft dysfunction can lead to reduced renal mass, hyperphosphatemia, increase FGF23, low calcitriol, low Ca and secondary hyperparathroidism.
Explain the effects of malabsorption on bone.
Important causes are pancreatic/liver dysfuction, celiac disease, Chron’s disease,short bowel syndrome,and instestinal blinding of Ca by chelating agents (oxalate,phytate, high dietary PO4 and fats).
Vit D is A fat soluble affected by malabsorption leading to ostemalacia
What are the contributing factors of osteomalacia?
Osteomalacia is mostly due to a lack of available calcium, phosphorus, or vitamin D. Causative factors of osteomalacia include;
nutritional deficiency,
diminished absorptive capabilities (often due to gastrointestinal disorders),
renal insufficiency.
What are the clinical presentation and radiological findings of osteomalacia?
mostly Asymptomatic and may present with symptoms of hypocalcemia in severe cases ,chronic cases of Vit D deficiency can lead to bone deformities .
Radiological findings ;
Milk man syndrome , pseudo fractures .
What are the bone changes in kidney transplant recipients?
depends mainly on pre transplant status , mostly tertiary hyperparathyroidism and high possibility of hungry bone syndrome after parathroidectomy .
Explain the effects of malabsorption on bone.
Vit D is A fat soluble vit affected by malabsorption leading to ostemalacia
Also any calcium chelators can cause same problem .
-What are the clinical presentation and radiological findings of osteomalacia? A.Clinical presentation
Mostly asymptomatic disease
Symptoms of hypocalcemia in severe disease e.g.,malyagias, muscle spasm, bone pain and deformities, tetany, & seizures
B.Radiological findings
Looser line or Milkman pseuodofracture on the concave side of bone
Cupping,flaring, and metaphyseal widening in the distal radius
-What are the bone changes in kidney transplant recipients?
There may be no changes with normal allograft function
Hypophosphatemia, low FGF23 with improved allograft function
Tertiary hyperparathyroidism with long standing CKD prior to transplantation
Risk of parathyroidectomy due to tertiary hyperparathyroidism
Hungry bone syndrome as a complications of parathroidectomy
Allograft dysfunction can lead to reduced renal mass, hyperphosphatemia, increase FGF23, low calcitriol, low Ca and secondary hyperparathroidism
-Explain the effects of malabsorption on bone.
Depriving osteocytes of its hormonal control
Depriving osteoid of its constituent calcium
The end results are decrease bone density and fracture
Important causes are pancreatic/liver dysfuction, celiac disease, Chron’s disease,short bowel syndrome,and instestinal blinding of Ca by chelating agents (oxalate,phytate, high dietary PO4 and fats)
osteomalacia is undermineralization of newly formed osteoid leading to failure of its conversion to osteon, so it occurs due to deficiency of ca,or oo4 or their regulator vit D. according to the cause it can be classified into deficiency, malabosrptive, renal loss and osteodystrophy.
osteomalacia can be asymptomatic discovered accidently during evaluation of x-ray, or symptomatic. the main syptom is pain which is usually dull-aching, started in lower plevis and thigh, increased by movement and weight lifting. the condition is assoscitated with ms weakness and wasting affect proximal ms.
lab abnormalities include icreased ( alk.phosphatase, PTH), decreased ( vit D, ca, po4).
radiological findings include reduced bone density, specific x-ray signs like 1-cod fish sign: which occurs due to softing and concavity of vertebral bodies, 2- looser zones: radiolucent zones 1-2 mm in diameter appear mostly likely in neck of femur, looks like pseudofracture.
the bone abnormality post kidney transplantion is osteoporosis, which occurs fastly in 1st six months, then progress slowly or stabilize. the risk factors include glucocorticoids which are toxic to osteoblasts and activate osteoclasts. CNI, especially cyclosporine increase osteoporotic effect of corticosteroid
malabsorption will cause decrease absoption of fat solublel vitamins like vit d, and calcium and phosphorus
1.The contributing factors of osteomalacia.
malabsorption due to gastrointestinal disorder which includes bariatric surgery .. IBS , hepatobiliary diseases
drugs including phenytoin,carbamazepin.
