Renal cell carinoma presenting as hypertension inpregnancy

J. FYNN1 and A. K. G. VENYO2

1Departments of Obstetrics and Gynaecology and 2Urology, North Manchester General Hospital, Manchester, UK

Case report

A 33-year-old primigravida was seen at the antenatal clinic at 12

weeks with ‘essential hypertension’. She had been started on

labetolol 200 mg t.d.s. prior to referral due to blood pressure of

220/110 mmHg. She was asymptomatic and there was no past

history of recurrent urinary tract infection (UTI) or any renal

disease.

The patient was obese, with a body mass index (BMI) of

44 kg m7 2. Her laboratory investigations, full blood count, urea

and electrolytes were normal and as such as continued on the

labetolol. At 18 weeks she was admitted with mild bleeding per

vaginum. The condition was satisfactory. The case was reviewed

and the decision was taken to investigate for cause of the

hypertension. Renal ultrasound revealed a suspicious 15-cm mass

in the upper pole of the right kidney. The patients was referred to a

tertiary centre for further management.

Magnetic resonance imaging (MRI) scanning showed a

126 14 cm soft tissue signal mass in the upper pole of the right

kidney. The right kidney was displaced downwards and the right

adrenal appeared slightly irregular and prominent. The mass was

considered primarily renal rather than adrenal. There was no

evidence seen to suggest the soft tissue mass was within the right

renal vein or the inferior vena cava. There was no associated para-

aortic lymphadenopathy. The left kidney was outlined normally

and the liver appeared normal. There was some high signal material

present on both T1 and T2 images, which suggests haemorrhage in

the mass lesion.

Twenty-four-hour urinary metanephrine level was normal.

Anomaly scan of fetus was normal. Two-weekly growth scans of

the fetus were normal. Prophylactic corticosteroid was given. Blood

pressure was controlled on increasingly higher doses of labetolol. At

26 weeks, due to the increasing size of the mass, she had combined

surgery during which she had emergency ceasarean section followed

by a radical right nephrectomy. She was delivered of a live baby girl

weighing 600 g. The baby died at 7 days old from prematurity. The

patient otherwise made satisfactory postoperative progress and was

discharged home at 2 weeks post-operatively. Histology examina-

tion revealed a T2N0M0 renal cell carcinoma. The right adrenal

gland was unremarkable. At follow-up after 3 years, the patient has

had a daughter, 2 years old, and was currently a few weeks into her

third pregnancy. The hypertension had resolved and there has been

no evidence of recurrence.

Discussion

Chronic hypertension is a common finding in pregnancy. It is

estimated that 3% of pregnant woman would be seen per year with

chronic hypertension in the United States (Sibai 2002). Because the

majority of the patients would have essential hypertension (90%), it

is likely that one would overlook the secondary causes (10%)

(Report of the National High Blood Pressure Education Program

2000) which are potentially curable, but if undiagnosed could prove

fatal. These secondary causes include coarctation of the aorta,

endocrine disorders (diabetes mellitus with vascular involvement,

phaeochromocytoma, thyrotoxicosis, Cushing’s disease, hyperal-

dosteronism), collagen vascular disease disorder (lupus, scleroder-

ma) and renal disease (glomerulonephritis, interstitial nephritis,

polycystic kidneys, renal artery stenosis).

A rare cause of hypertension in pregnancy is renal cell

carcinoma. Over 70 cases of renal cell carcinoma in pregnancy

have been reported in the literature (Kobayashi et al., 2000).

Walker and Knight (1986) reported that 18% of renal tumours

presented as hypertension in pregnancy. The most common mode

of presentation is a palpable mass (88%), the others being pain

(50%) and haematuria (47%). Other rare reported presentations

are haemolytic anaemia and hypercalcaemia (Monga et al., 1995;

Usta et al., 1998). In a more recent review of renal carcinoma in

pregnancy, Smith et al. (1994) have suggested that it is being

increasingly discovered during ultrasound examination for other

reasons.

Diagnostic evaluation of the pregnant patient with suspected

renal cell carcinoma invovles first sending urine for cytological

analysis. The preferred imaging technique is abdominal ultrasound

and magnetic imaging, as this avoids radiation exposure to the fetus

(Gladman et al., 2002). In non-pregnant patients, however, IVP and

computerised tomography are commonly used.

The management of a pregnant woman with a possbile malignant

solid renal mass follows certain principles, as reported by Gladman

et al. (2002). First, the welfare of the woman takes precedence over

that of the fetus, unless she wishes otherwise. Secondly, manage-

ment of the patient should take place in the multidisciplinary setting

involving urologists, neonatologist, obstetricians, radiologists,

anaesthetists, histopathologists, oncologist and midwives. Thirdly,

the standard surgical treatment of most stages of renal carcinoma is

a radical nephrectomy involving en bloc removal of the entire

kidney and perinephric fat within the Gerota fascia.

