The authors report the case of a 32-year-old woman, white, with no relevant medical, surgical or obstetric history. The current pregnancy arose through medically assisted techniques due to primary infertility.

During the first half of the pregnancy, the patient developed hypertension that was difficult to control despite combined medical therapy with alpha-methyldopa 500mg every hours, propranolol 20mg every 8hours and nifedipine CR 30mg once a day.

At 24 weeks gestation, following further elevation of blood pressure (BP) (194/131mmHg), visual disturbances, proteinuria and worsening renal function, the patient was transferred to a hospital with specialist perinatal support services and admitted to a maternal–fetal intensive care unit. The clinical setting and laboratory tests confirmed chronic hypertension with superimposed pre-eclampsia; intravenous perfusion of labetalol and magnesium sulfate was therefore begun and betamethasone was administered for fetal pulmonary maturation according to the department's protocol. On the third day of hospital stay, the patient's clinical condition worsened despite therapy, and she developed ascites, limb edema, periorbital edema and other signs of volume overload. Laboratory tests revealed hypoalbuminemia and worsening renal function (Table 1). Fetal ultrasound showed a good biophysical profile (8/8), despite fetal growth restriction and absent end-diastolic flow; ductus venosus Doppler was normal, and regular fetal monitoring was instituted.

On the fourth day of hospital stay, a diagnosis of acute pulmonary edema in the context of hypertensive crisis was made and appropriate therapeutic measures were taken. On the sixth day, there was further worsening of the mother's pulmonary status requiring invasive mechanical ventilation, followed by fetal death; the patient was transferred to a general intensive care unit. The fetus was stillborn two days later, and the patient's condition slowly improved.

A thorough etiological study was performed in the postpartum period, including renal and endocrine studies and investigation of hereditary and acquired thrombophilia.

Renal ultrasound showed a well-defined mass in the lower pole of the right kidney. Renal magnetic resonance imaging was performed to clarify its nature and relations, which showed a well-defined, macronodular mass measuring 85mm at its widest point, with radial expression and a central necrotic scar with high contrast uptake, suggestive of renal oncocytoma (Figs. 1 and 2).

Figure 1.

Nuclear magnetic resonance image of renal oncocytoma – transverse view.

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Figure 2.

Nuclear magnetic resonance image of renal oncocytoma – coronal view.

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Total right nephrectomy was subsequently performed and the surgical specimen was sent for pathoanatomical and immunohistochemical study. This confirmed a solid tumor measuring 85×70×65mm, consisting of granular and eosinophilic cytoplasm, positive for Cam 5.2 and negative for CD10, and focally positive for CK7 and vimentin, compatible with a diagnosis of renal oncocytoma.

The patient's BP normalized in the postoperative period.

After two years of clinical surveillance, the patient became pregnant again. The second pregnancy was monitored from the first trimester at our institution and was uneventful, with normal BP. At 36 weeks, it was decided to perform a cesarean section due to abnormal fetal presentation and oligamnios, resulting in the birth of a healthy boy weighing 2165g, with an Apgar score of 7/10.

Renal oncocytoma accounts for 5–7% of primary renal neoplasms. It is usually diagnosed in asymptomatic patients following diagnostic exams for non-urological reasons.1

On histopathological study, renal oncocytoma presents as a well-defined, solid mass in the renal parenchyma with a central sclerosed area, although it should be remembered that this classical finding is present in only a third of cases.1–3 Diagnosis therefore requires thorough histopathological study to document the presence of tumor cells arranged in nests, cords, or tubules, with eosinophilic cytoplasm and no mitosis, and exclude the coexistence of a clear-cell tumor, found in 10–32% of cases in the literature.2,4,5

This type of tumor usually has a benign behavior and excellent prognosis. Even large masses are encapsulated and as such are rarely invasive or associated with metastasis.5–8

Diagnosis of renal oncocytoma during pregnancy is uncommon. In 1989, Fraser et al.3 published the first case report of a renal tumor diagnosed at 23 weeks gestation following investigation of right lower back pain in a healthy 31-year-old woman. This case had a good perinatal outcome despite pre-eclampsia.

In the case presented here, the renal oncocytoma was diagnosed following investigation of the cause of hypertension detected in the first half of the pregnancy that was refractory to combined therapy, culminating in early onset of severe pre-eclampsia associated with acute pulmonary edema requiring invasive ventilation, followed by fetal death.

Pre-eclampsia is defined as hypertension (BP of over 140/90mmHg in two measurements at least 6h apart) and proteinuria of over 300mg/24h. It is a complex maternal–fetal syndrome of early onset that results from inadequate trophoblast invasion. The complications associated with this syndrome include acute renal failure, eclampsia, acute pulmonary edema, placental abruption fetal growth restriction and fetal death. Such manifestations or the development of pre-eclampsia at early gestational ages are taken by some authors as a criterion of severe disease that justifies thorough investigation of the underlying causes.

This case presented with hypertension before the 20th week of gestation that could not be controlled despite combined antihypertensive therapy, and was associated with significant maternal morbidity and fetal death. Thorough investigation to exclude a secondary cause led to a diagnosis of renal oncocytoma and resolution of the patient's hypertension.

The clinical behavior of renal oncocytoma remains poorly characterized during pregnancy and may lead to an adverse maternal and fetal outcome despite its theoretically benign behavior.

The authors highlight the importance of excluding a secondary cause of hypertension in cases that are difficult to control.

The authors have no conflicts of interest to declare.