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Hemodialysis is not essential for the development of destructive spondylarthropathy in patients with chronic renal failure.

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BRIEF REPORT
HEMODIALYSIS IS NOT ESSENTIAL FOR THE DEVELOPMENT OF
DESTRUCTIVE SPONDYLARTHROPATHY IN PATIENTS WITH
CHRONIC RENAL FAILURE
MICHEL ALCALAY, MARIE-CHRISTINE GOUPY, ISABELLE AZAIS, and DANIEL BONTOUX
Since 1984, there have been several reports of a
destructive spondylarthropathy occurring in patients
who have received hemodialysis over a long period of
time. Two cases of a similar syndrome were observed in
nonhemodialyzed patients with chronic renal failure,
one of whom underwent a lumbar disc excision. The
results of disc examination and of radiographic and
biologic investigations prompted reconsideration of factors previously considered to be pathogenetic (amyloidosis,
hydroxyapatite crystal deposition, aluminum toxicity),
except one: secondary hyperparathyroidism.
In 1984, Kuntz et a1 described a syndrome of
destructive spondylarthropathy in hemodialysis patients that comprised lesions of the intervertebral discs
and adjacent vertebral plates, predominantly in the
cervical spine, occurring over a period of several
months and leading to a radiographic pattern of discal
thinning, erosions, and geodes of the adjacent plates in
the absence of osteophytosis (1). The patients described by Kuntz had been undergoing hemodialysis
for several years (mean 8). Sebert et a1 reported 3 new
cases of destructive spondylarthropathy in patients
who had undergone hemodialysis for several years (2).
Factors promoting the development of destructive
spondylarthropathy are thought to be secondary
_____
From the Department of Rheumatology, Centre Hospitalier
et Universitaire de Poitiers, Poitiers, France.
Michel Alcalay: Professor of Rheumatology; MarieChristine Goupy, MD: Chef de Clinique Assistant; Isabelle Azais,
MD: Chef de Clinique Assistant; Daniel Bontoux: Professor of
Rheumatology.
Address reprint requests to M. Alcalay, Service de
Rheumatologie, HBpital de la MiWrie, BP 577,86021 Poitiers cedex,
France.
Submitted for publication August 28, 1986; accepted in
revised form February 26, 1987.
Arthritis and Rheumatism, Vol. 30, No. 10 (October 1987)
hyperparathyroidism, aluminum toxicity, deposit of
apatite crystals in the discs (l), amyloidosis (found in
the discs of 3 patients) (2), or other factors associated
with hemodialysis. We report 2 cases of destructive
spondylarthropathy in nonhemodialyzed patients with
chronic renal failure.
CASE REPORTS
Patient 1. Patient 1 was a woman who had been
treated since 1939 for tophaceous gout and since 1966
for chronic interstitial nephropathy with renal impairment without hypertension. Her therapy included
colchicine, allopurinol, indomethacin, calcium carbonate, aluminum salts (intermittently), and a low-protein
diet.
In July 1984, radiographic studies taken in
another hospital because of apyretic lumbar pain
showed L3-L4 discopathy that resembled spondylodiscitis. Her erythrocyte sedimentation rate (ESR)
was 76 mm/hour.
At surgery, the L3-L4 disc showed noninflammatory degeneration and was therefore completely
removed. The disc, as well as a few fragments of disc
L2-L3, was fixed in Bouin’s fluid and prepared for
embedding in paraffin during the 6-hour period following surgery. Histologic study showed no signs of
spondylodiscitis.
In January 1985, the patient was seen at our
department of rheumatology because of a new episode
of pain. Radiographs showed the development of
L2-L3 discopathy (Figure 1). The patient was apyretic. The ESR was 103 mmlhour, and results of a
differential blood cell count were normal with 5,900
leukocytes/mm3. Other laboratory results were as fol-
BRIEF REPORTS
1183
Figure 1. Lumbar spine radiographs of patient 1 after L3-L4 disc
excision, showing L Z L 3 disc space narrowing and erosions of
adjacent vertebral plates. White bars are clasps from previous
surgery.
that were suggestive of hyperparathyroidism: subperiosteal resorption of the left sacroiliac joint, both
sides of the right thumb first phalanx, and the right fifth
metacarpal bone.
