Renal osteodystrophy: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
Line 6: Line 6:
{{SK}}Chronic kidney disease- mineral bone disorder
{{SK}}Chronic kidney disease- mineral bone disorder
==Overview==
==Overview==
Renal osteodystrophy is<nowiki/> defined as 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 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 .
Renal osteodystrophy is<nowiki/> defined as 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 a major role in renal osteodystrophy. Renal osteodystrophy 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 describes a wider clinical syndrome based on bone turnover, bone mineralization, and bone volume. To investigate renal osteodystrophy, blood levels of [[parathyroid hormone]] (PTH), [[calcium]], [[phosphorus]], [[alkaline phosphatase]], [[bicarbonate]] should initially be ordered. Imaging studies should focus on finding [[calcification]] in soft tissues. A 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 biopsies are 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==
* Renal osteodystrophy was first defined by Kidney Disease: Improving Global Outcomes [[(KDIGO)]] in 2006.
* 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 [[Aluminium|aluminum s]]<nowiki/>alts. 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>
* It was discovered in the 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 [[Aluminium|aluminum s]]<nowiki/>alts. As a result, bone disease due to deposition of [[aluminium|aluminum]] 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==
* Renal osteodystrophy can be classified according to histology into following subtypes:<ref name="HruskaEpstein1995">{{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="MoeDrüeke20062">{{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>
* Renal osteodystrophy can be classified according to histology into the following subtypes:<ref name="HruskaEpstein1995">{{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="MoeDrüeke20062">{{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"
! colspan="4" |Histologic Classification of Renal Osteodystrophy
! colspan="4" |Histologic Classification of Renal Osteodystrophy
Line 20: Line 20:
|Description
|Description
|Pathogenesis
|Pathogenesis
|frequency(%)
|frequency (%)
|-
|-
|[[Osteitis fibrosa]]
|[[Osteitis fibrosa]]
Line 70: Line 70:
== Pathophysiology  ==
== Pathophysiology  ==


The following factors in chronic kidney disease are considered to be the main contributors<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>
The following factors in chronic kidney disease are considered to be the main contributors to renal osteodystrophy:<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>
* [[Hyperphosphatemia]], when [[GFR]] falls below 60 ml/min in [[chronic kidney disease]] there is impaired renal phosphorus excretion resulting in [[hyperphosphatemia]].
* [[Hyperphosphatemia]]: when [[GFR]] falls below 60 ml/min in [[chronic kidney disease]] there is impaired renal phosphorus excretion resulting in [[hyperphosphatemia]].
* [[Hypocalcemia]], because of decreased excretion of [[phosphate]] by the damaged kidneys.
* [[Hypocalcemia]], because of decreased excretion of [[phosphate]] by the damaged kidneys.
* Low activated [[Vitamin D3|vitamin D<sub>3</sub>]] levels happens because the damaged kidneys are unable to convert [[Vitamin D3|vitamin D<sub>3</sub>]] into its active form, [[calcitriol]], this results in further [[hypocalcemia]].
* Low activated [[Vitamin D3|vitamin D<sub>3</sub>]] levels happen because the damaged kidneys are unable to convert [[Vitamin D3|vitamin D<sub>3</sub>]] into its active form, [[calcitriol]], which results in further [[hypocalcemia]].
* [[Hyperphosphatemia]] combined with hypocalcemia results in hyperparathyroidism  
* [[Hyperphosphatemia]] combined with hypocalcemia results in hyperparathyroidism  
* Elevated level of [[Hyperparathyroid]] leads to [[Osteitis fibrosa cystica|Osteitis fibrosa]] .
* Elevated level of [[Hyperparathyroid]] leads to [[Osteitis fibrosa cystica|Osteitis fibrosa]].
* High levels of [[fibroblast growth factor 23]] are found in [[chronic kidney disease]].
* High levels of [[fibroblast growth factor 23]] are found in [[chronic kidney disease]].
{| class="wikitable"
{| class="wikitable"
Line 167: Line 167:
** [[Hypocalcemia]]
** [[Hypocalcemia]]
** [[Hyperphosphotemia|Hyperphosphatemia]]
** [[Hyperphosphotemia|Hyperphosphatemia]]
** [[1,25D defeciency|Vit D deficiency]]
** [[Vit D deficiency]]
** Parathyroid gland [[hyperplasia]]
** Parathyroid gland [[hyperplasia]]
** Systemic [[acidosis]]
** Systemic [[acidosis]]
Line 174: Line 174:


==Differentiating Renal Osteodystrophy from Other Diseases==
==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.
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<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* Primary hyperparathyroidism will cause [[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  presents as hypercalcemia, hyperparathyroidism, and normal or slightly elevated phosphate in patients with longterm chronic kidney disease and mineral bone disorder (CKD-MBD)
* Tertiary hyperparathyroidism causes 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.
* [[Osteoporosis]], patients will have normal renal function.
* Vitamin D deficiency will have normal or slight reduction in renal function.
* Vitamin D deficiency will cause normal or slight reduction in renal function.