2.The clinical presentation and radiological findings of osteomalacia
clinical presentation
in severe cases can present as myalgia, muscle spasm, seizures, tetany.
Radiographic finding includes looser zones, or pseudo fractures which is a classic finding in osteomalacia.
it also shows decreased distinctness of vertebral body trabeculae due to the inadequate mineralization of osteoid.
3.The bone changes in kidney transplant recipients
The reduction in FGF-23 levels is due to the increased phosphorus from the transplanted graft. There is a risk of tertiary hyperparathyroidism, which depends on the duration of ESKD, phosphorus control, and PTH levels. They are an also at risk of severe hypocalcemia post-parathyroidectomy due to hungry bone syndrome. As kidney disease further progresses, either in the native or transplanted kidney, phosphorus excretion declines, leading to hyperphosphatemia. This leads to the elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to elevation of PTH. Persistent elevation of PTH can lead to tertiary hyperparathyroidism and osteitis fibrosa cystica.
4.The effects of malabsorption on bone.
there are some GI conditions causes malabsorption absorptive osteomalacia , loss of bone density and fractures.
this malabsorption has direct effect on the skeletal and osteocytes of hormonal control and osteoid of its constituent calcium.
What are the contributing factors of osteomalacia?
-Nutritional lack of vit d ca or phosphate
-Lack of sun
-Age, Obesity
-Gi disorders( short bowel , pancreatitis)
-Renal Osteodystrophy
–
What are the clinical presentation and radiological findings of osteomalacia?
Clinical Presentation of Osteomalacia – asymptomatic or featues of low calcium msucle pain , bone pain, tetany ,seizure)
Radiological features- Ground glass appearance , indistinct trabeculae, slipped femoral epiphyses
What are the bone changes in kidney transplant recipients?
if they had ckdmbd prior to tx it will take time to resolve assuming they get good graft function
post tx they have low phosphate due to FGF23 being high and takes time to go down
they can also become hypercalcaemic if they were on cinacalcet or have tertiary hyperparathyorid
assuming they have good graft function and it declines they will suffer the same consequences of ckd mbd as usual ckd population. worth bearing on mind that is they take might make it worse for them too.
Contributing factors of Osteomalacia
Clinical manifestation of Osteomalacia
Radiologically osteomalacia appears as
Bone changes in kidney transplantation
Effects of malabsorption on bone
What are the contributing factors of osteomalacia?
What are the clinical presentation and radiological findings of osteomalacia
?
The clinical presentation: often asymptomatic but, when severe, mainly reflects symptoms of hypocalcemia (e.g. myalgias, muscle spasms,bone pain, tetany, and seizures).
Radiological findings: bones appear osteopenic on radiographs often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen. Milkman pseudofractures, looser lines, can be seen. Characteristic osteomalacic hip fractures resemble slipped femoral capital epiphyses. MRI and technetium bone scans might show stress fractures. Histologic characteristics of osteomalacia are trabeculae covered with long, wide osteoid seams due to the lack of mineralization. On bone biopsy with tetracycline labeling, smudged, indistinct tetracycline labels occur from the impaired mineralization.
What are the bone changes in kidney transplant recipients?
There is reduction in FGF-23 levels due to enhanced phosphorus from functioning transplanted graft. There is a risk of tertiary hyperparathyroidism which is depending on the length of ESKD, previous phosphorus control, and PTH levels. They are also at risk of severe hypocalcemia post parathyroidectomy due to hungry bone syndrome. As kidney disease progresses, either in the native or transplanted kidney, phosphorus excretion declines leading to hyperphosphatemia. This leads to elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to increased elevation of PTH. Persistent, unregulated elevation of PTH can lead to tertiary hyperparathyroidism and osteitis fibrosa. Conversely, over-suppression of PTH via administration of calcitriol can also have negative consequences in the form of osteomalacia. Therefore, it is essential that patients regulate their phosphorus intake to prevent hyperparathyroidism and maintain good bone health
Explain the effects of malabsorption on bone.
