Renal osteodystrophy: Difference between revisions

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{{SK}}Chronic kidney disease- mineral bone disorder
{{SK}}Chronic kidney disease- mineral bone disorder
==Overview==
==Overview==
Renal osteodystrophy i<nowiki/>s the term used to describe the complex metabolic bone disorders that occur as a complication of [[Chronic kidney disease|chronic renal insufficiency]]. Secondary [[hyperparathyroidism]] and 1,25-dihydroxycholecalciferol (Vitamin D3) deficiency are major contributors to renal osteodystrophy. It is basically defined as an alteration of bone morphology in patients with [[chronic kidney disease]] and is considered to be a component of chronic kidney disease - mineral bone disorder (CKD-MBD). Renal osteodystrophy is an important cause of morbidity, decreased quality of life, and extravascular [[Calcification|calcifications]] that have been associated with increased cardiovascular mortality. The classification of renal osteodystrophy is based on a unified system that describes a wider clinical syndrome based on bone turnover, bone mineralization, and bone volume. For investigating renal osteodystrophy, blood levels of [[parathyroid hormone]] (PTH), [[calcium]], [[phosphorus]], [[alkaline phosphatase]], [[bicarbonate]] should be ordered initially. Imaging studies should focus on finding [[calcification]] in soft tissues. <nowiki/>If there are inconsistencies in the biochemical markers, unexplained bone pain, or unexplained fractures, the bone [[biopsy]] would be indicated. However, bone biopsy is infrequently used in clinical practice due to invasiveness and lower cost effectiveness. The major objective in the prevention and management of renal osteodystrophy is either prevention of [[hyperparathyroidism]] or treatment if present already .
Renal osteodystrophy i<nowiki/>s the term used to describe the complex metabolic bone disorders which are present in [[Chronic kidney disease|chronic renal insufficiency]]. Secondary [[hyperparathyroidism]] and 1,25-dihydroxycholecalciferol (Vitamin D3) deficiency play major role in renal osteodystrophy. It is defined as an alteration of bone morphology in patients with [[chronic kidney disease]] and is considered to be a component of chronic kidney disease - mineral bone disorder (CKD-MBD). Renal osteodystrophy is an important cause of morbidity, decreased quality of life, and extravascular [[Calcification|calcifications]] that have been associated with increased cardiovascular mortality. The classification of renal osteodystrophy is based on a unified system that describes a wider clinical syndrome based on bone turnover, bone mineralization, and bone volume. For investigating renal osteodystrophy, blood levels of [[parathyroid hormone]] (PTH), [[calcium]], [[phosphorus]], [[alkaline phosphatase]], [[bicarbonate]] should be ordered initially. Imaging studies should focus on finding [[calcification]] in soft tissues. Bone [[biopsy]] is indicated<nowiki/> if the results of biochemical markers are not consistent, there is  unexplained bone pain, or presence of unexplained bone fractures. However, bone biopsy is infrequently used in clinical practice due to invasiveness and lower cost effectiveness. The major objective in the prevention and management of renal osteodystrophy is either prevention of [[hyperparathyroidism]] or treatment if present already .


==Historical Perspective==
==Historical Perspective==
* International work group convened in 2006 by Kidney Disease: Improving Global Outcomes [[(KDIGO)]] recommended that the term, renal osteodystrophy, be exclusively used to define bone pathology associated with CKD, chronic kidney disease.<ref name="pmid16641930">{{cite journal |vauthors=Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K, Ott S, Sprague S, Lameire N, Eknoyan G |title=Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO) |journal=Kidney Int. |volume=69 |issue=11 |pages=1945–53 |date=June 2006 |pmid=16641930 |doi=10.1038/sj.ki.5000414 |url=}}</ref>
* Renal osteodystrophy was first defined by Kidney Disease: Improving Global Outcomes [[(KDIGO)]] in 2006.
* During the 1970s and 1980s, it was discovered that an accumulation of aluminum from water used for dialysis and aluminum salts used as phosphate binders caused osteomalacia and an adynamic bone disease. The identification of these disorders broadened the spectrum of renal osteodystrophy and led to changes in the composition of dialysis fluids and the substitution of calcium carbonate for aluminum salts. As a result, the frequency of aluminum-related bone disease is decreasing.<ref name="HruskaEpstein19952">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
* It was found out in 1970s and 1980s, that aluminum in water that is used for dialysis and aluminum salts that are used as phosphate binders caused osteomalacia and an adynamic bone disease. The identification of these disorders led to define renal osteodystrophy, since then the composition of dialysis fluids was changed and calcium carbonate was substituted for aluminum salts. As a result, bone disease due to deposition of aluminium is decreasing.<ref name="HruskaEpstein19952">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>


==Classification==
==Classification==
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Table 2 '''.[[TMV Classification]]''':
Table 2 '''.[[TMV Classification]]'''  


It is done on the basis of interpretation of bone biopsy,and uses three histologic descriptors- bone turnover, mineralization  
It is done on the basis of results of bone biopsy, and uses three histologic descriptions- bone turnover, bone mineralization  


and volume. it provides a clinically relevant description of the bone pathology as assessed by [[histomorphometry]], which in turn define the [[pathophysiology]] and thereby guide therapy.<ref name="MoeDrüeke20063">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref>  
and bone volume. After the bone pathology is assessed by [[histomorphometry|histomorphometry,]] it helps to define the [[pathophysiology]] and to choose the right therapy.<ref name="MoeDrüeke20063">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref>  
{| class="wikitable"
{| class="wikitable"
!Turnover
!Turnover
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== Pathophysiology : ==
== Pathophysiology ==