==Epidemiology and Demographics==
==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.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
* The [[prevelence]] of renal osteodystrophy is 8,000 per 100,000 in the adult population in US. Incidence of renal osteodystrophy 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 is 24.4% to 63%.
**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.
** Aluminum, high [[strontium]] levels and iron overload play a major role in the development of renal osteodystrophy in patients who undergo dialysis.


==Risk Factors==
==Risk Factors==
*The major risk factor in the development of Renal Osteodystrophy is:
*The major risk factor in the development of renal osteodystrophy is:
** Chronic Renal Disease
** Chronic Renal Disease
**Dialysis
**Dialysis
Line 194: Line 194:


==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
*Common complications of Renal osteodystrophy include  
Common complications of renal osteodystrophy include:
** Bone fractures
* Bone fractures
** Vascular calcifications leading to [[atherosclerosis]], coronary artery calcification, [[hypertension]], left ventricular hypertrophy, and [[congestive heart failure]].
* Vascular calcifications leading to [[atherosclerosis]], coronary artery calcification, [[hypertension]], left ventricular hypertrophy, and [[congestive heart failure]].
** 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 [[Kidney transplantation|renal transplant]], otherwise it is associated with increase risk of bone fractures, [[cardiovascular]] calcification, 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 ======
* Renal osteodystrophy is associated with an increased risk of bone fractures, [[cardiovascular]] calcification, 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>
* However, prognosis is generally good after a [[Kidney transplantation|renal transplant]].


==Diagnosis==
==Diagnosis==
Line 218: Line 220:
}}</ref>
}}</ref>


* However bone biopsy are infrequently performed because it is [[invasive]] and expensive procedure.
* However, bone biopsies are infrequently performed because it is an [[invasive]] and expensive procedure.


'''Serum biomarkers''': 
'''Serum biomarkers''': 
*The following biomarkers are used in the diagnosis of renal osteodystrophy
 
** Serum [[calcium]]
The following biomarkers are used in the diagnosis of renal osteodystrophy
** Serum phosphorous  
* Serum [[calcium]]
** [[Alkaline phosphatase]] (total or bone-specific)
* Serum phosphorous  
** [[Parathyroid hormone]](PTH)  
* [[Alkaline phosphatase]] (total or bone-specific)
*** '''PTH''' levels are considered to be the best noninvasive option to assess 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>
* [[Parathyroid hormone]](PTH)  
** '''PTH''' levels are considered to be the best noninvasive option to assess 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 framework is used to describe the risk for different 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
Line 244: Line 247:


===History and Symptoms===
===History and Symptoms===
*The patients with renal osteodystrophy are usually asymptomatic. When symptomatic, they usually present with:
*Patients with renal osteodystrophy are usually asymptomatic. When symptomatic, they usually present with:
** Bone pain
** Bone pain
** Joint pain
** Joint pain
Line 258: Line 261:
** Congestive heart failure
** Congestive heart failure
** Heart murmur
** Heart murmur
** Increase Pulse Pressure( due to aortic calcification)
** Increase Pulse Pressure (due to aortic calcification)
** [[Ischemia]] and [[necrosis]] of skin called calciphylaxix.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>
** [[Ischemia]] and [[necrosis]] of skin called calciphylaxix.<ref>https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy</ref>


=== Laboratory Findings ===
=== 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.
*  Measurement of [[bone turnover]] on a bone biopsy is determined by labeling the bone with [[tetracycline]]. The procedure is done at two separate times approximately 2 weeks apart. The distance between the two areas of tetracycline deposition is measured and 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, dietary phosphorous , 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 shows increased osteoblastic activity. High levels are seen in severe osteitis fibrosa.  
* [[Alkaline phosphatase]] levels (total or bone-specific) are elevated and show 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>


Line 272: Line 275:
**PTH <100 pg/mL suggests adynamic bone disease and a decreased risk of osteitis fibrosa cystica and or MUO(mixed uremic osteodystrophy)
**PTH <100 pg/mL suggests adynamic bone disease and a decreased risk of osteitis fibrosa cystica and or MUO(mixed uremic osteodystrophy)
**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 in predicting 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 280: Line 283:


=== X-ray ===
=== X-ray ===
* Routine [[radiographic]] screening are not done for bone disease in patients with end-stage renal disease (ESRD).
* Routine [[radiographic]] screenings are not done for bone disease in patients with end-stage renal disease (ESRD).
* Radiographic findings are less sensitive for diagnosis than PTH levels.
* Radiographic findings are less sensitive for diagnosis than PTH levels.
* Imaging is usually performed for patients with unexplained bone pain or fractures.  
* Imaging is usually performed for patients with unexplained bone pain or fractures.  
Line 287: Line 290:
**New bone formation especially at the radial aspect of the middle phalanges.
**New bone formation especially 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.
* [[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]]<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 in showing soft tissue calcification 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]] dysfunctiong
** [[Diastolic]] dysfunction
** Left Ventricular [[Hypertrophy]]
** Left Ventricular [[Hypertrophy]]
** [[Valvular calcifications]]
** [[Valvular calcifications]]
Line 302: Line 305:


===Other Imaging Findings===
===Other Imaging Findings===
*There are no other imaging findings associated with Renal Osteodystrophy
*There are no other imaging findings associated with renal osteodystrophy.


===Other Diagnostic Studies===
===Other Diagnostic Studies===
* '''[[DEXA bone densitometry]]''' will show 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:===
===Medical Therapy:===
Line 311: Line 314:


'''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 mandatory in the end-stage renal disease, to keep serum phosphate concentration with in the normal limits.  
* A low-phosphate diet is mandatory in the end-stages of renal disease, to keep serum phosphate concentration within the normal limits.  
* A phosphate binder, either calcium carbonate68 or calcium acetate69 is required to be taken with each meal.
* A phosphate binder, either calcium carbonate68 or calcium acetate69 is required to be taken with each meal.
* Aluminum-containing phosphate binders should be avoided.
* Aluminum-containing phosphate binders should be avoided.
Line 319: Line 322:
*To prevent or suppress oversecretion of [[parathyroid hormone]], calcium concentrations should be maintained at the high end of the normal range.
*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.
* 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.
* To control hyperphosphatemia, the increased [[dialysate calcium]] concentration may cause hypercalcemia. If so, 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.
* 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]] - They reduce bone pain, improve bone histologic characteristics, and suppress parathyroid hormone secretion by increasing serum calcium concentrations and inhibiting parathyroid hormone gene [[transcription]].<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
* [[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]].<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


===Surgery===
===Surgery===
Line 332: Line 335:
=== Primary Prevention ===
=== Primary Prevention ===
* Timely recognition and treatment of hyperparathyroid patients.
* Timely recognition and treatment of hyperparathyroid patients.
* Early recognition and treatment of renal diseases to prevent chronic renal failure and consequently Renal osteodystrophy<ref name="MallucheFaugere19892">{{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>
* Early recognition and treatment of renal diseases to prevent chronic renal failure and consequently renal osteodystrophy<ref name="MallucheFaugere19892">{{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>.


===Secondary Prevention===
===Secondary Prevention===
* Vit D administration with every session of [[dialysis]]
* Vitamin D administration with every session of [[dialysis]]
* Use of [[aluminium]] free phosphate binders.<ref name="MallucheFaugere19893">{{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>
* Use of [[aluminium|aluminum]]-free phosphate binders.<ref name="MallucheFaugere19893">{{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>


==References==
==References==

Revision as of 01:05, 14 July 2018

WikiDoc Resources for Renal osteodystrophy

Articles

Most recent articles on Renal osteodystrophy

Most cited articles on Renal osteodystrophy

Review articles on Renal osteodystrophy

Articles on Renal osteodystrophy in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Renal osteodystrophy

Images of Renal osteodystrophy

Photos of Renal osteodystrophy

Podcasts & MP3s on Renal osteodystrophy

Videos on Renal osteodystrophy

Evidence Based Medicine

Cochrane Collaboration on Renal osteodystrophy

Bandolier on Renal osteodystrophy

TRIP on Renal osteodystrophy

Clinical Trials

Ongoing Trials on Renal osteodystrophy at Clinical Trials.gov

Trial results on Renal osteodystrophy

Clinical Trials on Renal osteodystrophy at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Renal osteodystrophy

NICE Guidance on Renal osteodystrophy

NHS PRODIGY Guidance

FDA on Renal osteodystrophy

CDC on Renal osteodystrophy

Books

Books on Renal osteodystrophy

News

Renal osteodystrophy in the news

Be alerted to news on Renal osteodystrophy

News trends on Renal osteodystrophy

Commentary

Blogs on Renal osteodystrophy

Definitions

Definitions of Renal osteodystrophy

Patient Resources / Community

Patient resources on Renal osteodystrophy

Discussion groups on Renal osteodystrophy

Patient Handouts on Renal osteodystrophy

Directions to Hospitals Treating Renal osteodystrophy

Risk calculators and risk factors for Renal osteodystrophy

Healthcare Provider Resources

Symptoms of Renal osteodystrophy

Causes & Risk Factors for Renal osteodystrophy

Diagnostic studies for Renal osteodystrophy

Treatment of Renal osteodystrophy

Continuing Medical Education (CME)