Several gastrointestinal conditions can cause malabsorption of nutrients and absorptive osteomalacia, decreased bone density, and fractures.
Malabsorption of nutrients from GIT has profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of its constituent calcium.
Malabsorption is in two forms: (1) Pancreatic insufficiency, pancreatitis, cystic fibrosis, and hepatobiliary diseases, including cirrhosis and alcoholism, reduce the secretion of bile and pancreatic enzymes and impair the ability to digest and absorb fats including the fat-soluble vitamins, A, D, E, and K, contributing to an absorptive vitamin D-deficient osteomalacia and low serum 25(OH) D. (2) Enteric malabsorption is due to the loss of absorptive surfaces of the duodenum and proximal jejunum. Loss of absorptive villi can be due to inflammatory diseases such as Crohn’s disease, celiac disease, and sprue, surgical short bowel syndrome, or small intestinal bacterial overgrowth syndrome. Other forms of absorptive osteomalacia occur due to intestinal binding of calcium.
Here are the answers:
What are the contributing factors of osteomalacia?
What are the clinical presentation and radiological findings of osteomalacia?
The clinical presentation: often asymptomatic but, when severe, mainly reflects symptoms of hypocalcemia (e.g. myalgias, muscle spasms,bone pain, tetany, and seizures).
Radiological findings: bones appear osteopenic on radiographs often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen. Milkman pseudofractures, looser lines, can be seen. Characteristic osteomalacic hip fractures resemble slipped femoral capital epiphyses. MRI and technetium bone scans might show stress fractures. Histologic characteristics of osteomalacia are trabeculae covered with long, wide osteoid seams due to the lack of mineralization. On bone biopsy with tetracycline labeling, smudged, indistinct tetracycline labels occur from the impaired mineralization.
What are the bone changes in kidney transplant recipients?
There is reduction in FGF-23 levels due to enhanced phosphorus from functioning transplanted graft. There is a risk of tertiary hyperparathyroidism which is depending on the length of ESKD, previous phosphorus control, and PTH levels. They are also at risk of severe hypocalcemia post parathyroidectomy due to hungry bone syndrome. As kidney disease progresses, either in the native or transplanted kidney, phosphorus excretion declines leading to hyperphosphatemia. This leads to elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to increased elevation of PTH. Persistent, unregulated elevation of PTH can lead to tertiary hyperparathyroidism and osteitis fibrosa. Conversely, over-suppression of PTH via administration of calcitriol can also have negative consequences in the form of osteomalacia. Therefore, it is essential that patients regulate their phosphorus intake to prevent hyperparathyroidism and maintain good bone health.
Explain the effects of malabsorption on bone.
Several gastrointestinal conditions can cause malabsorption of nutrients and absorptive osteomalacia, decreased bone density, and fractures.
Malabsorption of nutrients from GIT has profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of its constituent calcium.
Malabsorption is in two forms: (1) Pancreatic insufficiency, pancreatitis, cystic fibrosis, and hepatobiliary diseases, including cirrhosis and alcoholism, reduce the secretion of bile and pancreatic enzymes and impair the ability to digest and absorb fats including the fat-soluble vitamins, A, D, E, and K, contributing to an absorptive vitamin D-deficient osteomalacia and low serum 25(OH) D. (2) Enteric malabsorption is due to the loss of absorptive surfaces of the duodenum and proximal jejunum. Loss of absorptive villi can be due to inflammatory diseases such as Crohn’s disease, celiac disease, and sprue, surgical short bowel syndrome, or small intestinal bacterial overgrowth syndrome. Other forms of absorptive osteomalacia occur due to intestinal binding of calcium.
Explain the effects of malabsorption on bone.
A range of gastrointestinal conditions can cause malabsorption of nutrients and absorptive osteomalacia, decreased bone density, and fractures. Malabsorption of nutrients from the gastrointestinal tract has profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of its constituent calcium.The subject of malabsorption is quite complex and, for our purposes, will be broadly considered in two forms.
