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CASE REPORT
Pregnancy outcome in a renal transplant recipient withresidual mild tertiary hyperparathyroidism
Adam Morton,a Fiona Dalzell,b Nicole Isbel,c Tony Pradob
Case report
A 26 year old woman presented for preconception
counselling. Eight years previously, she had received a live
related kidney transplant for end-stage renal failure due to
reflux nephropathy. Five years later, bilateral native ne-
phrectomies were performed because of severe hyperten-
sion, with angiography excluding significant stenosis of the
renal transplant artery. Inactive problems were previous dis-
seminated tuberculosis and herpes zoster. Her medications
included azathioprine, prednisolone, felodipine, atenolol,
hydralazine, ranitidine, sodium bicarbonate and iron. Serum
creatinine had ranged between 0.14 and 0.18 mmol/L dur-
ing the preceding two years, 24-hour urine protein was
0.72 g/day, haemoglobin was 97 g/dL and serum urate was
0.34 mmol/L.
There was evidence of mild residual tertiary hyper-
parathyroidism with ionised calcium 1.4 mmol/L (normal
1.2–1.3 mmol/L), corrected calcium 2.74 mmol/L (2.15–
2.6 mmol/L) and serum parathyroid hormone 14 pmol/L
(1–7 pmol/L). Bone mineral density a year earlier was
normal. She was commenced on iron and folate supple-
ments, and methyldopa and labetalol were substituted for
atenolol, hydralazine and felodipine with good control of
blood pressure on home and office monitoring.
No information on outcomes of pregnancy complicated
by tertiary hyperparathyroidism could be obtained from a
literature search, nor on personal communications with
leading authorities in the areas of transplantation, renal
disease and pregnancy. Six months later she conceived. At
13 weeks, serum testing estimated a risk of trisomy 21 of
1:16. This was assumed to be a false result related to her
renal dysfunction. A nuchal translucency scan estimated the
risk at 1:7000. By 17 weeks of gestation, haemoglobin had
fallen to 82 g/dL with serum ferritin 222 Ag/L. Darbopoetin
30 Ag a week was commenced with the haemoglobin rising
to 118 g/dL over the next eight weeks. At 30 weeks of
gestation, her blood pressure rose without other evidence of
superimposed pre-eclampsia. Darbopoetin was ceased and
nifedipine was added because of intolerance of higher doses
of methyldopa. At 32 weeks of gestation, she was admitted
to the hospital because of progressive hypertension. Serum
creatinine had risen from 0.14 to 0.16 mmol/L in the pre-
ceding week (normal for pregnancy 0.04–0.07 mmol/L),
serum urate was 0.4 mmol/L, the degree of proteinuria was
stable,and there was loss of variability on cardiotocogram.
After betamethasone administration, caesarean section was
performed with delivery of a male infant with birthweight
1568 g. The mothers’ blood pressure and renal function im-
proved after delivery with excellent blood pressure control
on irbesartan alone and serum creatinine of 0.12 mmol/L at
the time of discharge six days postpartum. She elected not
to breastfeed because of uncertainty regarding the safety
of azathioprine. During the course of pregnancy and the
postpartum period, her degree of hypercalcemia was stable
(Fig. 1). The paediatric team was notified of the risk of
neonatal hypocalcemia and tetany prior to delivery. Her
son’s calcium was checked on cord blood then on a daily
basis. He was noted to have mild hypocalcemia 24 hours
after delivery with ionised calcium 0.95 mmol/L (normal
1.00–1.18 mmol/L) and was treated with intravenous cal-
cium gluconate. Hyaline membrane disease was of mod-
erate severity requiring nasal continuous positive airway
pressure for five days, prematurity associated jaundice
was treated with phototherapy, patent ductus arteriosus
was treated with indomethacin and non-descent of the right
testicle was noted at birth. An ultrasound of the kidneys
and urinary tract was normal.
Discussion
Tertiary hyperparathyroidism occurs when there is hy-
percalcemia due to autonomously hyperfunctioning para-
thyroid tissue following prolonged parathyroid stimulation
by prior hypocalcemia in the setting of renal failure. It is
usually due to four-gland parathyroid hyperplasia, as distinct
from a single gland adenoma which makes up more than
BJOG: an International Journal of Obstetrics and GynaecologyJanuary 2005, Vol. 112, pp. 124–125
D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology www.blackwellpublishing.com/bjog
aMater Hospital, South Brisbane, AustraliabMater Private Clinic, South Brisbane, AustraliacPrincess Alexandra Hospital, Woolloongabba, Australia
Correspondence: Dr A. Morton, Mater Hospital, South Brisbane 4101,
Australia.
