I o i , 1

RENAL OSTEODYSTROPHY*
By MICHAEL WELLER, M.D.,t JACK EDEIKEN, M.D., and PHILIP j. H0I)ES, M.D.
PHILADELPHIA, PENNSYLVANIA
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ENAL osteodystrophy is the skeletal

response to long-standing chronic renal
disease. In the past, few patients with
chronic renal failure survived a sufficient
time for osseous abnormalities to become
manifest. With improvement in dialyzing
techniques, longevity is increased and
renal osteodvstrophv is a more frequent
finding. Although dialysis prolongs life,
the osseous abnormalities persist and pro-
gress, albeit at a slower rate. Since renal
osteodystrophy will occur with increasing
frequency, it is important to understand
basic bone physiology and be cognizant of
the roentgenographic features of the dis-
ease spectrum.
Renal osteodystrophy is a recognizable
complex of skeletal changes and includes:
(i) osteomalacia (adults) or rickets (chil-
dren); (2) osteitis fibrosa (hyperparathv-
roidism); and () osteosclerosis (Fig. i).
Soft tissue calcifications are common. All
of these features may not be present in the
same individual. The skeletal changes
may be due to several causes, classified by
Dent into glomerular and tubular forms.’2
IIG. 1. Uremia in a child produced widening of the
Giomerular renal disease is most often due
growth plate (rickets), osteosclerosis of the meta-
to chronic pyelonephritis and chronic gb- physis, and subperiosteal resorption due to sec-
merulonephri tis.2633 Tubular forms include ondarv hyperparathyroidism. Note the resorption
vitamin D resistant rickets, the Fanconi of the distal end of the clavicle.
syndrome, and renal tubular acidosis.
mechanisms are controversial, and there
“Glomerular” types are due to acquired
are two main theories: (i)acquired insensi-
renal disease, and tubular forms are due
tivity to all actions of vitamin D (ergo-
mainly to inborn metabolic errors. There-
sterol) ;1O,17,33,35,36,37 and (2) chronic acidosis
fore, we use the terms acquired (glomerular)
and excessive secretion of phosphorus into
and congenital (tubular) renal osteods-
the bowel.
trophy.
ACQUIRED INSENSITIVITY TO VITAMIN D (ANn-
ACQUiRED RENAL OSTEODYSTROPHY VIrAMIN D FACTOR)

PATHOPH YSIOLOGY Vitamin D has three known functions:

Acquired renal osteodystrophy is caused (i) to promote intestinal absorption of

by functional renal impairment. The basic calcium and phosphorus; (2) to exert a

* From the Department of Radiology, Jefferson Medical Center, Philadelphia, Pennsylvania.

t Resident in Radiology.
Professor of Radiology, Chief of Diagnostic Division.
§ Professor of Radiology, Chairman, Department of Radiology.

354
 \oi. 104, No. 2 Renal Osteodvstrophv 3-cs
tlirect effect oii bone mineralization; and
(3) to exert a minor phosphattiric action.
\Vhen these functions are lost, less circu-
bating ninerals are available to bone clue
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to decreased intestinal absorption. Bone

cannot utilize the circulating minerals
present, since the direct eflect On bone
ninera1ization is lost. The result is osteo-
malacia. Eventually there is a decrease in
serum calcium which stimulates the para-
thyroids to secrete large amounts of para-
thormone. Parathorrnone causes an in-
creased rate of bone resorption (to release l”ic. 2. Renal osteodvstrophy due to chronic PYC-
lonephritis. ‘I’here is widening of the sacroiliac
minerals in order to maintain seruin cab-
joints and the femoral growth plates. There is
cium levels) antI osteitis fibrosa results.
bilateral slipping of the capital-femoral epiphvses.
Two notal)le groups of studies support Note the osteoscierosis adjacent to the sacroiliac
this theory of acquired insensitivity to joints.
vitamin 1) or an anti-vitamin 1) factor.
Rachitic rat cartilage calcifies at a Ca_P
cause of renal osteodystrophv is unlikely,
product of 35, incubatetl with serum from
since abkalinization of the patient will not
control patients, but only at s with
serum from chronic renal disease patients.’2
cause skeletal healing unless vitamin I) is
Also, barge tioses of vitamin D (20,000- adtietl.’ 9,24,23, 35,39 Other chroni c acidoses,
e.g., diabetes mellitus and renal tubular
50,000 units per day) will cause healing of
renal osteotlvstrophv before the Ca-P prod- aciclosis, do not cause osteitis fibrosa.29

