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Journal of Medical Genetics 1989, 26, 631-636
Transient nephrotic syndrome after anaesthesia
resulting from a familial cryofibrinogen
precipitating at 35°C
Y LOLIN*, P A RAZISt, P O'GORMANt, M HJELM§, AND A S WIERZBICKI*
From *the Department of Chemical Pathology, The National Hospitals for Nervous Diseases, Queen Square,
London WCJ; tDepartment of Anaesthesia, University College Hospital, Gower Street, London WCI;
fDepartment of Chemical Pathology, Brook General Hospital, Shooters Hill Road, Blackheath, London SE18;
and §Department of Clinical Biochemistry, The HospitalforSick Children, Great Ormond Street, London WCI.
Transient nephrotic syndrome, haematuria, and cryofibrinogenuria in a child after
anaesthesia were found in association with a plasma cryofibrinogen that precipitated at 35°C.
Investigation of the family showed this to be a familial trait probably with dominant inheritance.
SUMMARY
In 1955, Korst and Kratochvill coined the term
cryofibrinogen to describe a plasma protein which
precipitated on cooling and redissolved on rewarming to 37°C. Since then, cryofibrinogenaemia
has been found to occur in 3% of hospital patients.2 3
It has been described in association with a variety of
conditions including malignancy,3 6 infection,' 7-9
autoimmune disorders,57 10 thromboembolic
disease, 3 5 711 glomerulonephritis,12 13 diabetes
mellitus,3 pregnancy,3 14 and in women taking oral
contraceptives.15 In rare instances when no underlying disease has been found, the cryofibrinogenaemia has been termed primary or essential.3 5 16
Cold related symptoms usually sugest the diagnosis, but they may be absent.3 5 6
Heat loss is a common accompaniment of anaesthesia18 because of the use of cold and dry gases,
exposure to a cool environment of often vasodilated
patients, heat loss from the operation site, the
infusion of cold fluids, and abolition of the shivering
reflex by muscle relaxants. It is greatest in children
because of their larger surface area to volume ratio,
with most heat loss occurring in the first operative
hour. We report an unusual presentation of the
complications of a cryofibrinogen that precipitated
at 35°C in a child after anaesthesia and a hitherto
undescribed familial form of the condition.
biopsy because of a history of postoperative myalgia
and 'myoglobinuria'. She was born after a normal
pregnancy and delivery with spina bifida occulta and
spinal dysraphism. She has two healthy sisters. The
father had congenital dislocation of the hips and one
of the paternal uncles is mentally subnormal. The
father and the maternal grandmother were the only
members of the family who were known to have had
operations, both as adults, with uncomplicated
recoveries. The proband had had seven operations
between the ages of two weeks and six years, all
under general anaesthesia, for the correction of foot
deformities and a right eye squint. Four of the
operations were followed by uneventful recoveries,
but three were followed by nausea, vomiting,
myalgia (with on one occasion a recorded creatine
kinase activity (CK) of 24 000 U/l), and the passage
of 'dark' urine, with spontaneous, full recovery
three to five days postoperatively. Inheritance of a
gene for malignant hyperpyrexia was excluded in
both parents. The child's temperature had never
been recorded as higher than 37 5°C, but had been
35°C (axilla) on at least one occasion. She had also
had measles, chickenpox, and 'gastroenteritis' that
had followed a 'normal' course. However, one
month before the present admission she had a 'cold'
and because she was febrile the mother had uncovered her for about an hour and had opened the
Case report
windows. Several hours later the child developed
the same symptoms and signs as above.
The proband, a seven year old girl, was admitted to
When admitted the child was well, cheerful, and
the National Hospital in June 1987 for a muscle active. She walked with orthopaedic supports and
wore nappies because of frequent incontinence.
Received for publication 21 March 1989.
Accepted for publication 20 April 1989.