The factors that contribute to pathophysiology of renal osteodystrophy in chronic kidney disease are:<ref name="GonzalezMartin19952">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology Dialysis Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref><ref name="MoeDrüeke20064">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref>
The following factors in chronic kidney disease are considered to be the main contributers<ref name="GonzalezMartin19952">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology Dialysis Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref><ref name="MoeDrüeke20064">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref><ref name="HruskaEpstein19953">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
<ref name="HruskaEpstein19953">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
* [[Hyperphosphatemia]] ,when [[GFR]] falls below 60ml/min in chronic Kidney disease there is impaired renal phosphorus excretion resulting in hyperphosphotemia
* [[Hyperphosphatemia]] , due to impaired renal phosphorus excretion with [[GFR]] below 60ml/min in chronic Kidney disease.
*  [[Hypocalcemia]], because of decreased excretion of phosphate by the damaged kidneys.
*  [[Hypocalcemia]], due to decreased excretion of phosphate by the damaged kidney.
* Low activated vitamin D<sub>3</sub> levels happens because the damaged kidneys are unable to convert vitamin D<sub>3</sub> into its active form, calcitriol, this results in further hypocalcaemia.
* Low activated vitamin D<sub>3</sub> levels are a result of the damaged kidneys' inability to convert vitamin D<sub>3</sub> into its active form, calcitriol, and result in further hypocalcaemia.
*  Hyperphosphatemia combined with hypocalcemia results in hyperparathyroidism  
*  Hyperphosphatemia combined with hypocalcemia leads to hyperparathyroidism  
* Elevated level of Hyperparathyroid leads to Osteitis fibrosa .
* Elevated level of Hyperparathyroid leads to Osteitis fibrosa .
* High levels of [[fibroblast growth factor 23]]
* High levels of [[fibroblast growth factor 23]] are found in chronic kidney disease.
{| class="wikitable"
{| class="wikitable"
! colspan="7" | Factors in the pathogenesis of hyperparathyroidism in chronic renal disease
! colspan="7" | Factors in the pathogenesis of hyperparathyroidism in chronic renal disease
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==Causes==
==Causes==
The common causes of renal osteodystrophy are:<ref>{{cite book | last = Nissenson | first = Allen | title = Current diagnosis & treatment | publisher = McGraw-Hill Medical | location = New York | year = 2009 | isbn = 978-0-07-144787-4 }}</ref>
The common causes of renal osteodystrophy are<ref>{{cite book | last = Nissenson | first = Allen | title = Current diagnosis & treatment | publisher = McGraw-Hill Medical | location = New York | year = 2009 | isbn = 978-0-07-144787-4 }}</ref>
* Disorder of bone and mineral metabolism associated with chronic renal disease.
* chronic renal disease
* [[Hypocalcemia]]
* [[Hypocalcemia]]
* [[Hyperphosphotemia]]
* [[Hyperphosphotemia|Hyperphosphatemia]]
* [[1,25D defeciency]]
* [[1,25D defeciency|Vit D deficiency]]
* Parathyroid gland [[hyperplasia]]
* Parathyroid gland [[hyperplasia]]
* Systemic [[acidosis]]
* Systemic [[acidosis]]
* [[Aluminum]] retention,(in dialysis patients)  
* [[Aluminum]] retention(in dialysis patients)  
* Accumulation of [[β2M]] in bone and joints.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* Accumulation of [[β2M]] in bone and joints<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>


==Differentiating Renal Osteodystrophy from Other Diseases==
==Differentiating Renal Osteodystrophy from Other Diseases==
[[Renal osteodystrophy]] must be differentiated from other diseases that cause abnormal bone mineralization, unexplained bone fractures and bone pain,it include
[[Renal osteodystrophy]] must be differentiated from the  diseases that cause abnormal bone mineralization, unexplained bone fractures and bone pain.
* Primary Hyperparathyroidism,which typically presents with [[hypercalcemia]], [[hyperparathyroidism]], and normal-to-low phosphate in patients with normal or minimally-reduced renal function<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* Primary Hyperparathyroidism will have [[hypercalcemia]], [[hyperparathyroidism]], and normal-to-low phosphate in patients with either normal or slightly reduced renal function<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* Tertiary Hyperparathyroidism typically presents as hypercalcemia, hyperparathyroidism, and normal-to-elevated phosphate in patients with longstanding CKD-MBD.
* Tertiary Hyperparathyroidism presents as hypercalcemia, hyperparathyroidism, and normal or slightly elevated phosphate in patients with longterm chronic kidney disease and mineral bone disorder (CKD-MBD)


* [[Osteoporosis]] and
* [[Osteoporosis]], patients will have normal renal function.
* Vitamin D deficiency will have normal or minimally reduced renal function.
* Vitamin D deficiency will have normal or slight reduction in renal function.


==Epidemiology and Demographics==
==Epidemiology and Demographics==
* Approximately 8% of the adult population in the US has a glomular filtration rate (GFR) less than 60 mL/min and is at risk of developing renal osteodystrophy and other manifestations of CKD-MBD.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* The prevelence of renal osteodystrophy is 8% in the adult population in US . The incidence increases in patients with chronic kidney disease who have glomerular filtration rate (GFR) less than 60 mL/min.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* Prevalence in developing countries:
* Prevalence in developing countries:
**The prevalence of renal osteodystrophy in developing countries 24.4% to 63%.
**The prevalence of renal osteodystrophy in developing countries is 24.4% to 63%.
** Aluminium related bone disease is a common cause. High strontium levels and iron overload in developing countries play a major role in the development of renal bone disease among dialysis patients.
** Aluminium,high strontium levels and iron overload plays a major role in the development of renalosteodystrophy in patients who undergo dialysis.