DOI: 10.1111/j .1471-0528.2004.00314.x
80% of cases of primary hyperparathyroidism. Residual
hyperparathyroidism after renal transplantation is common,
with as few as 22.6% of patients having normal parathyroid
hormone concentrations after transplantation.1–3 Predictive
factors include pre-transplantation parathyroid hormone
levels and post-transplantation graft function. Indications
for surgical intervention for persistent hyperparathyroidism
after renal transplantation include corrected calcium greater
than 3.0 mmol/L more than one year post-graft and symp-
tomatic hypercalcemia. This is the first case of pregnancy
outcome in a woman with tertiary hyperparathyroidism of
which we are aware. A recent review noted 145 cases of
primary hyperparathyroidism in pregnancy reported in the
literature to date.4 The management of primary hyperpara-
thyroidism in pregnancy is controversial. Maternal compli-
cations of primary hyperparathyroidism in pregnancy
including hyperemesis gravidarum, pancreatitis, hypercal-
cemic crisis and nephrolithiasis have been reported to occur
in up to 67% of mothers. Up to 80% of fetuses or neonates
in pregnancies to affected mothers have been reported to
have complications including miscarriage, stillbirth or
neonatal death in 31% of pregnancies, and neonatal tetany
in 19%. Based upon this, some authors recommend neck
exploration in the second trimester in all pregnant women
with primary hyperparathyroidism. These complication
rates, however, are from older literature where the maternal
disease was severe, and some authors suggest observation
is reasonable in those women who are asymptomatic with
mild hypercalcemia. Early neonatal hypocalcemia in
infants of diabetic mothers or those who are premature
usually occurs in the first 24–48 hours of life. Hypocalce-
mia in infants born to mothers with primary hyperparathy-
roidism tends to occur towards the end of the first week of
life, although this may present as late as 10 weeks of age.
Signs reported in affected infants include irritability, rapid
eye blinking and jerking, facial grimacing and convul-
sions. It would seem reasonable therefore to measure
serum calcium on a daily basis in infants of mothers with
hyperparathyroidism, although it is important to warn
mothers of the possibility of late onset hypocalcemia
and the need for assessment should their infant manifest
signs suggestive of this.
Other than mild neonatal hypocalcemia, the complica-
tions observed in this pregnancy are in keeping with the
degree of maternal renal dysfunction and hypertension
preconception, and seem unlikely to be related to the
mothers’ tertiary hyperparathyroidism. The neonatal course
was consistent with prematurity at 32 weeks. We conclude
that based upon this case, mild maternal tertiary hyperpara-
thyroidism is not a contraindication to pregnancy, and can
be safely observed without intervention. Serum testing for
trisomy 21 may be unreliable in the setting of renal
dysfunction and other means of quantifying risk such as
nuchal translucency should be used.5,6
References
1. Vlcek J, Binswanger U, Keusch G, Zaruba J. Hyperparathyroidism
after kidney transplantation: a retrospective case controlled study. Klin
Wochenschr 1991;69:669–673.
2. Torres A, Rodriguez AP, Concepcion MT, et al. Parathyroid function in
long-term renal transplant patients: importance of pre-transplant PTH
concentrations. Nephrol Dial Transplant 1998;13(Suppl 3):94–97.
3. Botha JF, Botha JR. Parathyroid function after successful renal
transplantation. S Afr J Surg 1997;35:113–116.
4. Schnatz PF, Curry SL. Primary hyperparathyroidism in pregnancy:
evidence-based management. Obstet Gynecol Surv 2002;57:365–376.
5. Cararach V, Casals E, Martinez S, et al. Abnormal renal function as a
cause of false-positive biochemical screening for Down’s syndrome.
Lancet 1997;350:1295.
6. Karidas CN, Michailidis GD, Spencer K, Economides DL. Biochemi-
cal screening for Down syndrome in pregnancies following renal
transplantation. Prenat Diagn 2002;22:226–230.
Accepted 9 May 2004
Fig. 1. Ionised calcium and parathyroid hormone levels during pregnancy and postpartum.
CASE REPORT 125
D RCOG 2004 BJOG: an International Journal of Obstetrics and Gynaecology 112, pp. 124–125