CASE REPORTS
775
British Journal of Obstetrics and Gynaecology September 1992, Vol. 99, pp. 715-776
Renal cell carcinoma: an unusual cause of second trimester hypertension JOHN J. MORRISON Research Registrar R A L P H E. R O B I N S O N Consultant Department o j Obstetrics and Gynaecology University of Cambridge Clinical School Rosir Maternity Hospital Robinson Way, Cambridge CB2 2SW, UK
Case report A 30-year-old woman in her second pregnancy was noted at her first hospital antenatal clinic visit at 14 weeks gestation to have elevated blood pressure of 150/105 mmHg. Physical examination was otherwise normal with no associated oedema or proteinuria. In her first pregnancy 5 years previously, labour had been induced at 38 weeks gestation because of hypertension and proteinuria (160/100 mmHg and 3+ respectively), at another hospital. She gave birth to a male infant whose weight was on the third centile. Her past medical history was uneventful. Admission was arranged for assessment of the hypertension. Urine microscopy was normal and culture of a midstream specimen showed no growth. Laboratory data included a haemoglobin concentration of 1 1.9 g/dl with normal red cell indices, a white cell count of I 1 x 109/1and a platelet count of 271 x 109/1. The blood urea nitrogen level was normal (1.9 mmol/l) and plasma electrolytes were normal: Na 138 mmol/l, K 3.6 mmol/l and C193 mmol/l. The blood glucose level was normal (3.7 mmol/l). Serum uric acid level was 2.9 mmol/l and the plasma creatinine concentration was 75 pmol/l. Blood pressure readings taken on a 2-h basis subsequently showed a consistently elevated pattern within the range of 140-150/95-105 mmHg. The total protein in a 24-h collection was normal (0.23 g/24 h) as were urinary sodium (177 mmo1/24 h), potassium (57 mmo1/24 h), urea (304 mmo1/24 h) and creatinine (1 6.1 mmol/l) levels. Creatinine clearance was normal for pregnancy at 149 ml/m and the urinary vanillylmandelic acid was normal at 33 pmo1/24 h. Treatment was started with labetalol 100 mg twice daily on the fourth hospital day and blood pressure readings settled within 48 h to 120-130/75-85 mmHg. She was discharged home on the seventh hospital day. The patient remained normotensive after this time and attended for a routine, detailed fetal ultrasound scan 3 weeks later. During this scan, an 8 to 10 cm mixed echogenic mass was noted in the upper pole of the left maternal kidney suggestive of renal cell carcinoma (Fig. 1). A chest X-ray was normal and blood liver function tests were all within the normal range. A radical left nephrectomy was performed at 19 weeks gestation. The histological Correspondence: Dr John J. Morrison.
picture was that of a renal cell carcinoma and the tumour capsule had not been breached (Fig. 2 ) . The labetalol treatment was discontinued at the time of surgery and the patient remained normotensive throughout the remainder of her pregnancy. She was admitted in early labour at 41 weeks gestation and gave birth spontaneously to a healthy female infant weighing 3440 g. Pathological examination of the placenta revealed no evidence of tumour deposits Computerized tomography 9 months after nephrectomy showed no evidence of recurrent disease.
Discussion This case illustrates the diagnostic challenge of the young pregnant patient with a rare disease. Primary renal neoplasms are uncommon in pregnancy and when they occur their presentation is usually quite different to this. Renal cell carcinoma is an adenocarcinoma that arises from the tubular epithelial cells. It may occur at any age but is most common in the sixth decade of life. There is a male to female ratio of 2: 1. A review of the literature revealed 71 reported primary renal neoplasms in pregnancy of which 35 (50%) were renal cell carcinomas (Walker & Knight 1986).The most common presenting feature in pregnant patients was a palpable mass (88%). Pain was the second most frequent finding (50%) and haematuria was found in 47% of cases. Our patient presented with hypertension alone causing a diagnostic dilemma as hypertension is often seen in pregnancy. In view of the clinical findings and laboratory data a diagnostic renal ultrasound scan was not performed during the initial assessment and hence the coincidental finding 3 weeks later. The low numbers of reported cases of renal cell carcinoma in pregnancy allow few conclusions to be drawn about the effects of pregnancy. There is some evidence that in long-term
Fig. 1. Ultrasound scan of left kidney showing mixed echogenic mass in the upper pole.