==Risk Factors==
==Risk Factors==
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* Extraskeletal calcification can also affect the heart valves and the cardiac [[conduction]] system.
* Extraskeletal calcification can also affect the heart valves and the cardiac [[conduction]] system.
* Calcification of skin [[arterioles]] may lead to a condition of ischemia and necrosis of the skin known as [[calciphylaxis]].
* Calcification of skin [[arterioles]] may lead to a condition of ischemia and necrosis of the skin known as [[calciphylaxis]].
'''[[Prognosis]]''' is generally good after Renal Transplant, otherwise it is associated with increase risk of bone fractures , cardiovascular calcifications ,poor quality of life and increased [[morbidity]] and [[mortality]] in patients with Chronic Kidney disease.<ref name="HruskaEpstein19955">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
'''[[Prognosis]]''' is generally good after renal transplant, otherwise it is associated with increase risk of bone fractures , cardiovascular calcifications ,poor quality of life and increased [[morbidity]] and [[mortality]] in patients with Chronic Kidney disease.<ref name="HruskaEpstein19955">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>


==Diagnosis==
==Diagnosis==
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===Diagnostic Study of Choice===
===Diagnostic Study of Choice===
====Bone biopsy====
====Bone biopsy====
* A definitive tool for diagnosis of renal osteodystrophy is bone [[biopsy]].


A definitive diagnosis of renal osteodystrophy and the identification of histologic subtype are made by bone [[biopsy]].
* however bone biopsy are infrequently performed because it is [[invasive]] and expensive procedure. 
 
however bone biopsy are infrequently performed because it is [[invasive]] and expensive procedure. 
 
Indication for bone biopsy:
Indication for bone biopsy:


According to KDIGO 2017 guidelines a bone biopsy is indicated if knowledge of the type of renal osteodystrophy will affect treatment decisions <ref>{{Cite journal
According to KDIGO 2017 guidelines a bone biopsy is indicated if finding of the type of renal osteodystrophy will affect the method of treatment <ref>{{Cite journal


  | author = [[Markus Ketteler]], [[Geoffrey A. Block]], [[Pieter Evenepoel]], [[Masafumi Fukagawa]], [[Charles A. Herzog]], [[Linda McCann]], [[Sharon M. Moe]], [[Rukshana Shroff]], [[Marcello A. Tonelli]], [[Nigel D. Toussaint]], [[Marc G. Vervloet]] & [[Mary B. Leonard]]
  | author = [[Markus Ketteler]], [[Geoffrey A. Block]], [[Pieter Evenepoel]], [[Masafumi Fukagawa]], [[Charles A. Herzog]], [[Linda McCann]], [[Sharon M. Moe]], [[Rukshana Shroff]], [[Marcello A. Tonelli]], [[Nigel D. Toussaint]], [[Marc G. Vervloet]] & [[Mary B. Leonard]]
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* [[Alkaline phosphatase]] (total or bone-specific)
* [[Alkaline phosphatase]] (total or bone-specific)
* [[Parathyroid hormone]](PTH)  
* [[Parathyroid hormone]](PTH)  
'''PTH''' levels are the best noninvasive option for assessment of bone turnover.<ref name="GonzalezMartin19953">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology Dialysis Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref> <ref name="HruskaEpstein19954">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
'''PTH''' levels are considered to be the best noninvasive option to assess h bone turnover.<ref name="GonzalezMartin19953">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology Dialysis Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref> <ref name="HruskaEpstein19954">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>


The following parameters are used to define the risk for specific subtypes of renal osteodystrophy :<ref name=":0">{{Cite journal
The following framework is used to describe the risk for different subtypes of renal osteodystrophy<ref name=":0">{{Cite journal


  | author = [[Sharon M. Moe]]
  | author = [[Sharon M. Moe]]
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}}</ref>
}}</ref>


 ●PTH <100 pg/mL suggests adynamic bone disease and a decreased risk of [[osteitis fibrosa cystica ]]and .
 ●PTH <100 pg/mL  means adynamic bone disease and a decreased risk of [[osteitis fibrosa cystica ]].


●PTH >450 pg/mL suggests osteitis fibrosa cystica and/or MUO(mixed uremic osteodystrophy)
●PTH >450 pg/mL means osteitis fibrosa cystica and/or MUO(mixed uremic osteodystrophy)


●Intermediate PTH levels between 100 and 450 pg/mL are not useful to predict the type of renal osteodystrophy. Intermediate values may be associated with normal or increased turnover or even reduced turnover. .<ref name="MoeDrüeke20065">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref>   
●Intermediate PTH levels between 100 and 450 pg/mL  Intermediate values may be due to normal or increased turnover or even reduced turnover.<ref name="MoeDrüeke20065">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref>   


===History and Symptoms===
===History and Symptoms===
Renal osteodystrophy may exhibit no symptoms; if it does they include:
Renal osteodystrophy usually show no symptoms; if it does they may include,
* Bone pain
* Bone pain
* Joint pain
* Joint pain
* Chest pain due to atherosclerotic disease
* Chest pain  
* [[Dyspnea]], due to CHF
* [[Dyspnea]]
* Palpitation or slow pulse due to conduction heart defects.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* Palpitation or slow pulse <ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>


===Physical Examination===
===Physical Examination===
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=== Laboratory Findings ===
=== Laboratory Findings ===
*  Measurement of [[bone turnover]] on a bone biopsy is assessed by labeling the bone with [[tetracycline]] at two separate times approximately 2 weeks apart. The distance between the two areas of tetracycline deposition can be used to calculate bone growth.
*  Measurement of [[bone turnover]] on a bone biopsy is determined by labeling the bone with [[tetracycline]].it is done at two separate times approximately 2 weeks apart. The distance between the two areas of tetracycline deposition is measured and it can be used to calculate bone growth.