There was severe wasting of the muscles below the
631
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632
Y Lolin, P A Razis, P O'Gorman, M Hjelm, and A S Wierzbicki
knees consistent with her spinal cord disorder and
she had a right third nerve palsy. The muscle biopsy
was performed on the left vastus lateralis under
general anaesthesia using etomidate for induction,
alfentanil, nitrous oxide in oxygen, and trichloroethylene from a 'halothane free' machine for
maintenance, under standard hospital theatre
conditions. During the 20 minute procedure the
child's extremities were left uncovered. Axilla
temperatures varied betwen 35°C and 36*5°C. The
operation and recovery from the anaesthetic were
uneventful, but the child remained nauseated and
irritable for the rest of the day. The next day she
developed a temperature of 37-5°C, complained of
pain in the thighs, was noted to have bilateral
lumbar tenderness, and started passing 'dark' urine.
She was treated with intravenous fluids only and by
the fifth postoperative day she was well again and
the urine was clear.
Detailed histories indicated that the maternal
grandmother had had symptoms suggestive of
Raynaud's phenomenon in the fingers for most of
her life, and that one maternal uncle developed joint
and muscle pains and a rash in cold weather.
However, in January 1988, nine members of the
family, including the proband, went for the first time
on a skiing holiday (in Austria), and encountered
low temperatures (fig 1). Seven of them developed
acrocyanosis over uncovered noses and cheeks when
exposed to the cold, the symploms being relieved
only after several hours in the warmth. The proband
was most affected. The mother had, however,
stayed indoors most of the time and remained
symptom free.
Initial investigation and results on proband
BLOOD
Routine preoperative investigations showed normal
haematological and biochemical indices except for a
slightly raised serum CK activity (83 U/l, reference
range 10 to 70). However, on the first postoperative
day the CK activity rose to 11 460 U/l (the serum
CK activity was 400 U/l one day after performing a
muscle biopsy under similar conditions in another
young patient) and the white blood cell count was
17-5x 109/l (84% neutrophils). The plasma and
serum samples received on that day were haemolysed. The blood urea remained normal throughout
her hospital stay and postoperative serum creatinine
level was normal. Further investigations showed
normal clotting studies, fibrinogen degradation
products of less than 10 mg/l, insignificant antibody
titres to an extensive panel of viruses (including the
Epstein Barr virus and mycoplasma pneumoniae), a
negative autoantibody screen and 1gM cold agglutinins, which, however, reacted at less than 20°C.
URINE
32'C
32C
33"C
35°C
**
32tC*
35C
33'C
35'C
35°C
*
28'C
Cryofibriniogen detected
Cryofibrinogen absent
*
A
A
*
**
***
?
Cold related symptoms before stu(ly
Presence of acrocyanosis on skiing holiday
Absence of acrocyanosis on skiing holiday
Uncle with mental subnormality
Father with congenital dislocation of hipts
Proband with spina bifida
Symptomatology unknown
FIG 1 Pedigree of family showing the subjects
with or without cryofibrinogenaemia, with or without
cold related symptoms, or with other disease. The
cryofibrinogen precipitating temperatures are indicated.
A routine mid stream urine (MSU) sample
examined before surgery was clear and contained no
protein, casts, or cells. A sample received during the
first postoperative day contained brown and white
granular material, comprising a third of the total
volume after centrifugation, and with a clear supernatant. There was no excess of porphyrins. Dipstick
(Labsticks, Ames, Slough, UK) analysis showed the
presence of heavy proteinuria and haematuria.
Microscopy showed red and white blood cells,
granular casts, and large amounts of amorphous
deposit. The protein content of the supematant
(biuret method) was 10 gIl. Agarose electrophoresis
(Coming Medical, Halstead, Essex) of the whole
urine, the x 100 concentrated supematant, and of
the sediment showed albumin and a,, a2, and I8
bands with, in addition, a prominent band in the 0b
region (fig 2). Immunoelectrophoresis of the whole
urine, supematant, and sediment, using antisera
against heavy (Guildhay, Surrey) and light immunoglobulin chains (both bound and free) (Daco,
Denmark) and fibrinogen (Daco, Denmark),
showed an excess of free light chains around the
origin and fibrinogen in the j6 region. Myoglobinuria was excluded by spectroscopy, by electro-
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633
Transient nephrotic syndrome after anaesthesia
2
3Ia
3b
lc
4
_>
FIG 2 The electrophoretic patterns of the plasma, serum, and urine obtained on the first postoperative day, and of the urine
samples from the fifth postoperative day. I=plasma. 2=serum. 3a=supernatant concentratedx 100. 3b=sediment.
