Renal osteodystrophy: Difference between revisions
Nazia Fuad (talk | contribs) (→X-ray) |
Nazia Fuad (talk | contribs) |
||
Line 310: | Line 310: | ||
===Echocardiography or Ultrasound=== | ===Echocardiography or Ultrasound=== | ||
There are no echocardiography/ultrasound findings associated with [disease name]. | There are no echocardiography/ultrasound findings associated with [disease name]. | ||
===CT scan=== | ===CT scan=== | ||
CT scan findings associated with Renal Osteodystrophy are the same that r related to chronic kidney disease However, . | |||
===MRI=== | ===MRI=== |
Revision as of 18:48, 9 July 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: nazia fuad[1]Synonyms 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.[2]
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[3]
Classification
Table 1. Histologic Classification of Renal Osteodystrophy[4]
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 exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Causes
Renal Osteodystrophy mainly caused by Chronic Kidney Diseases
OR
Common causes of [disease] include [cause1], [cause2], and [cause3].
OR
The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].
OR
Differentiating ((Page name)) 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
The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.
OR
In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.
OR
In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate of [number range]%.
Patients of all age groups may develop [disease name].
OR
The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.
OR
[Disease name] commonly affects individuals younger than/older than [number of years] years of age.
OR
[Chronic disease name] is usually first diagnosed among [age group].
OR
[Acute disease name] commonly affects [age group].
There is no racial predilection to [disease name].
OR
[Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].
[Disease name] affects men and women equally.
OR
[Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.
The majority of [disease name] cases are reported in [geographical region].
OR
[Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].
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 [6]
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 :[7]
●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
The majority of patients with [disease name] are asymptomatic.
OR
The hallmark of [disease name] is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of [disease name]. The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].
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 [disease name].
OR
An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
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 [disease name].
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 [disease name].
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.
.[8]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[9]
Secondary Prevention
- Vit D administration with every session of dialysis
- use of aluminium free phosphate binders.[10]
References
- ↑ 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.
- ↑ 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.
- ↑ Moe S, Drüeke T, Cunningham J, Goodman W, Martin K, Olgaard K, Ott S, Sprague S, Lameire N, Eknoyan G (June 2006). "Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO)". Kidney Int. 69 (11): 1945–53. doi:10.1038/sj.ki.5000414. PMID 16641930.
- ↑ 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.
- ↑ 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.
- ↑ 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) - ↑ 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) - ↑ 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.
- ↑ 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.
- ↑ 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
- osteoporosis
- osteopenia
- osteomalacia
- hyperparathyroidism
- multiple myeloma
- soft tissue calcification including collagen vascular disease
- hydroxyapatite crystal deposition disease
- hypervitaminosis