* Serum calcium, levels are typically low.
* Serum calcium, levels are typically low.
* Serum phosphorous is elevated depending on the stage of chronic kidney disease, adherence to dietary phosphorous restriction, and use of phosphate binders.
* Serum phosphorous is elevated depending on the stage of chronic kidney disease, dietary phosphorous , and use of phosphate binders.
* Alkaline phosphatase (total or bone-specific) are elevated and may indicate increased osteoblastic activity. very high levels are suggestive of severe osteitis fibrosa  
* Alkaline phosphatase (total or bone-specific) are elevated and shows increased osteoblastic activity. High levels are seen in severe osteitis fibrosa.
'''PTH''' levels are the best noninvasive option for assessment of bone turnover. <ref name="HruskaEpstein19958">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
'''PTH''' levels are the best noninvasive option for assessment of bone turnover.<ref name="HruskaEpstein19958">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>


the following parameters are used to define the risk for specific subtypes of renal osteodystrophy :<ref name=":0" />
the following parameters are used to define the risk for specific subtypes of renal osteodystrophy.<ref name=":0" />


 ●PTH <100 pg/mL suggests adynamic bone disease and a decreased risk of osteitis fibrosa cystica and or MUO.
 ●PTH <100 pg/mL suggests adynamic bone disease and a decreased risk of osteitis fibrosa cystica and or MUO.
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●PTH >450 pg/mL suggests osteitis fibrosa cystica and/or MUO.
●PTH >450 pg/mL suggests osteitis fibrosa cystica and/or MUO.


●Intermediate PTH levels between 100 and 450 pg/mL are not useful to predict the type of renal osteodystrophy. Intermediate values may be associated with normal or increased turnover or even reduced turnover. .  <ref name="MoeDrüeke20066">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref> 
●Intermediate PTH levels between 100 and 450 pg/mL are not useful to predict the type of renal osteodystrophy. Intermediate values may be associated with normal or increased turnover or even reduced turnover. <ref name="MoeDrüeke20066">{{cite journal|last1=Moe|first1=S.|last2=Drüeke|first2=T.|last3=Cunningham|first3=J.|last4=Goodman|first4=W.|last5=Martin|first5=K.|last6=Olgaard|first6=K.|last7=Ott|first7=S.|last8=Sprague|first8=S.|last9=Lameire|first9=N.|last10=Eknoyan|first10=G.|title=Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)|journal=Kidney International|volume=69|issue=11|year=2006|pages=1945–1953|issn=00852538|doi=10.1038/sj.ki.5000414}}</ref> 


=== Electrocardiogram ===
=== Electrocardiogram ===
Line 321: Line 318:


=== X-ray ===
=== X-ray ===
*  Routine [[radiographic]] screening are not performed for bone disease in patients with end-stage renal disease (ESRD).
*  Routine [[radiographic]] screening are not done for bone disease in patients with end-stage renal disease (ESRD).


* Radiographic findings are less sensitive for diagnosis than PTH levels and do not establish the type of bone disease.
* Radiographic findings are less sensitive for diagnosis than PTH levels.


* Imaging may be done for patients with unexplained bone pain or fractures.  
* Imaging are usually performed for patients with unexplained bone pain or fractures.  
* Characteristic radiographic findings of osteitis fibrosa cystica include subperiosteal resorption and new bone formation, particularly at the radial aspect of the middle phalanges.
* Radiographic findings of osteitis fibrosa cystica include subperiosteal resorption and new bone formation specially at the radial aspect of the middle phalanges.
* [[Resorptive]] loss of bone may be also observed at the terminal phalanges, distal ends of the clavicles, and in the skull.
* [[Resorptive]] loss of bone can be seen at the terminal phalanges, distal ends of the clavicles, and in the skull.


* Radiographs may also reveal soft tissue calcification, particularly including the [[vasculature]],<ref name="GonzalezMartin19954">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology Dialysis Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref>
* Radiographs are helpful to show soft tissue calcification, particularly that involves the [[vasculature]],<ref name="GonzalezMartin19954">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology Dialysis Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref>


===Echocardiography or Ultrasound===
===Echocardiography or Ultrasound===
echocardiography will show
Echocardiography will show
* [[Diastolic]] dysfunction,
* [[Diastolic]] dysfunctiong
* Left Ventricular [[Hypertrophy]]
* Left Ventricular [[Hypertrophy]]
* [[Valvular calcifications]]
* [[Valvular calcifications]]
Line 347: Line 344:


===Other Diagnostic Studies===
===Other Diagnostic Studies===
 '''[[DEXA bone densitometry]]''' may reveal low bone density.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
 '''[[DEXA bone densitometry]]''' will show low bone density.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
 
==Treatment==
==Treatment==
===Medical Therapy:<ref name="GonzalezMartin19955">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology [[Dialysis]] Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref>===
===Medical Therapy:<ref name="GonzalezMartin19955">{{cite journal|last1=Gonzalez|first1=E. A.|last2=Martin|first2=K. J.|title=Renal osteodystrophy: pathogenesis and management|journal=Nephrology [[Dialysis]] Transplantation|volume=10|issue=supp3|year=1995|pages=13–21|issn=0931-0509|doi=10.1093/ndt/10.supp3.13}}</ref>===
The mainstays of the [[prevention]] and treatment of renal osteodystrophy continue to be phosphate binders and supplemental calcium.
Phosphate binders and supplemental calcium are mainly used for [[prevention]] and treatment of renal osteodystrophy.