(1) Pancreatic insufficiency, pancreatitis, cystic fibrosis, and hepatobiliary diseases, including cirrhosis and alcoholism, reduce the secretion of bile and pancreatic enzymes and impair the ability to digest and absorb fats including the fat-soluble vitamins, A, D, E, and K, contributing to an absorptive vitamin D-deficient osteomalacia and low serum 25(OH) D.
(2) Enteric malabsorption is due to the loss of absorptive surfaces of the duodenum and proximal jejunum. Loss of absorptive villi can be due to inflammatory diseases such as Crohn’s disease, celiac disease, and sprue, surgical short bowel syndrome, or small intestinal bacterial overgrowth syndrome.
Other forms of absorptive osteomalacia occur due to intestinal binding of calcium. Calcium absorption from the gastrointestinal tract is regulated by vitamin D and PTH. Vitamin D is fat-soluble and is dependent on bile salts for absorption, which primarily takes place in the proximal duodenum and proximal jejunum. Chelating agents such as oxalate (in spinach), phytate (in coarse cereals), or excessive concentrations of phosphate or free fatty acids make calcium more difficult to absorb as calcium can bind to these molecules creating materials that are insoluble in body fluids.
What are the bone changes in kidney transplant recipients?
Depending on the length of end-stage renal disease status, previous phosphorus control, and PTH levels, transplant patients are often at risk of tertiary hyperparathy- roidism requiring parathyroidectomy. They are also at risk of severe hypocalcemia post parathyroidectomy due to hungry bone syndrome. In end-stage renal disease patients, persistently elevated PTH levels deplete bone of calcium and phosphorus stores. Once the parathyroid gland is removed, calcium and phosphorus are aggressively taken up by bone. This leads to a precipitous drop in serum calcium and phosphorus concentration risking acute arrhythmia and respiratory failure if unaddressed.
As kidney disease advances, either in the native or transplanted kidney, phosphorous excretion declines leading to hyperphosphatemia. This leads to elevation of FGF-23 and decreased calcitriol synthesis resulting in hypocalcemia. Hypocalcemia leads to increased elevation of PTH. Persistent, unregulated elevation of PTH can lead to ter- tiary hyperparathyroidism and osteitis fibrosa. Conversely, over-suppression of PTH via administration of calcitriol can also have negative consequences in the form of osteomalacia. Therefore, it is essential that patients regulate their phosphorus intake to prevent hyperparathyroidism and maintain good bone health.
What are the clinical presentation and radiological findings of osteomalacia?
The clinical presentation of osteomalacia is often asymptomatic but, when severe, mainly reflects symptoms of hypocalcemia, including myalgias, muscle spasms, and bone pain. More severe symptoms related to hypocalcemia include tetany and seizures; chronic vitamin D deficiency can lead to long bone and limb angular deformities.
On radiographs, bones appear osteopenic often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen on the concave sides of bones. These are termed Looser lines, also called Milkman pseudofractures, after the aptly named radiologist, Louis Milkman, who described the radiological appearance of pseudofractures in osteomalacia .
Characteristic osteomalacic hip fractures resemble slipped femoral capital epiphyses and may occur over time with minimal symptoms. Stress fractures are common and may be seen by MRI and technetium bone scans; they may not be apparent radiographically until a healing callus is present. Histologic characteristics of osteomalacia are trabeculae covered with long, wide osteoid seams due to the lack of mineralization, contributing to the ground glass radiologic appearance of trabeculae .On bone biopsy with tetracycline labeling, smudged, indistinct tetracycline labels occur from the impaired mineralization.
What are the contributing factors of osteomalacia?