776
C A S E REPORTS
(Bloom et al. 1973). Progesterone, for this reason, has been proposed in the treatment of renal cell carcinoma (Concolino et al. 1978). The overall effect of the elevated circulating levels of both oestrogen and progesterone is unknown. To our knowledge there have been no cases of fetal metastasis and the effect of future pregnancies on tumour recurrence is unknown. The recommended treatment for renal cell carcinoma in pregnancy is radical surgical excision. During the first and second trimesters it is not necessary to interrupt the pregnancy to perform radical renal surgery. The situation is generally similar in the third trimester except under circumstances such as severe hypertension, spontaneous tumour rupture, heavy bleeding or difficulty with the trans-abdominal approach to the renal vessels due to uterine size when a caesarean section should be performed.
Acknowledgments We would like to thank Mr P. Doyle for allowing us to report this patient. We are grateful to Dr J. Tudor and Dr J. Amo for their help with the ultrasonography and histology, respectively.
References
Fig. 2. A view of a section from the tumour showing sheets of tumour cells. There are cells with characteristic clear cytoplasm and areas of granular cytoplasm.
follow up there is a generally better clinical course and survival than would be expected (Ney et al. 1971). The increased hormonal levels may have opposite effects, since experimental studies in rodents have reported that oestrogens can cause kidney tumours, while progesterone exerts a protective effect
Bloom H. J., Dukes G. E. & Mitchley B. L. (1973)Hormone-dependent tumours of the kidney. B r J Cancer 1 7 , 6 1 1 4 4 5 . Concolino F., Marocchi A,, Conti C., Tenaglia R., Di Silverio F. & Bracci U. (1978) Human renal cell carcinoma as a hormonedependent tumour. Cancer Res 38,4340-4344. Ney C., Posner A. C. & Ehrlich J. C. (1971) Tubular adenoma of the kidney during pregnancy. Obstet Gynecol37,267-276. Walker J . L. & Knight E. L. (1986)Renal cell carcinoma in pregnancy. Cancer 58, 2343-2347. Received 5 May 1992 Accepted 16 May 1992
775
British Journal of Obstetrics and Gynaecology September 1992, Vol. 99, pp. 715-776
Renal cell carcinoma: an unusual cause of second trimester hypertension JOHN J. MORRISON Research Registrar R A L P H E. R O B I N S O N Consultant Department o j Obstetrics and Gynaecology University of Cambridge Clinical School Rosir Maternity Hospital Robinson Way, Cambridge CB2 2SW, UK
Case report A 30-year-old woman in her second pregnancy was noted at her first hospital antenatal clinic visit at 14 weeks gestation to have elevated blood pressure of 150/105 mmHg. Physical examination was otherwise normal with no associated oedema or proteinuria. In her first pregnancy 5 years previously, labour had been induced at 38 weeks gestation because of hypertension and proteinuria (160/100 mmHg and 3+ respectively), at another hospital. She gave birth to a male infant whose weight was on the third centile. Her past medical history was uneventful. Admission was arranged for assessment of the hypertension. Urine microscopy was normal and culture of a midstream specimen showed no growth. Laboratory data included a haemoglobin concentration of 1 1.9 g/dl with normal red cell indices, a white cell count of I 1 x 109/1and a platelet count of 271 x 109/1. The blood urea nitrogen level was normal (1.9 mmol/l) and plasma electrolytes were normal: Na 138 mmol/l, K 3.6 mmol/l and C193 mmol/l. The blood glucose level was normal (3.7 mmol/l). Serum uric acid level was 2.9 mmol/l and the plasma creatinine concentration was 75 pmol/l. Blood pressure readings taken on a 2-h basis subsequently showed a consistently elevated pattern within the range of 140-150/95-105 mmHg. The total protein in a 24-h collection was normal (0.23 g/24 h) as were urinary sodium (177 mmo1/24 h), potassium (57 mmo1/24 h), urea (304 mmo1/24 h) and creatinine (1 6.1 mmol/l) levels. Creatinine clearance was normal for pregnancy at 149 ml/m and the urinary vanillylmandelic acid was normal at 33 pmo1/24 h. Treatment was started with labetalol 100 mg twice daily on the fourth hospital day and blood pressure readings settled within 48 h to 120-130/75-85 mmHg. She was discharged home on the seventh hospital day. The patient remained normotensive after this time and attended for a routine, detailed fetal ultrasound scan 3 weeks later. During this scan, an 8 to 10 cm mixed echogenic mass was noted in the upper pole of the left maternal kidney suggestive of renal cell carcinoma (Fig. 1). A chest X-ray was normal and blood liver function tests were all within the normal range. A radical left nephrectomy was performed at 19 weeks gestation. The histological Correspondence: Dr John J. Morrison.