'''Control of Serum Phosphate '''<ref name="HruskaEpstein19955">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
'''Control of Serum Phosphate '''<ref name="HruskaEpstein19955">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
* A low-phosphate diet is integral to the management of end-stage renal disease, to maintain a normal serum phosphate concentration.  
* A low-phosphate diet is mandatory in the end-stage renal disease, to keep serum phosphate concentration with in the normal limits.  
* A phosphate binder, either calcium carbonate68 or calcium acetate,69 taken with each meal in proportion to the phosphate content of the meal, is usually also required;
* A phosphate binder, either calcium carbonate68 or calcium acetate69 is required to be taken with each meal.
* Aluminum-containing phosphate binders should be avoided. Reducing dialysate magnesium concentrations and adding magnesium-containing binders to decrease the calcium salts may allow both the control of serum phosphate concentrations and higher doses of calcitriol70 .
* Aluminum-containing phosphate binders should be avoided.
'''Control of Serum Calcium'''<ref name="HruskaEpstein19956">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
'''Control of Serum Calcium'''<ref name="HruskaEpstein19956">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>


Calcium malabsorption is very common in end-stage renal disease because of deficient 1,25-dihydroxycholecalciferol.
Calcium malabsorption is seen in end-stage renal disease because of deficient 1,25-dihydroxycholecalciferol.
*Serum calcium concentrations need to be maintained at the high end of the normal range in order to prevent or suppress oversecretion of parathyroid hormone.
*To prevent or suppress oversecretion of parathyroid hormone, calcium concentrations should be maintained at the high end of the normal range.
* 71 A dialysate calcium concentration of 7 mg per deciliter (1.75 mmol per liter) provides an influx of approximately 800 mg per treatment.
* 71 A dialysate calcium concentration of 7 mg per deciliter provides approximately 800 mg calcium per treatment.
* . When calcium salts are required to control hyperphosphatemia, the increased dialysate calcium concentration may cause hypercalcemia. The dialysate calcium concentration should be reduced to 5 mg per deciliter (1.25 mmol per liter), a level that will not affect the calcium balance and will allow for sufficient oral intake of calcium salts to maintain normal serum phosphate concentrations.73 The timing of oral calcium intake is important; calcium taken between meals is more a calcium supplement than a phosphate binder.
* To control hyperphosphatemia, the increased dialysate calcium concentration may cause hypercalcemia ,in such situation the dialysate calcium concentration should be reduced to 5 mg per deciliter. this level will not affect the calcium balance.
* The timing of taking oral calcium is crucial as calcium taken between meals is more like a calcium supplement than a phosphate binder.
'''Use of Vit D analogue'''<ref name="HruskaEpstein19957">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
'''Use of Vit D analogue'''<ref name="HruskaEpstein19957">{{cite journal|last1=Hruska|first1=Keith A.|last2=Epstein|first2=Franklin H.|last3=Teitelbaum|first3=Steven L.|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=333|issue=3|year=1995|pages=166–175|issn=0028-4793|doi=10.1056/NEJM199507203330307}}</ref>
* [[Calcitriol]]  [[alfacalcidol]], [[dihydrotachysterol]], and [[calcifediol]] - These agents lessen bone pain, improve bone histologic characteristics, and suppress parathyroid hormone secretion by both raising serum calcium concentrations and inhibiting parathyroid hormone gene [[transcription]].
* [[Calcitriol]]  [[alfacalcidol]], [[dihydrotachysterol]], and [[calcifediol]] - They reduce bone pain, improve bone histologic characteristics, and suppress parathyroid hormone secretion by increasing serum calcium concentrations and inhibiting parathyroid hormone gene [[transcription]].


===Surgery===
===Surgery===
* subtotal [[parathyroidectomy]]  
* subtotal [[parathyroidectomy]]  
Mainstay of treatment for Renal Osteodystrophy is medical therapy. Surgery is usually reserved for patients with hyperparathroid bone disease  
* The treatment for Renal Osteodystrophy is medical therapy. Surgery is usually reserved for patients with hyperparathroid bone disease  
 
* Renal Transplant<ref name="MallucheFaugere1989">{{cite journal|last1=Malluche|first1=Harmut H.|last2=Faugere|first2=Marie-Claude|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=321|issue=5|year=1989|pages=317–319|issn=0028-4793|doi=10.1056/NEJM198908033210509}}</ref>
* Renal Transplant<ref name="MallucheFaugere1989">{{cite journal|last1=Malluche|first1=Harmut H.|last2=Faugere|first2=Marie-Claude|title=Renal Osteodystrophy|journal=New England Journal of Medicine|volume=321|issue=5|year=1989|pages=317–319|issn=0028-4793|doi=10.1056/NEJM198908033210509}}</ref>


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nazia Fuad M.D.