uct rises,1S seemingly substantiating a I. OSTEOMALACIA AND RICKETS

direct mineralizing effect of vitamin
Osteomalacia anti/or rickets is the com-
D.1 ,I4,3b
monest feature of renal osteodystroph’.
CHRONIC ACIDOSIS AND INTESTINAL. PHOSPHAnE The difference in adults (osteomalacia)
SECRETiON
and children (rickets) reflects only the
The older pathogenetic theory attributes stage of bone maturation present when the
the osseous changes to chronic acidosis.7’ deficiency occurs.
11,24,25,27 Chronic acidosis occurs with renal
OSrEOMA I.ACIA
failure anti is associated with increased
serum phosphorous bevels. This results in This occurs in both diffuse anti localized
the secretion of large amounts of phosphate forms. The former is tlue to diminution in
into the bowel. Intestinal calcium is then the number of trabecubae, anti a corn pensa-
bound to phosphate in the bowel lumen, tori thickening of primary stress trabe-
forming insoluble calcium sabts which can- culae, thus accounting for the “increased
not be absorbed. Hvpocalcemia eventually trabecular pattern” often (lescribed. The
ensues. focal form is known as “Milkman’s frac-
There is much evidence to refute the tures,” or “Looser’s nodes.” These pseudo-
above explanation. Careful metabolic fractures are really incomplete compres-
studies fail to show any increase in insol- sion fractures with little or no callus re-
ubbe calcium-phosphate salts in the stool. sponse.’3’36 Ratliobucency persists due to
Moreover, aluminum hydroxide given the failure of calcification of osteoid callus.
orally to bind intestinal phosphate will not Local pain is the most common complaint,
result in increaseti calcium absorption or anti the medial scapular border, ribs, and
blood levels,19 and will not bring about pubic anti ischiab rami are the most com-
bony healing. Chronic acidosis as the sole mon sites. Steinbach and Noetzli36 have
 356 Michael Weller, Jack Edeiken anti Philip J. Hotles OCI0BER, i68

observed a tendency toward bilateral svm- thickness of the rachitic growth plate is
rnetry of pseudofractures. 3.2 mm. in Steinbach and Noetzli’s series,
with the control thickness being i .o mm.3
RICKETS
Metaphyseal cupping and fraying occur,
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Any mechanism which prevents calcium as weib as bowing of bong bones and the
deposition in the zone of provisional cal- “rachitic rosary” of the ribs (Fig. , 1-D).
cification causes rickets. Roentgenographi- The changes are similar to those of dietary
cally, the growth plate is widened due to rickets, although occasionally more severe
continuing proliferation of cartilage which due to their occurrence in older, heavier
cannot calcify (Fig. 1 and 2). The average patients with a longer disease course.34

or the b - due to osteoma , i ne r

with little healing. (D) ‘ pelvis shows marked deossification and deformity of the proximal femurs.
Abundant undermineralized osteoid is present at the proximal ends of the femurs.
 \oi.. 104, No. 2 Renal Osteodystrophy 357

11. OS’l’EI’l’IS FIIIROSA

(isteitis hbrosa is caused by increased

parathvroid activity. The stimulus for
parathormone production is hypocalcemia,
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hyperphosphatemia, or both. The effect of