3c= whole urine concentrated x 100 (allfirst postoperative day). 4= whole urine concentrated x300 (fifth postoperative day).
S=myoglobin marker. -_--=the band in the Pb region.
phoresis using a myoglobin marker, and by
ammonium sulphate precipitation. 19 A further urine
sample obtained on the fifth postoperative day was
clear and after concentrating it x300, only a trace of
albumin was found on the electrophoretic pattern
with no free light chains or fibrinogen being
detected after immunoelectrophoresis (fig 2).
Muscle biopsy histology showed a predominance
of type I fibres, with the few type II fibres present
being very atrophic. The appearance was consistent
with long standing denervation owing to spinal
dysraphism.
The detection of free light chains and fibrinogen
in the urine on the first postoperative day suggested
the possibility of a cryofibrinogenuria and thus
cryofibrinogenaemia, and led to a retrospective
inspection of both heparin and EDTA plasmas and
serum, obtained on the first postoperative day, for
cryoproteins. Although the samples had been
frozen, a precipitate which could be partially dissolved on warming at 37°C for 30 minutes was noted
in both plasmas on thawing but not in serum.
Cryofibrinogen studies on the proband and her
family
The proband and, where possible, each member of
the family was investigated for the presence of
cryofibrinogenaemia on at least three separate
occasions in October and November 1987. The
proband had been well since her previous admission.
Methods
The blood samples were collected with disposable
plastic syringes and 20 gauge needles into 5 and
10 ml plastic and glass screw top bottles containing
lithium heparin, EDTA, or no anticoagulant, and
transported to the laboratory in a 37°C water bath.
They were allowed to clot for three hours at 37°C
and were centrifuged at room temperature at 3000
rpm for 10 minutes. Aliquots of each serum, EDTA,
and heparin plasmas were stored at 4, 15, 28, 30, 33,
34, 35, 36, and 37°C and examined for the presence
of a deposit every half hour. A portion of all the sera
and the EDTA and heparin plasmas was also first
incubated at 37°C and for half hourly intervals
thereafter at temperatures decreasing by 1°C until a
deposit was noted or the temperature of 25° was
reached. The time for the precipitate to redissolve
completely at 37°C was noted. The precipitation and
dissolution of the clots in the same samples were
carried out several times. Control blood samples
from two healthy volunteers from the laboratory
were examined in parallel under identical conditions.
Aliquots of the EDTA plasmas and sera from the
patient, her two sisters, and her mother were also
electrophoresed at the above temperatures. Scanning densitometry of the plasmas was used to
calculate the fibrinogen levels from total protein
concentrations. Deposits from their cold EDTA
plasmas were also isolated, washed three times in
0*9% saline, dissolved, precipitated again, washed,
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Y Lolin, P A Razis, P O'Gorman, M Hjelm, and A S Wierzbicki
634
TABLE The fibrinogen content in the same ED TA
plasmas from the patient, her two sisters, and her mother,
calculated from the peaks obtained after the samples
were electrophoresed (with previous incubation at
the corresponding temperature for half an hour)
on agarose gel at decreasing temperatures. The differences
in the fibrinogen amount were thought to reflect the
amount of cryoprecipitation occurring during the
incubation stage. The albumin levels are shown
in parentheses to show the consistency of other protein
separations as temperatures fall.