Synonyms and keywords:Chronic kidney disease- mineral bone disorder

Overview

Renal osteodystrophy is the term used to describe the complex metabolic bone disorders which are present in chronic renal insufficiency. Secondary hyperparathyroidism and 1,25-dihydroxycholecalciferol (Vitamin D3) deficiency play major role in renal osteodystrophy. It is defined as an alteration of bone morphology in patients with chronic kidney disease and is considered to be a component of chronic kidney disease - mineral bone disorder (CKD-MBD). Renal osteodystrophy is an important cause of morbidity, decreased quality of life, and extravascular calcifications that have been associated with increased cardiovascular mortality. The classification of renal osteodystrophy is based on a unified system that describes a wider clinical syndrome based on bone turnover, bone mineralization, and bone volume. For investigating renal osteodystrophy, blood levels of parathyroid hormone (PTH), calcium, phosphorus, alkaline phosphatase, bicarbonate should be ordered initially. Imaging studies should focus on finding calcification in soft tissues. Bone biopsy is indicated if the results of biochemical markers are not consistent, there is unexplained bone pain, or presence of unexplained bone fractures. However, bone biopsy is infrequently used in clinical practice due to invasiveness and lower cost effectiveness. The major objective in the prevention and management of renal osteodystrophy is either prevention of hyperparathyroidism or treatment if present already .

Historical Perspective

  • Renal osteodystrophy was first defined by Kidney Disease: Improving Global Outcomes (KDIGO) in 2006.
  • It was found out in 1970s and 1980s, that aluminum in water that is used for dialysis and aluminum salts that are used as phosphate binders caused osteomalacia and an adynamic bone disease. The identification of these disorders led to define renal osteodystrophy, since then the composition of dialysis fluids was changed and calcium carbonate was substituted for aluminum salts. As a result, bone disease due to deposition of aluminium is decreasing.[1]

Classification

Table 1. Histologic Classification of Renal Osteodystrophy[2][3]

Histologic Classification of Renal Osteodystrophy
Disorder Description Pathogenesis frequency(%)
Osteitis fibrosa  Peritrabecular fibrosis, increased

remodeling — resorption and

formation.

Secondary hyperparathyroidism, secondary

role of cytokines and growth factors

50
Osteomalacia  Increased osteoid, defective

mineralization

Aluminum deposition, plus

unknown factors

7
Mixed disease  Features of both osteitis fibrosa

and osteomalacia

Secondary hyperparathyroidism

and aluminum deposition,

plus unknown factors

13
Mild disease  Slightly increased remodeling Early or treated secondary

hyperparathyroidism

3
Adynamic renal

bone disease

Hypocellular bone surfaces,

no remodeling

Aluminum deposition, parathyroid hormone

suppression, and other factors

(deficiency of bone growth factors or

increased suppressors of bone remodeling)

27

Table 2 .TMV Classification

It is done on the basis of results of bone biopsy, and uses three histologic descriptions- bone turnover, bone mineralization

and bone volume. After the bone pathology is assessed by histomorphometry, it helps to define the pathophysiology and to choose the right therapy.[4]

Turnover Mineralization Volume
Low Low
Normal
Normal Normal
Abnormal
High High

Pathophysiology

The following factors in chronic kidney disease are considered to be the main contributers[5][6][7]

  • Hyperphosphatemia ,when GFR falls below 60ml/min in chronic Kidney disease there is impaired renal phosphorus excretion resulting in hyperphosphotemia
  •  Hypocalcemia, because of decreased excretion of phosphate by the damaged kidneys.
  • Low activated vitamin D3 levels happens because the damaged kidneys are unable to convert vitamin D3 into its active form, calcitriol, this results in further hypocalcaemia.
  •  Hyperphosphatemia combined with hypocalcemia results in hyperparathyroidism
  • Elevated level of Hyperparathyroid leads to Osteitis fibrosa .
  • High levels of fibroblast growth factor 23 are found in chronic kidney disease.
 Factors in the pathogenesis of hyperparathyroidism in chronic renal disease
phosphorus retention Hypocalcemia Low Calciterol Skeletal

resistance

Altered

parathyroid

function

↓Renal mass + +
↑Phosphorus + + + ?
↓Calcium +
↓Calciterol + + +
Skeletal resistance +
Desensitization to PTH +
↓Vit D recepters +
Altered cell growth +
Acidosis +

Causes

The common causes of renal osteodystrophy are[8]

Differentiating Renal Osteodystrophy from Other Diseases

Renal osteodystrophy must be differentiated from the diseases that cause abnormal bone mineralization, unexplained bone fractures and bone pain.

  • Primary Hyperparathyroidism will have hypercalcemia, hyperparathyroidism, and normal-to-low phosphate in patients with either normal or slightly reduced renal function[10]
  • Tertiary Hyperparathyroidism presents as hypercalcemia, hyperparathyroidism, and normal or slightly elevated phosphate in patients with longterm chronic kidney disease and mineral bone disorder (CKD-MBD)
  • Osteoporosis, patients will have normal renal function.
  • Vitamin D deficiency will have normal or slight reduction in renal function.

Epidemiology and Demographics

  • The prevelence of renal osteodystrophy is 8% in the adult population in US . The incidence increases in patients with chronic kidney disease who have glomerular filtration rate (GFR) less than 60 mL/min.[11]
  • Prevalence in developing countries:
    • The prevalence of renal osteodystrophy in developing countries is 24.4% to 63%.
    • Aluminium,high strontium levels and iron overload plays a major role in the development of renalosteodystrophy in patients who undergo dialysis.