Discal fragments, which had been taken at
surgery and embedded in paraffin, were studied. Light
microscopy examinations for amyloid, following
thioflavine T staining with observation under 449A
ultraviolet light by episcopy, and following Congo red
staining with observation under monochromatic and
polarized light, were negative. Electron microscopic
study for amyloid, carried out following rehydration of
an embedded fragment, refixation in 2.5% glutaraldehyde, postfixation with osmic acid, and embedding in
araldite for study under a Philips 300 transmission
electron microscope, was also negative. No crystalline
structure was visible, either by electron microscopy or
light microscopy. The patient was diagnosed as having
a destructive spondylarthropathy similar to hemodia-
lows: hemoglobin 98 gmhiter, serum creatinine 240
pmoles/liter, urinary protein 0.2 gm in 24 hours,
urinary red blood cells 6,90O/minute, urinary leukocytes 36,80O/minute, serum calcium 2.7 mmoles/liter,
serum phosphorus 1.3 mmoles/liter, phosphorus tubular absorption 6996, serum parathyroid hormone (titrated by radioimmunoassay kit; Oris Industries, Gif Sur
Yvette, France) 7.5 IU/liter (normal 1-5), urinary
cyclic AMP 805 nmoles/mmole creatinine (normal
250-700), serum uric acid 367 pmoleshiter, serum lead
0.72 pmoleshter (normal 1-3), blood aluminum by
atomic absorption spectrophotometry 0.46 pmoles/
liter (normal 0-1.1). Screens for infection by blood
culture, serology, tuberculin skin test, and needle aspiration of discs L2-L3 and L3-L4 all gave negative
results. Her HLA type was Aw24, AOO; Bw21, B5.
An iliac crest bone biopsy specimen showed
clear signs of hyperparathyroidism: osteoclastic resorption surfaces 5.59% (normal 3.6 ? 1.1%, mean ?
SD), osteoid volume 15.27% (normal 1.1 & 0.9%),
osteoid surface 56.14% (normal 10.90 ? 6.98%). Test
results for aluminum, by Aluminon staining, were
negative. Cervical spine radiographs, which were conducted despite the absence of any pain, showed major
reorganization of the vertebral discs, predominantly in
C4-C5, where there was a massive geode developing
in the 2 adjacent vertebral bodies (Figure 2).
Radiographs Of the entire
besides signs of Severe tophaceous arthropathies of
the hands and feet, only minor, nonspecific alterations
Figure 2. Cervical spine lateral view from patient 1, showing C 4 C 5
and C%C6 pseudospondylodiscitis, C4-CS pseudospondylolisthesis, and fusion of the posterior arches of C2-C3-C4.
1184
lysis spondylarthropathy. Her clinical course was
good, with resumption of ambulation after 18 months.
Patient 2. Patient 2, a man born in 1915, presented with 3 episodes of gout in 1973. He was
subsequently treated with allopurinol and, since 1977,
had been treated for renal failure and hypertension
caused by postinfectious chronic interstitial nephropathy, which required a low-protein, sodium-free diet.
In October 1984, a transient deterioration in renal
function due to noncompliance with the diet required 2
hemadialysis sessions, after which the patient’s condition restabilized.
In February 1985, the patient reported spontaneous development of lumbar pain. Spinal radiographic studies showed TI 1-T12 erosive discopathy
(Figure 3), with cervical discopathy between C2 and
C6 (Figure 4) in the absence of any cervical pain.