Temperature
Fibrinogen content in EDTA plasmas (gil)
CC)
Proband
37
35
34
33
32
30
28
25
4
6-72
5-74
5-74
4-40
390
3-90
4-00
4-11
3-43
(42-8)
(41-0)
(43-1)
(44-0)
(43-1)
(44-0)
(43.2)
(42-0)
(42-4)
Mother
Sister I
Sister 2
7-11
5-25
4-95
4-35
481
4-10
4-22
3-30
3-11
4-64
4-75
4-65
4-61
4-80
4-71
3-10
3-0
2-90
5-55
4-88
4-88
4-14
2-60
2-51
2-63
2-10
2-10
)=the concentration of albumin calculated from the albumin peak on the
same electrophoretic pattern. The actual albumin concentration measured on
Technicon AA II was 43 g/l. The reference range for plasma fibrinogen in the
laboratory is 1-46 to 3-8 g/l.
and after dissolving in saline immunoelectrophoresed against antisera to IgG, IgA, IgM, and
fibrinogen. In addition a washed precipitate from
the patient's EDTA plasma was dissolved in saline,
some added to a control EDTA plasma, and two
dimensional immunoelectrophoresis carried out on
both.
Results
A cryoprotein, precipitating at between 32 and 35°C
within one hour of incubation, was noted in the
EDTA as well as heparin plasmas, but not sera,
from the proband and nine members of her family
on each of the three occasions when tested (fig 1). A
cryoprotein was also detected in the EDTA and
heparin samples from one other mem-ber of the
family, precipitating within one hour of incubation,
but at 280C (fig 1, table). The precipitates comprised at least a quarter of the sample volume, redissolved totally on warming at 37°C, usually within
30 seconds although larger clots needed up to three
minutes, and could be precipitated and redissolved
totally several times. No cryoprecipitate was noted
in control EDTA and heparin plasmas and sera.
The concentrations of the total fibrinogen in the
EDTA plasmas from the proband, her mother, and
her two sisters, electrophoresed at 37°C, are shown
in the table together with the concentrations of the
fibrinogen remaining in solution at decreasing
temperatures. At 37°C the total fibrinogen level in
all four subjects was significantly higher than the
upper limit of the laboratory reference range. In
three of them visible clotting was noted at 35°C and
in one at 28°C. In all there was a significant fall in
the fibrinogen remaining in solution at the relevant
temperatures. After immunoelectrophoresis, the
washed clots from the samples of the four subjects
were confirmed as being fibrinogen, although a faint
additional reaction was also noted with IgG antiserum. After two dimensional immunoelectrophoresis no difference in electrophoretic mobility
between the proband's cryofibrinogen and the
fibrinogen from a control EDTA sample was noted.
Discussion
Although secondary cryofibrinogenaemia is relatively common in adults, the primary form is rare.5 16
In children both are rare. There have been occasional
reports of transient or chronic secondary cryofibrinogenaemia,8 9 20 21 but to our knowledge there
have been only two reports of persistent primary
cryofibrinogenaemia. 16 2
Trace amounts of cryoprecipitate in heparin
plasma left overnight at 4°C are frequently observed.
Although many reasons for that have been sugheparin (as anticoagulant in the blood
gested,
bottle) is thought to be the most important factor.2 24
The demonstration of a cryoprecipitate in plasma
using other anticoagulants such as EDTA,25 the
possibility of repeated precipitation and dissolution,17 as well as identification of the clot by
immunochemistry,17 indicate the definite presence
of a cryofibrinogen, which, if in a quantity of more
than 1 g/1,7 17 is of pathological significance. The
above could all be found in our study. In addition,
parallel examination of control plasmas under
identical conditions yielded no cryoprecipitate.
The clinical pre;sentation of the child was unusual.