Risk Factors

The major risk factor in the development of Renal Osteodystrophy is:

Natural History, Complications, and Prognosis

Common complications of Renal osteodystrophy include

Prognosis is generally good after renal transplant, otherwise it is associated with increase risk of bone fractures , cardiovascular calcifications ,poor quality of life and increased morbidity and mortality in patients with Chronic Kidney disease.[12]

Diagnosis

Diagnostic Study of Choice

Bone biopsy

  • A definitive tool for diagnosis of renal osteodystrophy is bone biopsy.
  • however bone biopsy are infrequently performed because it is invasive and expensive procedure. 

Indication for bone biopsy:

According to KDIGO 2017 guidelines a bone biopsy is indicated if finding of the type of renal osteodystrophy will affect the method of treatment [13]

Serum biomarkers: 

The following biomarkers are used in the diagnosis of renal osteodystrophy

PTH levels are considered to be the best noninvasive option to assess h bone turnover.[14] [15]

The following framework is used to describe the risk for different subtypes of renal osteodystrophy[16]

 ●PTH <100 pg/mL  means adynamic bone disease and a decreased risk of osteitis fibrosa cystica .

●PTH >450 pg/mL means osteitis fibrosa cystica and/or MUO(mixed uremic osteodystrophy)

●Intermediate PTH levels between 100 and 450 pg/mL  Intermediate values may be due to normal or increased turnover or even reduced turnover.[17]   

History and Symptoms

Renal osteodystrophy usually show no symptoms; if it does they may include,

  • Bone pain
  • Joint pain
  • Chest pain
  • Dyspnea
  • Palpitation or slow pulse [18]

Physical Examination

Patients with renal osteodystrophy usually appear sick. Physical examination of patients with Renal Osteodystrophy may include

Laboratory Findings

  •  Measurement of bone turnover on a bone biopsy is determined by labeling the bone with tetracycline.it is done at two separate times approximately 2 weeks apart. The distance between the two areas of tetracycline deposition is measured and it can be used to calculate bone growth.
  • Serum calcium, levels are typically low.
  • Serum phosphorous is elevated depending on the stage of chronic kidney disease, dietary phosphorous , and use of phosphate binders.
  • Alkaline phosphatase (total or bone-specific) are elevated and shows increased osteoblastic activity. High levels are seen in severe osteitis fibrosa.

PTH levels are the best noninvasive option for assessment of bone turnover.[20]

the following parameters are used to define the risk for specific subtypes of renal osteodystrophy.[16]

 ●PTH <100 pg/mL suggests adynamic bone disease and a decreased risk of osteitis fibrosa cystica and or MUO.

●PTH >450 pg/mL suggests osteitis fibrosa cystica and/or MUO.

●Intermediate PTH levels between 100 and 450 pg/mL are not useful to predict the type of renal osteodystrophy. Intermediate values may be associated with normal or increased turnover or even reduced turnover. [21] 

Electrocardiogram

Ekg findings in patients with renal osteodystrophy may include[22]

X-ray

  •  Routine radiographic screening are not done for bone disease in patients with end-stage renal disease (ESRD).
  • Radiographic findings are less sensitive for diagnosis than PTH levels.
  • Imaging are usually performed for patients with unexplained bone pain or fractures.
  • Radiographic findings of osteitis fibrosa cystica include subperiosteal resorption and new bone formation specially at the radial aspect of the middle phalanges.
  • Resorptive loss of bone can be seen at the terminal phalanges, distal ends of the clavicles, and in the skull.
  • Radiographs are helpful to show soft tissue calcification, particularly that involves the vasculature,[23]

Echocardiography or Ultrasound

Echocardiography will show

CT scan

CT scan findings associated with Renal Osteodystrophy are the same that r related to chronic kidney disease .

MRI

There are no MRI findings .

Other Imaging Findings

There are no other imaging findings associated with Renal Osteodystrophy

Other Diagnostic Studies

 DEXA bone densitometry will show low bone density.[24]

Treatment

Medical Therapy:[25]

Phosphate binders and supplemental calcium are mainly used for prevention and treatment of renal osteodystrophy.

Control of Serum Phosphate [12]

  • A low-phosphate diet is mandatory in the end-stage renal disease, to keep serum phosphate concentration with in the normal limits.
  • A phosphate binder, either calcium carbonate68 or calcium acetate69 is required to be taken with each meal.
  • Aluminum-containing phosphate binders should be avoided.

Control of Serum Calcium[26]

Calcium malabsorption is seen in end-stage renal disease because of deficient 1,25-dihydroxycholecalciferol.

  • To prevent or suppress oversecretion of parathyroid hormone, calcium concentrations should be maintained at the high end of the normal range.
  • 71 A dialysate calcium concentration of 7 mg per deciliter provides approximately 800 mg calcium per treatment.
  • To control hyperphosphatemia, the increased dialysate calcium concentration may cause hypercalcemia ,in such situation the dialysate calcium concentration should be reduced to 5 mg per deciliter. this level will not affect the calcium balance.
  • The timing of taking oral calcium is crucial as calcium taken between meals is more like a calcium supplement than a phosphate binder.