Etiological Classification of Rickets and Osteomalacia
I.Deficiency Rickets and Osteomalacia
A. Vitamin D deficiency
B. Calcium deficiency
C. Phosphorus deficiency
D. Chelators in diet
II.Absorptive Rickets and Osteomalacia
A. Gastric abnormalities
B. Biliary disease
C. Enteric absorptive defects
III.Renal Tubular Rickets and Osteomalacia
A. Proximal tubular lesions
B. Proximal and distal tubular lesions
C. Distal tubular lesions (renal tubular acidosis)
1. Primary
2. Secondary
IV.Renal Osteodystrophy
What are the clinical presentation and radiological findings of osteomalacia?
it could be asymptomatic or with severe cases may leads to muscle and bone pain
patient may have tetany or seizures.
contribution factors for osteomalacia include the following ;
vit D deficiency
low Ca and po4
RTA proximal and distal type
What are the bone changes in kidney transplant recipients?
Usually after RTX the level of FGF23 will decrease as it is secreted through the kidney because of that eraly post-operative period complicated with hypophatemia. and this will reduce the CV risk .
malabsorption can lead to severe Ca and PO4 deficiency which will be resulting in reduced bone density and finally cause fractures, Malabsorption can result in depriving osteocytes of hormonal control and osteoid of calcium.
1. Сontributing factors of osteomalacia are:
Deficiency of vitamin D, calcium and phosphate deficiency. Chelation in diets.
Absorption problem like gastric, biliary or enteropathy.
Renal problems like proximal and distal tubular lesions (RTA) and ROD.
2.Clinical findigs are a wide range from asymptomatic till severe with symptoms of myalgias, muscle spasms and bone pain. More severe symptoms related to hypocalcemia are tetany and seizure. Chronic Vitamin D Deficencies can lead to long bones and limb angular deficincies.
Radiologic findigs are :
osteopenic with ground glass appearance and indistinct trabecula
stress fracture with radiodence lines adjacent to region of radiolucency may be seen on concave side of bone(also termed looser line, or named Milkmann pseudofracture).
Characteristic osteomalacic fracture include slipped femoral capital epiphyses.
3 Bone Changes in Kidney transplant patient are related to kidney transplant function. Studies shows that Hypophosphatemia lead to improved allograft function and improvement in cardiovascular calcification. This improvement is due to enhanced phophorus secretion and lowering FGF23 after Transplantation.
Depending on the length on CKD , patients may be at risk of tretiary hyperparathyreoidismus requiring parathyreoidectomy.
After parathyreoidectomy , transplant patient are at risk of hypocalcemia due to Hungry bone syndrome.This may lead in severe cases to acutre respiratory failure and acute arrythmias.
4. Malabsorption can have dramatic effects on bones leading to osteomalacia.
Pancreatic insufficiency , pancreatitis, cystic fibrosis, hepatobiliary diseases, Crohn , celiac disease and sprue and loss of enteric absorptive surface in duodenum and proximal jejunum can reduce absorption of fat and fat soluble vitamins contributing to osteomalacia and low vitamin D.
Bariatric surgeries can lead also to osteomacia and icreased risk of fracture especially hip fracture with 6-10 % risk of bone loss 1year after surgery. The risk of fractures include fragility fracture at the hip, spine and wrist after bariatric surgery. Management of malnutrition especially after bariatric procedures are important are can be done using high dose of calcium, vitamin D analogs like ergocalciferol and monitoring 25(OH) D, PTH , serum and urine calcium and using DEXA scan.
vitamin D deficiency ,malabsorption .drugs ,renal osteodystrophy
clinical presentation is bone pain and proximal myopathy
radiological:
On radiographs, bones appear osteopenic often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen on the concave sides of bones. These are termed Looser lines, also called Milkman pseudofractures,
1. Сontributing factors of osteomalacia are:
Deficiency of vitamin D, calcium and phosphate deficiency. Chelation in diets.
Absorption problem like gastric, biliary or enteropathy.
Renal problems like proximal and distal tubular lesions (RTA) and ROD.
1-What are the contributing factors of osteomalacia?
Mostly due to deficiency in vitamin D, Calcium and Phosphate,Gastrointestinal disorders interfere with absorption of calcium and phosphorus
Renal Tubular disorders and renal osteodystrophy
2-What are the clinical presentation and radiological findings of osteomalacia?
