Reversible Renal Infarctions Associated with Pheochromocytoma: A Case Report
Pheochromocytoma is a rare neuroendocrine tumor that arises from the chromaffin cells of the adrenal medulla, leading to excessive production of catecholamines such as epinephrine and norepinephrine. These hormones can cause severe hypertension, headaches, palpitations, and sweating, among other symptoms. While the cardiovascular complications of pheochromocytoma are well-documented, renal involvement is less frequently reported. This case report describes a unique presentation of reversible bilateral renal infarctions associated with pheochromocytoma, highlighting the importance of early diagnosis and treatment to achieve a favorable outcome.
A 47-year-old male presented to the hospital with a 3-year history of uncontrolled hypertension, with the highest recorded blood pressure of 210/160 mmHg. He also reported intermittent severe headaches, pallor, and sweating. Although he occasionally took dihydropyridine calcium-channel blockers, he did not regularly monitor his blood pressure. His medical history was unremarkable for kidney disease, thromboembolic events, or renal artery injury. On admission, his blood pressure was 160/80 mmHg, with a heart rate of 90 beats/min and a respiratory rate of 18 breaths/min. Urinalysis revealed slight hematuria, and transient elevations in serum creatinine and blood urea nitrogen were observed, which normalized within 2 days after fluid replacement. Coagulation studies, including prothrombin time, activated partial thromboplastin time, and D-dimer levels, were within normal ranges. However, plasma levels of epinephrine and norepinephrine were significantly elevated at 7829.60 pg/mL and 6121.70 pg/mL, respectively, far exceeding the reference intervals of 9.16–254.60 pg/mL and 86.30–551.60 pg/mL.
An abdominal computed tomography (CT) scan revealed an 8.5 cm tumor in the right adrenal gland and multiple wedge-shaped perfusion defects in both kidneys, consistent with renal infarctions. Echocardiography showed no evidence of arterial thrombus, and a 24-hour Holter study revealed no arrhythmias. Based on these findings, the patient was diagnosed with pheochromocytoma and multiple renal infarctions. To manage his blood pressure, oral phenoxybenzamine was administered. After two weeks of antihypertensive therapy, the patient underwent surgical resection of the tumor on April 29, 2014. Histopathological examination confirmed the diagnosis of pheochromocytoma. No specific treatment was administered for the renal infarctions.
During a 4-year follow-up period, the patient remained normotensive with normal serum creatinine levels, and no thromboembolic events occurred. A repeat abdominal CT scan performed on May 15, 2018, showed complete resolution of the wedge-shaped perfusion defects in the kidneys, indicating the reversibility of the renal infarctions following tumor removal.
Pheochromocytoma is known to cause multiple target organ injuries due to the effects of catecholamine excess. While renal involvement is uncommon, it can manifest as renal failure or polyuria secondary to severe hypertension. Renal infarction, however, is an extremely rare complication, with an incidence of only 0.007% among all emergency admissions. The etiology of renal infarction often includes cardioembolic diseases, renal artery lesions, and hypercoagulable states, but more than half of cases remain unclassified. Diagnosis typically relies on characteristic findings on CT scans, such as wedge-shaped perfusion defects. Despite aggressive treatments like thrombolysis, renal infarction is usually irreversible and can lead to recurrent thromboembolic events, renal impairment, and even death.
In this case, the patient had no history of cardioembolic diseases, renal artery injury, or hypercoagulable states, and coagulation studies were normal. The reversible nature of the renal infarctions following tumor resection suggests that catecholamine-mediated vasoconstriction was the primary mechanism. The removal of the pheochromocytoma eliminated the excessive production of catecholamines, leading to the restoration of normal renal blood flow and the resolution of the infarctions.
This case highlights an uncommon presentation of renal infarctions associated with pheochromocytoma. It underscores the importance of considering pheochromocytoma in patients with unexplained renal infarction and severe hypertension. Early diagnosis and timely surgical intervention can lead to complete remission and a favorable prognosis. Clinicians should be vigilant about the potential for renal injury in patients with pheochromocytoma and consider appropriate diagnostic and therapeutic measures.
The findings from this case also contribute to the limited literature on renal infarctions associated with pheochromocytoma. To date, only four adult cases have been reported, with atrial thrombosis, renal artery embolism, and vasospasm proposed as possible mechanisms. This case is unique in that it provides long-term follow-up data and demonstrates the reversibility of renal infarctions following tumor resection. It emphasizes the role of catecholamine-induced vasoconstriction in the pathogenesis of renal infarction in the context of pheochromocytoma.
In conclusion, this case report illustrates the reversible nature of renal infarctions associated with pheochromocytoma and highlights the importance of early diagnosis and treatment. For patients with unexplained renal infarction and severe hypertension, screening for pheochromocytoma should be considered. Timely tumor resection can lead to complete remission and a favorable outcome. Clinicians should be aware of the potential for renal injury in patients with pheochromocytoma and take appropriate measures to ensure optimal patient care.
doi.org/10.1097/CM9.0000000000000759
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