Use of Vit D analogue[27]

Surgery

  • subtotal parathyroidectomy
  • The treatment for Renal Osteodystrophy is medical therapy. Surgery is usually reserved for patients with hyperparathroid bone disease
  • Renal Transplant[28]

Primary Prevention

  • Timely recognition and treatment of hyperparathyroid patients.
  • Early recognition and treatment of renal diseases to prevent chronic renal failure and consequently Renal osteodystrophy[29]

Secondary Prevention

References

  1. ↑ Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  2. ↑ Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  3. ↑ Moe, S.; Drüeke, T.; Cunningham, J.; Goodman, W.; Martin, K.; Olgaard, K.; Ott, S.; Sprague, S.; Lameire, N.; Eknoyan, G. (2006). "Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)". Kidney International. 69 (11): 1945–1953. doi:10.1038/sj.ki.5000414. ISSN 0085-2538.
  4. ↑ Moe, S.; Drüeke, T.; Cunningham, J.; Goodman, W.; Martin, K.; Olgaard, K.; Ott, S.; Sprague, S.; Lameire, N.; Eknoyan, G. (2006). "Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)". Kidney International. 69 (11): 1945–1953. doi:10.1038/sj.ki.5000414. ISSN 0085-2538.
  5. ↑ Gonzalez, E. A.; Martin, K. J. (1995). "Renal osteodystrophy: pathogenesis and management". Nephrology Dialysis Transplantation. 10 (supp3): 13–21. doi:10.1093/ndt/10.supp3.13. ISSN 0931-0509.
  6. ↑ Moe, S.; Drüeke, T.; Cunningham, J.; Goodman, W.; Martin, K.; Olgaard, K.; Ott, S.; Sprague, S.; Lameire, N.; Eknoyan, G. (2006). "Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)". Kidney International. 69 (11): 1945–1953. doi:10.1038/sj.ki.5000414. ISSN 0085-2538.
  7. ↑ Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  8. ↑ Nissenson, Allen (2009). Current diagnosis & treatment. New York: McGraw-Hill Medical. ISBN 978-0-07-144787-4.
  9. ↑ https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy
  10. ↑ https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy
  11. ↑ https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy
  12. ↑ 12.0 12.1 Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  13. ↑ Markus Ketteler, Geoffrey A. Block, Pieter Evenepoel, Masafumi Fukagawa, Charles A. Herzog, Linda McCann, Sharon M. Moe, Rukshana Shroff, Marcello A. Tonelli, Nigel D. Toussaint, Marc G. Vervloet & Mary B. Leonard. "Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters". Kidney international. 92 (1): 26–36. PMID 28646995. Unknown parameter |= ignored (help); Unknown parameter |month= ignored (help)
  14. ↑ Gonzalez, E. A.; Martin, K. J. (1995). "Renal osteodystrophy: pathogenesis and management". Nephrology Dialysis Transplantation. 10 (supp3): 13–21. doi:10.1093/ndt/10.supp3.13. ISSN 0931-0509.
  15. ↑ Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  16. ↑ 16.0 16.1 Sharon M. Moe. "Management of renal osteodystrophy in peritoneal dialysis patients". Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis. 24 (3): 209–216. PMID 15185768. Unknown parameter |= ignored (help); Unknown parameter |month= ignored (help)
  17. ↑ Moe, S.; Drüeke, T.; Cunningham, J.; Goodman, W.; Martin, K.; Olgaard, K.; Ott, S.; Sprague, S.; Lameire, N.; Eknoyan, G. (2006). "Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)". Kidney International. 69 (11): 1945–1953. doi:10.1038/sj.ki.5000414. ISSN 0085-2538.
  18. ↑ https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy
  19. ↑ https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy
  20. ↑ Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  21. ↑ Moe, S.; Drüeke, T.; Cunningham, J.; Goodman, W.; Martin, K.; Olgaard, K.; Ott, S.; Sprague, S.; Lameire, N.; Eknoyan, G. (2006). "Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)". Kidney International. 69 (11): 1945–1953. doi:10.1038/sj.ki.5000414. ISSN 0085-2538.
  22. ↑ https://radiopaedia.org/articles/renal-osteodystrophy
  23. ↑ Gonzalez, E. A.; Martin, K. J. (1995). "Renal osteodystrophy: pathogenesis and management". Nephrology Dialysis Transplantation. 10 (supp3): 13–21. doi:10.1093/ndt/10.supp3.13. ISSN 0931-0509.
  24. ↑ https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy
  25. ↑ Gonzalez, E. A.; Martin, K. J. (1995). "Renal osteodystrophy: pathogenesis and management". Nephrology Dialysis Transplantation. 10 (supp3): 13–21. doi:10.1093/ndt/10.supp3.13. ISSN 0931-0509.
  26. ↑ Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  27. ↑ Hruska, Keith A.; Epstein, Franklin H.; Teitelbaum, Steven L. (1995). "Renal Osteodystrophy". New England Journal of Medicine. 333 (3): 166–175. doi:10.1056/NEJM199507203330307. ISSN 0028-4793.
  28. ↑ Malluche, Harmut H.; Faugere, Marie-Claude (1989). "Renal Osteodystrophy". New England Journal of Medicine. 321 (5): 317–319. doi:10.1056/NEJM198908033210509. ISSN 0028-4793.
  29. ↑ Malluche, Harmut H.; Faugere, Marie-Claude (1989). "Renal Osteodystrophy". New England Journal of Medicine. 321 (5): 317–319. doi:10.1056/NEJM198908033210509. ISSN 0028-4793.
  30. ↑ Malluche, Harmut H.; Faugere, Marie-Claude (1989). "Renal Osteodystrophy". New England Journal of Medicine. 321 (5): 317–319. doi:10.1056/NEJM198908033210509. ISSN 0028-4793.

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