A 33-year-old Caucasian woman with end-stage renal failure secondary to systemic lupus erythematosus started PD in December 2008. She had previously been treated with PD without complication 17 years before, in the context of acute kidney injury, from which she recovered. Exact details of PD were unavailable, but it was recalled to be of short duration and probably of small fill volume. The patient denied any history of traumatic injury to the chest or diaphragmatic surgery.\nA Tenckhoff catheter was inserted 28 days before commencement of PD without complication. Her first exchange revealed asymptomatic slightly cloudy dialysate with 210 white cells [82% polymorphonuclear cells] and negative growth and was treated as culture-negative PD peritonitis.\nOne week later, she presented with sudden onset of dyspnea associated with right pleuritic chest pain. Chest X-ray (Figure ) showed right pleural effusion.\nThoracentesis was performed for symptomatic relief. Pleural fluid biochemistry results were consistent with transudate, according to Light's criteria (Table ). Culture of pleural aspirate showed no evidence of infection. Clinically, no evidence of lupus flare or nephrotic syndrome was noted.\nPleural fluid biochemistry results were consistent with PD-related hydrothorax. An effusion reaccumulated with further PD treatment. It was unclear whether poor dialysis (uremia) or ultrafiltration was contributing to the effusion. Tc-99 m DTPA scintigraphy was performed to confirm pleuroperitoneal leakage, showing prompt (within 15 minutes) appearance of tracer in the pleural space on the right side with no evidence of tracer entering the left hemithorax (Figure ). Thus, the etiology of hydrothorax likely was due to congenital diaphragmatic defects, exacerbated by persistently elevated intraabdominal pressure from PD.\nThe patient was temporarily transferred to hemodialysis via a tunneled line and underwent right video-assisted thoracoscopic surgery and talc pleurodesis. An intraoperative methylene blue test failed to identify the pleuroperitoneal defect. Two months after the procedure, she successfully recommenced PD without reoccurrence of hydrothorax.
A 16-year-old Indonesian boy with uncontrolled hypertension was referred from a remote area in an island to the pediatric nephrology clinic at Cipto Mangunkusumo Hospital, Jakarta, Indonesia. Twenty months prior to admission to our clinic, he experienced palpitation, diaphoresis, and left-sided chest pain without radiation, because of which he was brought to the emergency room. He experienced neither shortness of breath nor blurry vision. His blood pressure was 200/120 mmHg. The internist initiated the administration of 20 mg furosemide per oral (PO) and 12.5 mg captopril PO twice daily, together with 10 mg nifedipine PO 4 times daily. However, the patient’s symptoms and hypertension persisted, due to which his parents turned to herbal treatment and skipped further medical follow-up, although oral medications were continued.\nAs the boy’s palpitations persisted for 14 months, he was taken to another internist who prescribed 30 mg nebivolol PO every morning and 80 mg telmisartan PO every evening. Echocardiography revealed normal cardiac function. Kidney Doppler ultrasound disclosed a suspicion of right adrenal mass and kidney artery stenosis, therefore, he was referred to the pediatric nephrology clinic at our center.\nAt the clinic, he complained of palpitations with diaphoresis. We also discovered that he had lost a weight of 10 kg in the past 4 months. His BMI was 16.5 kg/m2 (undernourished with normal stature), and no skin lesions were noted (). He was hypertensive (blood pressure [BP] 140/83 mmHg) and tachycardic (heart rate (HR) 107 times/minute), with similar BP and HR values in all limbs. Other physical examinations, including neurological examinations and funduscopy, revealed normal findings. Complete blood count, random glucose levels, hepatic enzyme levels, kidney functions, urinalysis, chest X-ray, and electrocardiography were unremarkable. Pheochromocytoma was suspected due to symptoms of catecholamine secretion. However, as the urine catecholamine test was unavailable in Indonesia, the urine sample was sent to a laboratory outside the country. Simultaneously, the patient underwent abdominal magnetic resonance imaging (MRI) ( and ) and 131I-meta-iodobenzylguanidine (MIBG) scintigraphy ( and ) were ordered. 131I-MIBG scintigraphy demonstrated the uptake of pathological tracer in the right suprarenal region corresponding to an adrenal tumor without metastatic lesions. The results of urine catecholamine test, which were received subsequently, confirmed our suspicion of pheochromocytoma (), after which the administration of terazosin was initiated.\nThe boy had always been healthy with no recorded history of high BP, chest pain, or palpitations. He was the first of 3 children in his family. His father had hypertension with obesity. Hereditary diseases were not acknowledged in the family. Since the past 2 years, he had stayed at a boarding school in a remote area. He denied smoking, alcohol use, and the intake of regular medications.\nOne week prior to the surgery, bisoprolol was added to his treatment regimen. Surgery was performed using the posterior retroperitoneoscopic right adrenalectomy approach for removing the tumor ( and ). Administration of 1 mg terazosin PO was maintained until 1 week after the surgery. As his hypertension gradually resolved, terazosin was then discontinued. The results of pathological examination suggesting pheochromocytoma are presented in to . A follow-up examination conducted 6 months after the surgery showed normal and stable BP without the use of any antihypertensive medications, and no other persistent signs associated with pheochromocytoma were noted.