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Renal Osteodystrophy

Renal Osteodystrophy

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Published by Ahmad Shaltout

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Published by: Ahmad Shaltout on Jul 01, 2010
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01/27/2013

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Renal osteodystrophy
= constellation of musculoskeletal abnormalities that occur withchronic renal failure as
a combination of 
o
osteomalacia (adults) / rickets (children)
o
2آ° HPT with osteitis cystica fibrosa + soft-tissue calcifications
o
osteosclerosis
o
soft-tissue + vascular calcifications
Classification:
o
Glomerular form = acquired renal disease: chronicglomerulonephritis (common)
o
Tubular form = congenital renal osteodystrophy:
Vitamin D resistant rickets = hypophosphatemic rickets
Fanconi syndrome = impaired resorption of glucose, phosphate, amino acids, bicarbonate, uric acid, sodium, water 
Renal tubular acidosis
Pathogenesis:
o
Renal insufficiency causes a decrease in vitamin D conversioninto the active 1,25(OH)
2
D
3
(done by 25-OH-D-1-a hydroxylase,which is exclusive to renal tissue mitochondria); vitamin D deficiencyslows intestinal calcium absorption; vitamin D resistance predominatesand calcium levels stay low (Ca أ— P product remains almost normalsecondary to hyperphosphatemia); low calcium levels lead toOSTEOMALACIA; additional factors responsible for osteomalacia areinhibitors to calcification produced in the uremic state, aluminumtoxicity, dysfunction of hepatic enzyme system
o
Renal insufficiency with diminished filtration results in phosphate retention; maintenance of Ca أ— P product lowers serumcalcium directly, which in turn increases PTH production (2آ° HPT); 2آ° HPT predominates associated with mild vitamin D resistance andleads to an increase in Ca أ— P product with SOFT-TISSUECALCIFICATION in kidney, lung, joints, bursae, blood vessels, heartas well as OSTEITIS FIBROSA
o
Mixture of (a) and (b): increased serum phosphate inhibitsvitamin D activation via feedback regulation
OSTEOPENIA (in 25-83%)
o
= diminution in number of trabeculae + thickening of stressedtrabeculae = increased trabecular pattern
Cause
:
combined effect of 
Osteomalacia
(reduced bone mineralization due toacquired insensitivity to vitamin D / antivitamin D factor)
Osteitis fibrosa cystica
(bone resorption)
Osteoporosis
(decrease in bone quantity)
Contributing factors:
chronic metabolic acidosis, poor nutritional status, pre- and posttransplantation
 
azotemia, use of steroids, hyperparathyroidism,low vitamin D levels
 Site
:
vertebral body (3-25%), pubic ramus, rib(5-25%)
o
Milkman fracture / Looser zones (in 1%)
o
metaphyseal fractures
RICKETS (children)
Cause:
in CRF normal vessels fail to develop in an orderly way alongcartilage columns in zone of provisional calcification; this resultsin disorganized proliferation of the zone of maturing +hypertrophying cartilage and disturbed endochondral calcification
 Location:
most apparent in areas of rapid growth such as knee joints- diffuse bone demineralization- widening of growth plate- irregular zone of provisional calcification- metaphyseal cupping + fraying- bowing of long bones, scoliosis- diffuse concave impression at multiple vertebral end plates, basilar invagination- slipped epiphysis (10%): capital femoral, proximal humerus, distal femur, distalradius, heads of metacarpals + metatarsals- general delay in bone age
SECONDARY HPT (in 6-66%)
Cause
:
inability of kidneys to adequately excrete phosphate leads tohyperplasia of parathyroid chief cells (2آ° HPT); excess PTH affectsthe development of osteoclasts, osteoblasts, osteocytes
o
hyperphosphatemia
o
hypocalcemia- increased PTH levels- subperiosteal, cortical, subchondral, trabecular, endosteal,subligamentous bone resorption- osteoclastoma = brown tumor = osteitis fibrosa cystica in 1.5–1.7% (due toPTH-stimulated osteoclastic activity; more common in 1آ° HPT)
 
- periosteal new-bone formation (8–25%)- chondrocalcinosis (more common in 1آ° HPT)
OSTEOSCLEROSIS (9-34%)
- One of the most common radiologic manifestations; most commonly with chronicglomerulonephritis; may be the sole manifestation of renal osteodystrophy- diffuse chalky density: thoracolumbar spine in 60% (rugger jersey spine); also in pelvis, ribs, long bones, facial bones, base of skull (children)
SOFT-TISSUE CALCIFICATIONS
= Uremic tumoral calcinosis = secondary tumoral calcinosis = pseudotumor calcinosisMost frequent cause of a periarticular calcified mass! 
Cause:?
metastatic
secondary to hyperphosphatemia (solubility product for calcium + phosphate [Ca
2+
أ— PO
4-2
]exceeds 60–75 mg/dL in extracellular fluid),hypercalcemia, alkalosis with precipitation of calciumsalts
dystrophic
secondary to local tissue injury 
Location:
arterial
(27-83%):
in medial + intimal elastic tissue
 Site
:
dorsal pedis a., forearm, hand, wrist, leg
 pipestem appearance without prominent luminalinvolvement
periarticular
(0.5-1.2%):
multifocal, frequently symmetric, may extendinto adjacent joint
chalky fluid / pastelike material
inflammatory response in surroundingtenosynovial tissue- discrete cloudlike dense areas- fluid-fluid level in tumoral calcinosis

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