One of the major issues in the management of cancer in

pregnancy is the timing of surgery. It has to take into consideration

the biological behaviour of the tumour and the neonatal survival

rates for the different gestations (Gladman et al., 2002). It is widely

accepted that the natural history of renal cell carcinoma is variable

and is influenced by a complex interplay of both the tumour- and

host-specific factors (Whang and Godley, 2003). Therefore it is

difficult to predict the clinical course in a particular individual.

Nevertheless, it is known that up to a quarter to a third of the non-

pregnant population have distant metastases at presentation

(Malkowicz et al., 2001). Secondly, the UCLA integrated staging

system which has been refined to a simple algorithm for predicting

clinical outcome and survival rates relies on the data such as TNM

stage Fuhrman tumour histological grade and performance status,

requires a surgically resected tumour (Zisman et al., 2002). Thirdly,

although there is no evidence that the clinical outcome of urological

malignancies are influenced by pregnancy, more recent data calls

for caution (Loughlin, 1995). Lambe et al. (2002), in a Swedish

population-based study, found a strong association between the

number of births and the risk of renal cell carcinoma. They also

noted that ever parous women were at a 40% increased risk of renal

cell carcinoma compared to nulliparous women. Indeed oestrogen

and progesterone receptors have been found in normal and

malignant renal cells (Ronchi et al., 1984). It has been speculated

that pregnancy-associated hormonal changes, particularly high

oestrogen levels, may act as promoters of malignant change by

stimulating renal cell proliferation either directly or via paracrine

growth factors (Concolino et al., 1993). Whether these observations

have any implications for the biological behaviour of malignant

renal cells in pregnancy is not clear, but a tendency towards

immediate rather than delayed surgery would be appropriate.

As neonatal survival rates increase with increasing gestation at

delivery, immediate surgery at early gestations is potentially

deleterious to fetal health. Also pertinent is whether pregnancy is

interrupted or allowed to continue if radical nephrectomy is carried

out.

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In the first trimester, immediate surgery is the general

recommendation (Loughlin, 1995; Gladman et al., 2002). Whether

pregnancy is terminated at this gestation should be based on the

patient’s wishes and therapeutic reasons, but it should be noted that

the risk of miscarriage and teratogenesis are both high at this

gestation, making termination a better option. Usta et al. (1998) are

of the opinion that this option is not necessary.

Management in the second trimester poses some challenges. In

the late second trimester, in keeping with Loughlin’s recommenda-

tion, surgery should be delayed to at least 28 weeks, where fetal

survival of over 90% is achievable in most tertiary units where this

operation would be performed anyway (Loughlin, 1995). However,

in the early second trimester, it is our opinion that immediate

surgery would probably be better than delaying, as the risk of fetal

loss is low (Fazeli-Matin et al., 1998; Gnessin et al., 2002; Jenkins et

al., 2003).

In the third trimester, where fetal lung maturity is established or

can be improved with antenatal corticosteroids, immediate surgery

seems expedient. It has been suggested that caesarean section

should not be performed automatically at the time of radical

nephrectomy as the kidney is removed through a flank incision

(Walker and Knight 1986). In cases complicated by severe

hypertension, spontaneous tumour rupture, heavy bleeding,

difficulty with transabdominal approach to the renal vessels due

to uterine size or a clear obstetric indication, a caesarean section

should be performed initially (Usta et al., 1998). If the diagnosis is

made near term renal surgery can be safely postponed until delivery

(Loughlin, 1995). If there is widespread metastatic disease, an

extremely rare occurrence, Hendry has suggested the pregnancy

should be terminated (Hendry, 1997). So far there have been no

reports of fetal metastases (Walker and Knight 1986).

There are few data on the effect of pregnancy on long-term

survival in renal cell carcinoma. Several authors have reported the

clinical course and survival is better than would be expected

(Walker and Knight, 1986). There is also lack of knowledge on the

effect of future pregnancy on tumour recurrence, but it seems, in the

absence of metastases as illustrated by our case, the risk is low. A

regional or national registry of cases of renal cell carcinoma in

pregnancy and outcome in subsequent pregnancies would offer

answers to these uncertainties.

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and Di Silverio F. (1993) Acquired cystic kidney disease: thehormonal hypothesis. Urology, 41, 170 – 175.

Fazeli-Matin S., Goldfarb D.A. and Novick A.C. (1998) Renal andadrenal surgery during pregnancy. Urology, 52, 510 – 511.

