Renal osteodystrophy

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 fuadSynonyms and keywords:↓↑

Overview

Renal osteodystrophy is the term used to describe the complex metabolic bone disorders that occur as a complication of chronic renal insufficiency.secondary hyperparathyroidism and 1a,25-dihydroxycholecalciferol (1a,25-dihydroxyvitamin D3) deficiency are major contributors to renal osteodystrophy .

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.

Classification

Table 1. Histologic Classification of Renal Osteodystrophy

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 .TNM Classification:

Turnover	Mineralization	Volume
Low		Low
	Normal
Normal		Normal
	Abnormal
High		High

Pathophysiology

the factors that contribute to pathophysiology of Renal osteodystrophy in chronic kidney disease are:

• hyperphosphatemia 
•  hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney.
• Low activated vitamin D₃ levels are a result of the damaged kidneys' inability to convert vitamin D₃ into its active form, calcitriol, and result in further hypocalcaemia.
•  hyperphosphatemia combined with hypocalcemia leads to hyperparathyroidism
• elevated level of hyperparathyroid leads to Osteitis fibrosa .
• High levels of fibroblast growth factor 23

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:

• Disorder of bone and mineral metabolism associated with chronic renal disease.
• Skeletal disorders associated with renal dysfunction.
• hypocalcemia, hyperphosphotemia, and 1,25D defeciency
• Parathyroid gland hyperplasia.
• Systemic acidosis, aluminum retention, accumulation of β2M in bone and joints.

Differentiating Renal Osteodystrophy from Other Diseases

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].

OR

[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].

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.

prevelence in developing countries:

.the prevelance of renal osteodystrophy in developing countries 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.

Risk Factors

Common risk factors in the development of Renal Osteodystrophy are:

Natural History, Complications, and Prognosis

If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

OR

Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].

OR

Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.

Diagnosis

Diagnostic Study of Choice

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 of invasive and expensive procedure. 

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

Serum biomarkers: 

serum calcium, phosphorous, parathyroid hormone (PTH), and alkaline phosphatase (total or bone-specific) .

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

the following parameters are used to define the risk for specific subtypes of renal osteodystrophy : 

●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. .    

History and Symptoms

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

• Bone pain
• Joint pain
• Bone deformation
• Bone fracture
• cardiovascular calcification
• atherosclerotic disease
• aortic calcification leading to LVH left ventricular hypertrophy and diastolic dysfunction

Physical Examination

Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

Laboratory Findings

An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].

OR

Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

OR

[Test] is usually normal among patients with [disease name].

OR

Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

OR

There are no diagnostic laboratory findings associated with [disease name].

Electrocardiogram

There are no ECG findings associated with Renal Osteodystrophy.

X-ray

 routine radiographic screening are not performed 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.Imaging may be done 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. Resorptive loss of bone may be also observed at the terminal phalanges, distal ends of the clavicles, and in the skull.

Radiographs may also reveal soft tissue calcification, particularly including the vasculature,

Echocardiography or Ultrasound

There are no echocardiography/ultrasound findings associated with Renal Osteodystrophy

CT scan

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

MRI

There are no MRI findings associated with.

OR

[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

There are no other diagnostic studies associated with [disease name].

OR

[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy:

The mainstays of the prevention and treatment of renal osteodystrophy continue to be phosphate binders and supplemental calcium.

Control of Serum Phosphate :

• A low-phosphate diet is integral to the management of end-stage renal disease, to maintain a normal serum phosphate concentration.
• 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;
• 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 .
• Control of Serum Calcium
• Calcium malabsorption is very common in end-stage renal disease because of deficient 1a,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.
• 71 A dialysate calcium concentration of 7 mg per deciliter (1.75 mmol per liter) provides an influx of approximately 800 mg 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.

.Surgery

• The mainstay of treatment for Renal Osteodystrophy is medical therapy. Surgery is usually reserved for patients with hyperparathroid

bone disease,these patients need subtotal parathyroidectomy

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

Secondary Prevention

• Vit D administration with every session of dialysis
• use of aluminium free phosphate binders.

Related Chapters

• osteoporosis
• osteopenia
• osteomalacia
• hyperparathyroidism
• multiple myeloma
• soft tissue calcification including collagen vascular disease
• hydroxyapatite crystal deposition disease
• hypervitaminosis

External links

Renal Osteodystrophy

Template:WikiDoc Sources