picture was that of a renal cell carcinoma and the tumour capsule had not been breached (Fig. 2 ) . The labetalol treatment was discontinued at the time of surgery and the patient remained normotensive throughout the remainder of her pregnancy. She was admitted in early labour at 41 weeks gestation and gave birth spontaneously to a healthy female infant weighing 3440 g. Pathological examination of the placenta revealed no evidence of tumour deposits Computerized tomography 9 months after nephrectomy showed no evidence of recurrent disease.
Discussion This case illustrates the diagnostic challenge of the young pregnant patient with a rare disease. Primary renal neoplasms are uncommon in pregnancy and when they occur their presentation is usually quite different to this. Renal cell carcinoma is an adenocarcinoma that arises from the tubular epithelial cells. It may occur at any age but is most common in the sixth decade of life. There is a male to female ratio of 2: 1. A review of the literature revealed 71 reported primary renal neoplasms in pregnancy of which 35 (50%) were renal cell carcinomas (Walker & Knight 1986).The most common presenting feature in pregnant patients was a palpable mass (88%). Pain was the second most frequent finding (50%) and haematuria was found in 47% of cases. Our patient presented with hypertension alone causing a diagnostic dilemma as hypertension is often seen in pregnancy. In view of the clinical findings and laboratory data a diagnostic renal ultrasound scan was not performed during the initial assessment and hence the coincidental finding 3 weeks later. The low numbers of reported cases of renal cell carcinoma in pregnancy allow few conclusions to be drawn about the effects of pregnancy. There is some evidence that in long-term
Fig. 1. Ultrasound scan of left kidney showing mixed echogenic mass in the upper pole.
776
C A S E REPORTS
(Bloom et al. 1973). Progesterone, for this reason, has been proposed in the treatment of renal cell carcinoma (Concolino et al. 1978). The overall effect of the elevated circulating levels of both oestrogen and progesterone is unknown. To our knowledge there have been no cases of fetal metastasis and the effect of future pregnancies on tumour recurrence is unknown. The recommended treatment for renal cell carcinoma in pregnancy is radical surgical excision. During the first and second trimesters it is not necessary to interrupt the pregnancy to perform radical renal surgery. The situation is generally similar in the third trimester except under circumstances such as severe hypertension, spontaneous tumour rupture, heavy bleeding or difficulty with the trans-abdominal approach to the renal vessels due to uterine size when a caesarean section should be performed.
Acknowledgments We would like to thank Mr P. Doyle for allowing us to report this patient. We are grateful to Dr J. Tudor and Dr J. Amo for their help with the ultrasonography and histology, respectively.
References
Fig. 2. A view of a section from the tumour showing sheets of tumour cells. There are cells with characteristic clear cytoplasm and areas of granular cytoplasm.
follow up there is a generally better clinical course and survival than would be expected (Ney et al. 1971). The increased hormonal levels may have opposite effects, since experimental studies in rodents have reported that oestrogens can cause kidney tumours, while progesterone exerts a protective effect
Bloom H. J., Dukes G. E. & Mitchley B. L. (1973)Hormone-dependent tumours of the kidney. B r J Cancer 1 7 , 6 1 1 4 4 5 . Concolino F., Marocchi A,, Conti C., Tenaglia R., Di Silverio F. & Bracci U. (1978) Human renal cell carcinoma as a hormonedependent tumour. Cancer Res 38,4340-4344. Ney C., Posner A. C. & Ehrlich J. C. (1971) Tubular adenoma of the kidney during pregnancy. Obstet Gynecol37,267-276. Walker J . L. & Knight E. L. (1986)Renal cell carcinoma in pregnancy. Cancer 58, 2343-2347. Received 5 May 1992 Accepted 16 May 1992