Clinical: mostly asymptomatic but maybe bone pain, muscle spasm, and myalgia.
Radiological:Osteopenia, ground glass in the bone, and unclear trabeculae; radiodense area close to radiolucency known as looser zone or milkman microfracture.Hip fractures manifest as slipping capital femoral epiphysis; MRI and technesium scan show asymptomatic microfractures.
3-What are the bone changes in kidney transplant recipients?
Changes in bone mineral abnormality as in serum calcium, phosphate can occur in patients with renal transplant depends on:
the functioning of the transplanted kidney ,hypophosphatemia leads to improved transplant graft survival,
length of ESRD
pre-transplant phosphate control and degree of hyperparathyroidism
4-Explain the effects of malabsorption on bone.
Different cause of git disease can cause malabsorption of nutrients essential of bone health resulting in reduced bone density and finally causing fractures,Malabsorption can result in depriving osteocytes from hormonal control and osteoid of calcium.
What are the clinical presentation and radiological findings of osteomalacia?
Clinical presentation: Mostly asymptomatic disease, Symptoms of hypocalcemia in severe disease e.g.,malyagias, muscle spasm, bone pain and deformities, tetany, & seizures
Radiological findings: Looser line or Milkman pseuodofracture on the concave side of bone, Cupping,flaring, and metaphyseal widening in the distal radius
Explain the effects of malabsorption on bone.
What are the contributing factors of osteomalacia?
What are the bone changes in kidney transplant recipients?
*Lack of vitamin D, and consequently low Ca and PO4
*GIT absorptive disorders
*Tubular Acidosis
*Renal Osteodystrophy
Clinical:bone pain, spasm, and myalgia, or severe symptoms such as tetany, convulsion, obtundation, and coma, or chronic vitamin D limb and long bone angular deformity.
Osteopenia, ground glass look in the bone, and unclear trabeculae; radiodense area close to radiolucency known as looser zone or milkman microfracture.
Hip fractures manifest as slipping capital femoral epiphysis; MRI and technesium scan show asymptomatic microfractures.
Long-standing ESKD patients have hyperphosphatemia, hypocalcemia, an increase in FGF23, hyperparathyroidism, and a low vitamin D level.
In Kidney Transplant recipient when graft function, Hungry bone disease happen where high PTH leads to phosphaturia and hypophosphatemia ensues, serum Ca also becomes low because Ca get deposited in bones.
profound effects on the skeleton due to the hormonal control loss in osteocytes and calcium deprivation in osteoid. this leads to lower bone density, higher risk of fractures, and a spectrum of bone illnesses including osteomalacia, renal osteodystrophy, and osteoporosis.
Hyperparathyroidism, a lack of osteoid mineralization, and bone resorption are symptoms of renal osteodystrophy. It is caused by an imbalance between calcium and phosphorus levels, leading to an increase in parathyroid hormone production and consequent bone loss.
Malabsorption can lead to decreased calcium absorption, leading in decreased bone density and increased risk of fractures.
Nutrient malabsorption can have negative effects on the skeleton, increasing the risk of fractures and causing a variety of bone disorders.
What are the contributing factors of osteomalacia?
What are the clinical presentation and radiological findings of osteomalacia?
What are the bone changes in kidney transplant recipients?
Explain the effects of malabsorption on bone.
**What are the contributing factors of osteomalacia?
1.Deficiency ricket and osteomalacia :calcium deficiency, phosphorous Def., vitamin D deficiency, chelators agent
2. Absorptive ricket and osteomalacia :gastric abnormalities, biliary problem, enteric malabsorption
3.renal cause:proximal renal tubular disease, distal and proximal tubular disease, distal renal tubular disease include primary and secondary
4.renal osteodystrophy
**What are the clinical presentation and radiological findings of osteomalacia?
Clinical :features of hypocalcimia bone pain, spasm and myalgia or severe symptoms in the form of tetany, convulsion obtundation and coma or chronic vitamin D limb and long bone angular deformaty
Radiological :osteopenia, ground glass appearance in the bone and indistinct trabeculae, radiodense area adjacent to radiolucency called looser zone or milkman microfracture
Hip fractures appear as slipped capital femoral epiphysis, MRI detect microfracture also technesium scan which is asymptomatic
**What are the bone changes in kidney transplant recipients?
Patients in ESKD specially long standing has hyperphosphatemia, hypocalcimia, increase FGF23, hyperparathyroidism and low vitamin D level.