Gladman M.A., MacDonald D., Webster J.J., Cook T. and Williams G.(2002) Renal cell carcinoma in pregnancy. Journal of the RoyalSociety of Medicine, 95, 199 – 201.

Gnessin E., Dekel Y. and Baniel J. (2002) Renal cell carcinoma inpregnancy. Urology, 60, 1111.

Hendry W.F. (1997) Management of urological tumours in pregnancy.British Journal of Urology, 80 (Supplement 1), 24 – 28.

Jenkins T.M., Mackey S.F., Benzoni E.M., Tolosa J.E. and SciscioneA.C. (2003) Non-obstetric surgery during gestation: risk factors forlower birthweight. Australian and New Zealand Journal of Obstetricsand Gynaecology, 43, 27 – 31.

Kobayashi T., Fukuzawa S., Miura K., Matsui Y., Fujikawa K., OkaH. and Takeuchi H. (2000) A case of renal cell carcinoma duringpregnancy: simultaneous cesarean section and radical nephrectomy.Journal of Urology, 163, 1515 – 1516.

Lambe M., Lindblad P., Wuu J., Remler R. and Hsieh C.C. (2002)Pregnancy and risk of renal cell cancer: a population-based study inSweden. British Journal of Cancer, 86, 1425 – 1429.

Loughlin K.R. (1995) The management of urological malignanciesduring pregnancy. British Journal of Urology, 76, 639 – 644.

Malkowicz B.S., Sanchez-Ortiz R.F. and Wein A.J. (2001) Adultgenitourinary cancer. In: Clinical Manual of Urology, 3rd edn, editedby Hanno P., Malkowicz S.B. and Wein A.J., pp. 487 – 560. NewYork, McGraw Hill.

Monga M., Benson G.S. and Parisi V.M. (1995) Renal cell carcinomapresenting as hemolytic anemia in pregnancy. American Journal ofPerinatology, 12, 84 – 86.

Report of the National High Blood Pressure Education ProgramWorking Group on High Blood Pressure in Pregnancy. (2000)American Journal of Obstetrics and Gynecology, 183, S1 – S22.

Ronchi E., Pizzocaro G., Miodini P., Piva L., Salvioni R. and DiFronzo G. (1984) Steroid hormone receptors in normal andmalignant human renal tissue: relationship with progestin therapy.Journal of Steroid Biochemistry and Molecular Biology, 21, 329 – 335.

Sibai B.M. (2002) Chronic hypertension in pregnancy. Obstetrics andGynecology, 100, 369 – 377.

Smith D.P., Goldman S.M., Beggs D.S. and Lanigan P.J. (1994) Renalcell carcinoma in pregnancy: report of three cases and review of theliterature. Obstetrics and Gynecology, 83, 818 – 820.

Usta I.M., Chammas M. and Khalil A.M. (1998) Renal cell carcinomawith hypercalcemia complicating a pregnancy: case report and reviewof the literature. European Journal of Gynaecological Oncology, 19,584 – 587.

Walker J.L. and Knight E.L. (1986) Renal cell carcinoma in pregnancy.Cancer, 58, 2343 – 2347.

Whang Y.E. and Godley P.A. (2003) Renal cell carcinoma. CurrentOpinion in Oncology, 15, 213 – 216.

Zisman A., Pantuck A.J., Wieder J., Chao D.H., Dorey F., Said J.W.,deKernion J.B., Figlin R.A. and Bellegrun A.S. (2002) Risk groupassessment and clinical outcome algorithm to predict the naturalhistory of patients with surgically resected renal cell carcinoma.Journal of Clinical Oncology, 20, 4559 – 4566.

Correspondence to: Dr John Fynn, 4 Churchside Close, Manchester M9 8HZ, UK. E-mail: crow13103@ntlworld.com

DOI: 10.1080/01443610400009600

Nail deformity in pregnancy

Q. A. WARRAICH1 and G. P. CUMMING2

1Department of Obstetrics and Gynaecology, Aberdeen Royal Infirmary, Aberdeen and 2Department of Obstetricsand Gynaecology, Dr Grays Hospital, Elgin, UK

Case report

A 29-year-old para 1+4, non-vegetarian woman presented at 16

weeks’ gestation at the antenatal clinic with a non-familial recurring

nail condition, occurring during pregnancy, and resolving comple-

tely postnatally. Interestingly, this condition occurred after the first

trimester so did not manifest in her miscarriages, which were all

early first trimester. It was characterised by a painless forward

longitudinal over curvature of the nail plates in both hands, most

obvious at the distal free edges. Her nails were otherwise normal in

appearance and rate of growth. Investigations revealed normal

serum electrolytes, including serum calcium, a negative serum beta

thalassaemia screen and normal thyroid function tests. However,

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