CME Programs on Renal osteodystrophy

International

Renal osteodystrophy en Espanol

Renal osteodystrophy en Francais

Business

Renal osteodystrophy in the Marketplace

Patents on Renal osteodystrophy

Experimental / Informatics

List of terms related to Renal osteodystrophy

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 defined as the complex metabolic bone disorders which are present in chronic renal insufficiency. Secondary hyperparathyroidism and 1,25-dihydroxycholecalciferol (Vitamin D3) deficiency play a major role in renal osteodystrophy. Renal osteodystrophy 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 describes a wider clinical syndrome based on bone turnover, bone mineralization, and bone volume. To investigate renal osteodystrophy, blood levels of parathyroid hormone (PTH), calcium, phosphorus, alkaline phosphatase, bicarbonate should initially be ordered. Imaging studies should focus on finding calcification in soft tissues. A 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 biopsies are 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 discovered in the 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 aluminum is decreasing.[1]

Classification

  • Renal osteodystrophy can be classified according to histology into the following subtypes:[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
  • Renal osteodystrophy can be subdivided according to TMV classification which uses three descriptions- bone turnover(T), bone mineralization(M)

and bone volume(V).

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

Pathophysiology

The following factors in chronic kidney disease are considered to be the main contributors to renal osteodystrophy:[5][6][7]

 Factors in the pathogenesis of hyperparathyroidism in chronic renal disease
phosphorus retention Hypocalcemia Low calcitriol Skeletal

resistance

Altered

parathyroid

function

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

Causes

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 cause hypercalcemia, hyperparathyroidism, and normal-to-low phosphate in patients with either normal or slightly reduced renal function[10]
  • Tertiary hyperparathyroidism causes 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 cause normal or slight reduction in renal function.

Epidemiology and Demographics

  • The prevelence of renal osteodystrophy is 8,000 per 100,000 in the adult population in US. Incidence of renal osteodystrophy 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%.
    • Aluminum, high strontium levels and iron overload play a major role in the development of renal osteodystrophy 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:

  • Bone fractures
  • Vascular calcifications leading to atherosclerosis, coronary artery calcification, hypertension, left ventricular hypertrophy, and congestive heart failure.
  • 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.
Prognosis

Diagnosis

Diagnostic Study of Choice

Bone biopsy

  • A definitive tool for diagnosis of renal osteodystrophy is bone biopsy according to KIDGO 2017 guidelines. [13]
  • However, bone biopsies are infrequently performed because it is an invasive and expensive procedure.

Serum biomarkers: 

The following biomarkers are used in the diagnosis of renal osteodystrophy

  • 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 bone turnover[17]   

History and Symptoms

  • Patients with renal osteodystrophy are usually asymptomatic. When symptomatic, they usually present with:
    • 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. The procedure is done at two separate times approximately 2 weeks apart. The distance between the two areas of tetracycline deposition is measured and 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 levels (total or bone-specific) are elevated and show 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(mixed uremic osteodystrophy)
    • PTH >450 pg/mL suggests osteitis fibrosa cystica and/or MUO.
    • Intermediate PTH levels between 100 and 450 pg/mL are not useful in predicting the type of renal osteodystrophy. Intermediate values may be associated with normal or increased turnover or even reduced turnover. [21] 

Electrocardiogram

X-ray

  • Routine radiographic screenings 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 is usually performed for patients with unexplained bone pain or fractures.
  • Radiographic findings of osteitis fibrosa cystica include:
    • Subperiosteal resorption and
    • New bone formation especially 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 in showing soft tissue calcification that involves the vasculature[23].

Echocardiography or Ultrasound

CT scan

  • CT scan findings associated with renal osteodystrophy are the same that are related to chronic kidney disease.

MRI

  • There are no MRI findings associated with renal osteodystrophy.

Other Imaging Findings

  • There are no other imaging findings associated with renal osteodystrophy.

Other Diagnostic Studies

Treatment

Medical Therapy:

Control of Serum Phosphate [12]

  • A low-phosphate diet is mandatory in the end-stages of renal disease, to keep serum phosphate concentration within 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[25]

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. If so, 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[26]

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[28].

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. ↑ https://www.orthopaedicsone.com/display/MSKMed/Renal+osteodystrophy
  9. ↑ Nissenson, Allen (2009). Current diagnosis & treatment. New York: McGraw-Hill Medical. ISBN 978-0-07-144787-4.
  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. ↑ 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.
  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. ↑ 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.</ref

    Surgery

    • Subtotal parathyroidectomy
    • The treatment for renal osteodystrophy is medical therapy. Surgery is usually reserved for patients with hyperparathyroid bone disease
    • Renal Transplant<ref name="MallucheFaugere1989">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.
  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.

Related Chapters

External links

Renal Osteodystrophy

Template:Nephrology


Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Renal_osteodystrophy&oldid=1482376"