In Kidney Transplant recipient when graft function this lead to excretion of phosphorous lead to hypophosphametic and decrease FGF23 which has effect on cardiovascular disease, some time patient my need for parathyroidectomy this lead to shifting of the calcium and phosphorus to the bone this is called hungry bone disease
**Explain the effects of malabsorption on bone
The malabsorption has profound effect on the bone by deprivation of the osteocyte of hormonal control and osteoid of its constitute Ca, lead to a decrease bone density and liable to fracture
What are the contributing factors of osteomalacia?
What are the clinical presentation and radiological findings of osteomalacia?
The clinical presentation of osteomalacia is often asymptomatic, but when severe it mainly is symptoms of hypocalcemia such as myalgias, muscle spasms, and bone pain.
Radiologically, osteomalacia is characterized by bones that appear osteopenic, often with a ground glass appearance and indistinct trabeculae. On radiographs, bones may also demonstrate Looser lines (also called Milkman pseudofractures), which are characteristic of osteomalacia and resemble slipped capital femoral epiphyses.
The epiphyseal plate can demonstrate cupping, flaring, and metaphyseal widening associated with deficient mineralization.
What are the bone changes in kidney transplant recipients?
Kidney transplant recipients may experience calcium, phosphorus, and bone pathology due to adverse interactions among the parathyroid gland, kidney, and bone.
This can manifest as renal osteodystrophy, which is a condition characterized by hyperparathyroidism, lack of osteoid mineralization (osteomalacia), and bone resorption. Patients with advanced kidney disease are also at risk of bone disorders that range from osteitis fibrosa to adynamic bone disease (osteomalacia).
Additionally, bone loss can occur after bariatric surgery due to metabolic bone changes. Special considerations must be taken into account when assessing the bone health of patients fitting these criteria, such as reduced calcium absorption, increased bone resorption, and increased risk of fractures.
To attenuate bone loss, dietary restrictions, and bone health management strategies must be implemented.
Explain the effects of malabsorption on bone.
Malabsorption of nutrients from the GI tract can have profound effects on the skeleton by depriving osteocytes of hormonal control and osteoid of their constituent calcium. this leads to decreased bone density, increased risk of fractures, and a range of bone disorders including osteomalacia, renal osteodystrophy, and osteoporosis.
Renal osteodystrophy is a condition characterized by hyperparathyroidism, lack of osteoid mineralization, and bone resorption. It is caused by an imbalance between calcium and phosphorus levels, leading to an increase in parathyroid hormone production and consequent bone loss.
Malabsorption can lead to decreased calcium absorption, resulting in decreased bone density and increased risk of fractures.
Malabsorption of nutrients can have serious effects on the skeleton, leading to a range of bone disorders and increased risk of fractures.
Osteomalacia is frequently asymptomatic, but when severe, it causes hypocalcemia-related myalgias, muscular spasms, and bone pain. Chronic vitamin D insufficiency may cause lengthy bone and limb angular deformities, tetany, and seizures from hypocalcemia.
Most transplant patients with a functional transplanted kidney do not encounter these pathologic interactions, although they may need to change their diet and phosphorus consumption. Hypophosphatemia improves cardiovascular and transplant graft survival. The working transplanted graft increases phosphorus, lowering FGF-23, which is connected to cardiovascular mortality. 24,25 Depending on end-stage renal disease duration, phosphorus management, and PTH levels, transplant patients may need parathyroidectomy for tertiary hyperparathyroidism. The hungry bone syndrome may cause severe hypocalcemia after parathyroidectomy.
removing osteocytes from the hormonal control they normally have, and removing the calcium, which is an essential component of osteoid.