Radiographs of the dorsal and lumbar spine taken after
a fall in 1953 showed no abnormalities. Skeletal
scintigraphy showed areas of hyperfixation that corresponded to the radiographic lesions. Radiologic studies of the peripheral and sacroiliacjoints did not show
chondrocalcinosis o r sacroiliitis. However, there were
numerous alterations that were suggestive of hyperparathyroidism in the absence of any tophaceous
deposit: lytic lesions on the distal end of the right
second finger first phalanx and on the right thumb
Figure 3. Lateral radiographic view of the thoracic spine of patient
2 , showing Tll-TI2 disc space narrowing, erosions of the adjacent
vertebral plates, and angular alterations of the vertebral bodies.
BRIEF REPORTS
Figure 4. Radiograph of the cervical spine of patient 2 (lateral
view), showing erosions of the C2 inferior plate and C3-C4 disc
space narrowing, with erosions of adjacent vertebral plates.
metacarpal bone, together with subperiosteal resorption of the radial surfaces of the third, fourth, and fifth
metacarpal bones and of the second, third, fourth, and
fifth middle phalanges of both hands (Figure 5 ) ;
subperiosteal resorption of the medial aspect of each
upper tibia (Figure 6) and of several toe phalanges;
lytic lesions of each upper humerus; and granular
pattern of the skull, with subperiosteal resorption of
the calvarium inner surface at its top, and approximately 20, small, round lytic lesions scattered on the
calvarium.
Laboratory studies showed the following: ESR
85 mm/hour, normal differential blood cell count,
hemoglobin 94 gm/liter, serum creatinine 540 pmoles/
liter, serum uric acid 368 pmolesiliter, serum calcium
2.3 mmoles/liter, serum phosphorus 1.3 mmoles/liter,
alkaline phosphatase 710 IU/liter, parathyroid hormone (titrated by the same method used for patient 1)
18 IU/liter, and blood aluminum 0.15 pmolesfliter.
BRIEF REPORTS
1185
An increased ESR is common in patients undergoing
long-term hemodialysis. In our nonhemodialyzed patients, the elevated ESR probably is a result of disorders
induced by chronic renal insufficiency (3). Further studies eliminated the diagnoses of infectious spondylitis,
ankylosing spondylarthritis, articular chondrocalcinosis,
and idiopathic erosive spondylopathy .
Each of our patients had a history of gout, a
disease which may have discovertebral manifestations
( 4 3 . Though it cannot be ruled out definitely, however, the possibility that gout was the cause of the
spinal manifestations in our patients seems unlikely
when the following data are taken into consideration:
1) These manifestations are rare; only 9 symptomatic
patients have been described, including 1 without
peripheral tophi (5). 2) Hyperuricemia was present in
all the previously reported cases, and absent in our 2
Figure 5. Radiograph of the right hand of patient 2, showing numerous signs of secondary hyperparathyroidism.
Needle aspiration of disc Tll-T12 did not show any
pathogens or crystals and resulted in relief of pain.
The diagnosis was a destructive spondylarthropathy similar to the spondylarthropathy of hemodialysis. The patient's pain resolved in 1985, and at
that time, the ESR showed a decrease to 38 mm/hour.
DISCUSSION
These 2 patients with chronic renal insufficiency developed a spondylarthropathy similar to that
described by Kuntz et al (1) in 10 patients undergoing
long-term hemodialysis. The local increased uptake of
the isotope during bone scan noted in our patients was
lacking in some of the patients described by Kuntz et
al, but was present in patients later seen by those
authors (Kuntz D: personal communication). The
ESRs were increased in our patients as in the patients
Of Kuntz et
(Kuntz D: personal communication) and
of Sebert et a1 (Sebert JL: Personal communication), in
the absence of clinical and biologic signs of infection.
Figure 6. Front radiograph of the upper end of the left tibia of
patient 2, showing subperiosteal resorption of the medial aspect
(arrowhead).