parathormone is to increase osteoclasis.
The bone tiefects produced by local resorp-
tion are replaceti by fibrous tissue anti
giant cells. When this process becomes ex-
tensive, the calcium released may elevate
the blood levels to normal, so that if a pa-
0
tient with chronic renal disease has a nor-
11G. . (E) Aortogranl reveals absence of the left
mal serum calcium, osteitis fibrosa is in- renal artery and a IlypoplaStic right renal artery.
evitabby seen 011 the roentgenograrns.2Ostei- (Courtesy of I)octor John \V. Hope, Children’s
tis fibrosa begins early in renal tiecompen- Hospital of Philadelphia.)
sation anti max’ be observed in patients
dung of acute renal failure.34 Osteitis
bong-stantii ng hyperparathvroi tiisrn and
fibrosa is far more common in acquired
may be found in soft tissue, small and
( gbomerubar) forms of renal disease than
medium sizeti arteries (Fig. 6 antI 7), renal
the tubular svntirornes.36
parench vm a, carti 1age, and conj u n cti va
ROENIGEN FEATURES
fornices.24
The most constant and specific featuie
III. OS’I’EOSCLEROSIS
is subperiosteal bone resorption, most often
seen at the radial surface of the mitidle Osteosclerosis (hyperostosis) I1ost com-
phalanges. the resorption presents as a nonly occurs wi th chroni c pvebonephri-
peculiar “lace-like” or “palisade” appear- tis.” It most likely results from thera-
ance diagnostic of the condition. Subperi- peutic et}orts with vitamin D and calcium
osteal bone resorption also occurs in the a(iministration, rather than the primar
clavicle (Fig. i), the medial aspect of the disease.33’34’3
proximal tibia and humerus, anti the distal Niany investigators believe that osteo-
ulna, in that order (Fig. 4, 1, B and C). sclerosis results from an exaggeratetl osteo-
In the skull, spott\ deossification is a blastic response following bone resorp_
common feature of h’perparathvroidisrn tion.”6”8’2’36’4’ There may be a separate
and causes a “wooley” or “salt and pepper” fraction of parathormone, which stlmulates
appearance (Fig. ). Resorption of the osteoblasti c activi ty,’39’43 especi ally early
lamina dura is a rather constant feature in renal disease with mild parathvroid hy-
but it is not characteristic of the condition. peractivi ty and positive calcium balance.26
Metaphvseal fractures and slipped epi- In 1932, Selye3#{176}injected repeated small
phses may be prominent features of the doses of parathyroid extract into rats and
disease (Fig. 2). “Brown” tumors are not produced osteosclerosis, with or without
found frequently in secondary hvperpara- osteitis fibrosa, depending on the dose.
thvroidisrn. Destruction of the phalangeal Osteoscierosis may occur early in the course
tufts may occur. The resultant telescoping of osteitis fibrosa when hormone levels are
of the soft tissues of the fingers causes a relatively low.6”6’30’40
“pseudo-clubbing” appearance (Fig. 6). Thyrocalci tonin, elaborated by the para-
Destruction of the interphalangeal joints follicular cells of the thyroid, acts to foster
occurs anti may be confused with rheuma- osteoblastic activity even in the face of
toici arthritis.29’33 hipercalcemia, and is thought by some to
Soft tissue calcification3’23’36 occurs with cause osteosclerosis perhaps vi a decreased
 .35 \ I cli id \\‘cl Icr, J ack lldcikcn and PhiliP J . 1 I( n Ics ui k ,
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I ic. . Renal osteodvstrophv with characteristic bone changes of hvperparathvroidisnl. (1) Subperiosteal
resorption is most marked at the radial surface of the middle phalanges (arrow). There is destruction of
tufts. A) Subperiosteal resorption of ribs, clavicle, and the humeral shaft. (C) Resorption of the bones
adjacent to tile symphsis pubis and of the femoral neck.
 \OL. 104, No. Renal Osteodvstrophv 359

excretion, increased prothictioll, or both.9”5

Osteoscierosis alone is reporte(i with
chronic renal disease3 but is usually asso-
ciated with osteomalacia and osteitis fibrosa.
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ROEN I(;EN FEAFIJRES

Thickening and fusion of adjacent tra-

beculae produce an increased trabecular F;.

pattern on the roentgenograms, which pro-

gresses to a ditluse, chalks’ density anti ob-
scuration of the normal bone architecture.
In children, metaphvseal osteosclerosis is
exaggerated because of adjacent deossifica-
tion36 (Fig. I anti 2). In adults, the thoraco-
lumbar spine is the most common site, oc-
curring in 6 of the 6,3 cases in three corn-
bineti series.264’ Dent and HotisoIlli
‘ have
termed this picture “rugger-jerse’ spine”
t
tlue to the sclerosis at the superior and in-
ferior vertebral borders (Fig. ). Other
common sites include the pelvis, ribs, fem-
ora, and long bones. It may occur in the
facial bones, simulating leontiasis ossea,hI
and in the base of the skull, especially in
chiltlren (Fig. 9).