Although we had not excluded other causes for
myalgia and nephrotic syndrome, both were transient, occurred after a fall in body temperature, and
were thus most likely to have been caused by
the cryofibrinogen precipitating in the muscle and
renal microvasculature. Cryofibrinogenaemia is
frequently associated with proteinuria and glomerulonephritis.12 13 Persistent cryofibrinogenaemia
may even cause nephropathy.12 However, transient
heavy proteinuria has been described only once in
association with cryoproteinaemia and was thought
to be the result of 'reversible embolism' of the renal
vasculature.26 Cryofibrinogenuria is also rare,
occurring in only 5% of patients with cryofibrino-
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Transient nephrotic syndrome after anaesthesia
genaemia, particularly if, as in our patient, they are
also secreting an excess of free light chain immunoglobulins.27
The precipitation of the protein at 35°C was
unusual. The highest recorded precipitating
temperature to date for cryofibrinogen has been
27°C16 and for cryoglobulin 320C.28 The latter was
detected in the serum of an adult who died postoperatively in acute renal failure because of resulting globulin precipitation in the kidneys. Her lowest
body temperature was 34-8°C.
While congenital fibrinogen abnormalities,
including afibrinogenaemia, hypofibrinogenaemia,
and dysfibrinogenaemia, although rare, are well
documented,29 familial cryofibrinogenaemia has
not been described before to our knowledge.
Although this is the first such report, the condition
may not be uncommon. Most of the affected
members of the family gave no history of symptomatic cryofibrinogenaemia before the study and some
did so only after detailed questioning, but all
developed acrocyanosis when exposed for the first
time to very low temperatures. Though asymptomatic cryofibrinogenaemia is frequently found,S the
paucity of symptoms in our family was surprising,
since the fibrinogen precipitating temperatures were
high. One of the reasons may have been the rapid
dissolution of the clots which was total for larger
clots within three minutes and for smaller clots
within seconds of warming in vitro. Thus, any
precipitate formed in the extremities in vivo may
have dissolved rapidly on entering the central
circulation. The patient developed serious symptomatic cryofibrinogenaemia, that is, myalgia and
lumbar tenderness, only with cooling of large areas
of the body when precipitation of fibrinogen may
have been more extensive.
The cause of cryofibrinogenaemia is unknown.
There may be abnormal synthesis or postsynthetic
alterations in the protein. Interestingly, while the
family studies strongly suggest a dominant pattern of
inheritance of the abnormality, both parents of the
proband are affected (the child may thus be homozygous for the gene concerned). Although they
strongly deny consanguinity, they originate from the
Welsh mining valleys where some congenital
abnormalities are particularly frequent. Molecular
genetic studies on both sides of the proband's family
are in progress, as is the analysis of the amino acid
composition of the cryofibrinogen.
, The electrophoretic mobility of cryofibrinogen is
usually similar to that of normal fibrinogen5 6as was
the case in our study. The clotting studies may be
normal,'0 as in our proband, or abnormal." 16 It is
often associated with thromboembolic disease of
disseminated intravascular coagulation.3 24 There
635
is no correlation between the amount of cryofibrinogen and fibrinogen in the plasma of the same
subject examined serially. 2 However, the
proband, her mother, and her two sisters all had
raised total fibrinogen levels. They may thus have
abnormal both fibrinogen synthesis and clearance
from the circulation.
After the diagnosis in the proband, necessary
orthopaedic operations which had been postponed
will now be carried out since appropriate precautions
and therapy can be applied,2 1 17 31 and the awareness of the condition in the proband and family may
minimise future possibly life threatening complications.
The authors wish to thank Dr J A Morgan-Hughes
(National Hospitals for Nervous Diseases, London)
and Dr C M Weaver (University Hospital of Wales,
Cardiff) for allowing them to investigate the patient
and her family, and Mrs Linda Dudderidge for her
invaluable assistance in the preparation of this
manuscript.
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Correspondence to Dr Y Lolin, Department of
Chemical Pathology, The National Hospitals for
Nervous Diseases, Queen Square, London
WC1N 3BG.
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Transient nephrotic syndrome
after anaesthesia resulting from a
familial cryofibrinogen
precipitating at 35 degrees C.
Y Lolin, P A Razis, P O'Gorman, M Hjelm and A S
Wierzbicki
J Med Genet 1989 26: 631-636
doi: 10.1136/jmg.26.10.631
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