1186
patients. 3) Radiologic abnormalities generally consisted of degenerative changes in the cervical, thoracic, and lumbosacral spine; only 3 patients presented
with vertebral body collapse or destructive changes
(4). 4) Histologic examination of the surgically removed disc from our first patient, after fixation in
Bouin’s fluid, which may well have solubilized urate
crystals, did not show any crystal imprints. 5 ) Needle
aspiration of the involved intervertebral discs of our 2
patients did not produce any urate crystals, as demonstrated by microscopic examination under polarized
light.
Unlike the patients in previously published reports (1,Z), our patients were not undergoing regular
hemodialysis; patient 2 had received 2 sessions of
hemodialysis, but these had occurred 4 months before
the onset of lumbar pain. The duration of renal failure
was 16 years in the first patient and 8 years in the
second. To the best of our knowledge, this type of
complication has not previously been described in
nonhemodialyzed patients with renal failure. In light of
our observations, we must express reservations concerning the notion that the development of destructive
spondylarthropathy is a result of hemodialysis. Hemodialysis does not appear to be a sine qua non, and its
effect could be simply to prolong the life of hemodialysis
patients sufficiently to allow development of these
slowly constituted lesions, as suggested by the duration of renal failure in our 2 patients. This hypothesis
is supported by comparison with erosive arthropathy
in renal failure, which can occur both with repetitive
hemodialysis (6) or in the absence of hemodialysis (7).
Finally, we would note that neither patient had
hyperaluminemia, and unlike previous reports (1,2),
results of bone aluminum assays in patient 1 were
negative. Discal fragments from patient 1 showed
neither apatite crystals (1) nor amyloid deposits (2).
Conversely, as in the previously published cases, both
of our patients had hyperparathyroidism, as proven by
BRIEF REPORTS
biochemical, radiologic, and histologic evidence in
patient 1, and by biochemical and radiologic evidence
in patient 2. This condition is deleterious for bone (8)
as well as for intervertebral discs (9), and is possibly a
chief causal factor in the destructive spondylarthropathy of hemodialyzed and nonhemodialyzed patients
with chronic renal failure.
REFERENCES
1. Kuntz D, Naveau B, Bardin T, Drueke T, Treves R, Dryll
A: Destructive spondylarthropathy in hemodialyzed patients: a new syndrome. Arthritis Rheum 27:369-375,
1984
2. Sebert J-L, Fardellone P, Marie A, Deramond H,
Lambrey G, Legars D, Galibert P, Smadja A, Fournier A:
Destructive spondylarthropathy in hemodialyzed patients: possible role of amyloidosis (letter). Arthritis
Rheum 29:301-303, 1986
3. Shusterman NH, Kimmel PL, Kiechle FL, Williams S,
Morrison G, Singer I: Factors influencing erythrocyte
sedimentation in patients with chronic renal failure. Arch
Intern Med 145:1796-1799, 1985
4. Aaron SL, Miller JDR, Percy JS: Tophaceous gout in the
cervical spine. J Rheumatol 11:862-865, 1984
5. Varga J, Giampaolo C, Goldenberg DL: Tophaceous gout
of the spine id a patient with no peripheral tophi: case
report and review of the literature. Arthritis Rheum
28:1312-1315, 1985
6. Goldstein S, Winston E, Chung TJ, Chopra S, Pariser K:
Chronic arthropathy in long term hemodialysis. Am J
Med 78:82-86, 1985
7. Griffin CN Jr: Severe erosive arthritis of large joints in
chronic renal failure. Skeletal Radio1 12:29-33, 1984
8. Matrajt H, Bordier P, Tun-Chot S, Martin J, Hioco D:
Les lesions osseuses de I’hyperparathyroidisme:donnCes
histologiques nouvelles, L’actualitC Rhumatologique
PrCsentCe au Praticien. Vol. 1. Edited by S de Seze, A
Ryckewaert, MF Kahn, P Dreyfus. Paris, Expansion
Edit, 1968, pp 283-288
9. Dihlmann W: Hyperparathyroidism and intervertebral
disk. ROFO 135:353, 1981
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