‘FUISULAR SVNI)ROMES

Tubular syndromes cause renal osteo-

dystrophy less commonly than acquired A
disease, and exretorv impairment is not l 11G. (. Renal osteodvstrophv. There is destruction
of the phalangeal tufts vith ‘‘pseudo-clubi)ing
due to soft tissue telescoping. Arterial calcification
is lrnlinent. Note the sui)periosteai hone resorp-
tion at the ra(iial aspect of the middle phalanges.

prerequisite. Ihe plethora of syndromes

and eponvms often differ onl’ in the abnor-
mal excretion of specific metabolites. Skel-
etal changes are similar to acquired (glo_
merular) osteodvstrophi, with a few excep-
tions. There are three nlajor disease pat-
terns: (i) vitamin D resistant rickets;
(2) lanconi syndrome; and () renal tubu-
lar acidosis.
,tji .
V1’Fl\ll\ I) R1’I’.FA F RRKl1r

‘Ihese cliihlren present classic rachitic

changes, I)ne pain, muscular weakness,
I’I(;. . Ihere is deossihcation of the skull producing
occasional (iwarhsm, anti persistent phos-
a ‘‘salt and pepper’ appearallce. A small ‘‘brovn’’
tumor is present in the posterior portion of tile phaturia with flO systemic acidosis, amino-
parietal bone. aciduria, glycosuria, or proteinuria.ii It is
 360 Michael Weller, Jack Edeiken and Philip J. Hodes OCTOBER, 1968

rickets since the primary defect in resistant

rickets is probabl’ a combination of a
congenital renal phosphate leak combined
with intestinal malabsorption of calcium.
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The roentgenographi c features resem ble

those of glomerular rickets, although dwarf-
ism may be more marked.28 Bowing of
long bones, pseudofractures, and metaph’s-
eal osteosclerosis all occur. Even with
vitamin D an(i phosphate supplements, re-
currences are common anti deformities
may result.32

FANCONI SYNDROME

The more severe childhood form of this

tlisease has been termeti the Fanconi-de-
Toni-Debre or Fanconi-Lignac syndrome,
while the milder adult form is commonly
called the adult Fanconi syntirome. Al-
though many variations exist due to liffer-
ing tubular enz’matic defects, it is basi-
callv a triad of hyperphosphaturia, amino

- . ._ _.y the result of ad .. a-

tion of calcium without vitamin I).

probably familial or genetic in origin, al-

though spontaneous appearances are re-
ported.’4 Hyperphosphaturia leads to hy-
pophosphatem ia, and hypocalcemi a occurs
secondary to intestinal malabsorption. The
alkaline phosphatase is usually elevated.
Since large doses of vitamin D will cause
healing without alleviating urinary phos-
phate loss, it is unlikely that the disease is
solely due to resistance to vitamin D ac-
tion.’8’33 Fanconi, and earlier Johnson,
suggested the term “phosphate diabetes”
due to the persistent phosphaturia despite
healing with ergosterol.
Partial and complete healing occur with
phosphate infusion and oral supplementa
tion. However, the result is temporary un-
less calcium and vitamin D are added and
maintained.20’28 A parallel would seem to
FIG. 8. Renal osteodystrophy. Osteosclerosis of tile
exist between the pathophysiology of re- superior and inferior margins of the Vertebral
sistant rickets and acquired (glomerular) centra producing a “rugger-jersey” appearance.
 104, No. Renal Osteodvstrophy 36!