The final outcome is a lower bone density and an increased risk of fracture.
Key reasons include pancreas and liver dysfunction, celiac disease, Chron’s disease, short bowel syndrome, and intestinal blindness to calcium caused by chelating drugs. Other possible causes include short bowel syndrome and Chron’s disease
the contributing factors of osteomalacia are
I. Deficiency Rickets and Osteomalacia
A. Vitamin D deficiency
B. Calcium deficiency
C. Phosphorus deficiency
D. Chelators in diet
II. Absorptive Rickets and Osteomalacia
A. Gastric abnormalities
B. Biliary disease
C. Enteric absorptive defects
III. Renal Tubular Rickets and Osteomalacia
A. Proximal tubular lesions
B. Proximal and distal tubular lesions
C. Distal tubular lesions (renal tubular acidosis) 1. Primary 2. Secondary
IV. Renal Osteodystrophy
the clinical presentationof osteomalacia
is often asymptomatic but, presented with , myalgias, muscle spasms, and bone pain. Due to hypocalcemia More severe hypocalcemia presented with tetany and seizures;
chronic vitamin D deficiency can lead to long bone and limb angular deformities
Undermineralized newly formed bone is the hallmark of both osteomalacia and rickets, the juvenile form of osteomalacia
radiological findings of osteomalacia
. On radiographs, bones appear osteopenic often with a ground glass appearance and indistinct trabeculae. Stress fractures with radiodense lines adjacent to regions of radiolucency may be seen on the concave sides of bones.
Osteomalacia is demineralisation due to deficincy of calcium, phosphorus, or vitamin D.
factors of osteomalacia include
What are the clinical presentation and radiological findings of osteomalacia?
A.Clinical presentation
B.Radiological findings
reduced bone denisity
metaphyseal widening in the distal radius.
depends mainly on pre transplant status.
Osteomalacia is mostly due to a lack of available calcium, phosphorus, or vitamin D. Causative factors of osteomalacia include;
mostly Asymptomatic and may present with symptoms of hypocalcemia in severe cases ,chronic cases of Vit D deficiency can lead to bone deformities .
Radiological findings ;
Milk man syndrome , pseudo fractures .
depends mainly on pre transplant status , mostly tertiary hyperparathyroidism and high possibility of hungry bone syndrome after parathroidectomy .
Vit D is A fat soluble vit affected by malabsorption leading to ostemalacia
Also any calcium chelators can cause same problem .
-What are the contributing factors of osteomalacia?
-What are the clinical presentation and radiological findings of osteomalacia?
A.Clinical presentation
B.Radiological findings
-What are the bone changes in kidney transplant recipients?
-Explain the effects of malabsorption on bone.
osteomalacia is undermineralization of newly formed osteoid leading to failure of its conversion to osteon, so it occurs due to deficiency of ca,or oo4 or their regulator vit D. according to the cause it can be classified into deficiency, malabosrptive, renal loss and osteodystrophy.
osteomalacia can be asymptomatic discovered accidently during evaluation of x-ray, or symptomatic. the main syptom is pain which is usually dull-aching, started in lower plevis and thigh, increased by movement and weight lifting. the condition is assoscitated with ms weakness and wasting affect proximal ms.
lab abnormalities include icreased ( alk.phosphatase, PTH), decreased ( vit D, ca, po4).
radiological findings include reduced bone density, specific x-ray signs like 1-cod fish sign: which occurs due to softing and concavity of vertebral bodies, 2- looser zones: radiolucent zones 1-2 mm in diameter appear mostly likely in neck of femur, looks like pseudofracture.
the bone abnormality post kidney transplantion is osteoporosis, which occurs fastly in 1st six months, then progress slowly or stabilize. the risk factors include glucocorticoids which are toxic to osteoblasts and activate osteoclasts. CNI, especially cyclosporine increase osteoporotic effect of corticosteroid
malabsorption will cause decrease absoption of fat solublel vitamins like vit d, and calcium and phosphorus