aciduria, anti renal gI’cosuria with a nor- disturbance in infants anti children and
mal blood glucose.22 It is reported with while active, produces systemic acidosis
hypokalemia anti periodic weakness, neph- anti bone lesions but not nephrocalcinosis.
rogenic diabetes insipitius,22 ll1ti hvper- The adult form of renal tubular acidosis
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tiricuria.7 Althougli m ainl\’ genetic, the (Bu tler-Albright sv ndrome), is the severe
Fanconi syndrome may complicate heavy form. Systemic aci(iosis, bone lesions, and
metal intoxication anti multiple m eloma.22 nephrocalcinosis are seen. The basic defect
Cystinosis is no longer considered the un- in both forms is failure of tubular epithe-
deriving cause. hum to excrete the h’drogen ion, except
\\‘hen bone changes (10 occur, functional through coupling with the ammonia radi-
renal impairment is likely. Most cases heal cal. All the h’drogen that is filtered cannot
with large (loses of vitamin D,2223 or alka- be excreted through this pathway, and
linization plus erg3sterol, thus suggesting s’stem ic Ii perchlorem ic aci dosis results.
another link between acquired and tubular The serum phosphate rises as renal failure
osteo.ivstroph . Rickets, osteom alacia, os- ensues. Therap’ with vitamin D and
teitis fibrosa,” anti osteosclerosis may be alkalinization is only partially efficacious
present,uiSG the latter two in more pro- in causing bone healing.’2” 8,33

tracted cases. Bowing of long bones and The roentgen features include rickets
epiphyseal collapse and mu alposi tion cause anti/or osteomihicia, pseutiofractiires, and
limb deformities. Peculiar spurs and ossi- nephrocalci nosis. Ostei tis fibrosa is rare,#{176}
des at ligamentous insertions about the and osteoscierosis is not reported.
joints are described by Steinbach anti
SUMMARY
Noetzli36 in renal phosphaturia with or
without glycosuria, and are presumably Renal osteoti’stroph’ is a complex of
due to normal stresses placed on abnor- skeletal responses to renal disease, which
mally soft, u ntiermineralized bone. incluties : (i ) osteomalacia (adults) and

RENAL 1tiitJl.AR AC1I)OSIS

rickets (children); (2) osteitis fibrosa; and
( 3) osteosclerosis. The latter may be the
The Lightwood svntirom e or “salt-losing
result of treatment. Soft tissue calcifica-
nephritis” is the self-limited form of the
tions occur in long-standing disease.
Renal osteodvstrophv max’ be divided
into acquired or glomerular form (due most
often to chronic pvelonephritis), anti the
congenital or tubular form, e.g., vitamin D
resistant rickets, Fanconi sndrome, and
renal tubular acidosis. Impaired intestinal
absorption of calcium anti phosphorus may
be a common link between the two forms.
Roentgenographicallv, renal and tiietar’

rickets differ only in severity. The greater

degree of change in renal rickets may be

related to age of onset and body weight.
Osteonlalacia is difluse,or localized (pseudo-
fractures). Ostei tis fibrosa occurs most
characteristically as subperiosteal hone
resorption. Osteosclerosis is lilOSt COIlillioll
in the thoracolumbar spine at the superior
lu;. . Renal osteodvstrophv. i’here is loss of dc-
hnition of tile skull tables especially evident in the
and inferior vertebral borders. Soft tissue,
frontal and occipital areas and sclerosis along tile arterial, anti renal parenchvmal calcifica-
base of tile skull and in tile mastoids. tions occur late.
 362 Michael Weller, Jack Edeiken and Philip J. Hodes OCTOBER, 1968

The disease will become more prevalent Is. DOYLE, F. H. Some quantitative radiological
with increasing use of long-term dialysis. observations in primary and secondary hyper-
parathyroidism. Brit. 7. Radiol., i 966, 39,
Philip J. Hodes, M.D. 161-167.
Jefferson Medical Center z6. DRESKIN, E. A., and Fox, T. A. Adult renal
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iith and Walnut Streets osteitis fibrosa with metastatic calcification

Philadelphia, Pennsylvania 19107 and hyperplasia of one parathyroid gland: re-
port of case. Arch. mt. Med., 1950, 86, 5-
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