A 9-year-old Indonesian boy on CAPD was admitted to the emergency unit of our center due to dyspnea, swelling, and increased body weight. There was no fever, cough, or chest pain. Two years previously, he was diagnosed with end-stage renal disease (ESRD) secondary to bilateral renal hypoplasia; since then, he had been receiving CAPD comprising five cycles of 1-L exchanges with 1.5% dextrose-based solution for 22 months. Furthermore, he had no medical history of heart disease, peritonitis, hernia, thoracic and abdominal trauma, pneumonia, or thoracic and abdominal surgery, except for Tenckhoff catheter insertion. During the previous 3 days, his body weight had increased by 4 kg (12%), and he experienced ultrafiltration failure because although PD fluid at 1 L per cycle was being infused as usual, the effluent drainage was only approximately 0.6 L per cycle.\nPhysical examination revealed a respiratory rate of 34 breaths/min, heart rate of 120 beats/min, and blood pressure of 147/86 mm Hg. Oxygen saturation was 92% with nasal oxygen at 2 L/min. Auscultation of the lungs revealed diminished vesicular sounds in the right chest wall. Cardiac findings were normal. Arterial blood gas analysis results were as follows: pH: 7.467, pCO2: 4.51 kPa, pO2: 22.52 kPa, bicarbonate: 24.8 mmol/L, and base deficit: 2 mmol/L. His hemoglobin level was 131 g/L, albumin level was 34.6 g/L, BUN level was 7.08 mmol/L, and creatinine level was 840.33 µmol/L. Chest radiograph revealed right pleural effusion and bilateral pulmonary infiltrates (Fig. ). The chest tube drained 500 mL of transudative fluid. A comparison of serum, pleural fluid, and peritoneal fluid parameters has been presented in Table .\nAfter the excessive pleural fluid was completely removed, PD was continued via an installed chest tube (Fig. ). Intravenous cefotaxime was administered to treat pneumonia that occurred as an additional complication. Recurrent pleural effusion was subsequently found along with ultrafiltration failure. Pleural fluid culture did not show any microbial growth. Hydrothorax secondary to PPF was suspected, and PD was suspended from the 8th day of hospitalization. Hemodialysis (HD) was subsequently initiated.\nCT peritoneography was performed on the 9th day using 300 mg/mL of iohexol contrast agent immersed in PD fluid. Serial examinations at 30 and 180 min after administering the contrast agent showed excessive fluid in the right pleural cavity (Fig. ). PPF in the right posterolateral side was suspected.\nThe patient underwent VATS on the 20th day of hospitalization; however, no fistula was detected in the right chest cavity. Instead, adhesions between the parietal and visceral pleura with septated appearance were observed (Fig. ). Pleurodesis was performed using 20 mL of bleomycin for the right diaphragm. Following this, pleural effusion of the right lung resolved (Fig. ), and the patient underwent regular HD for 10 weeks. Subsequently, PD was gradually initiated until achieving 1 L of 1.5% dextrose-based dialysate solution with five daily exchanges. A 3-year follow-up showed normal PD without any recurrence of hydrothorax (Fig. ).
A 38-year-old Romanian female was admitted acutely with symptomatic uraemia. Her background was significant for minimal change disease, diagnosed in 2001 in Romania. She had received two courses of heavy immunosuppression for this and was then lost to follow up. She had no known heart disease. Her renal ultrasound showed small, shrunken kidneys, which confirmed the suspicion of advanced chronic kidney disease.\nAcute HD was initiated but, as the patient's preference was for PD, a Tenckhoff catheter was inserted. Five weeks later, PD training began. Her target PD prescription consisted of four cycles of two litre exchanges with standard dextrose-based standard solution. She was also prescribed one icodextrin-based dwell by day.\nAfter six days of PD training, she presented with dyspnoea that was exacerbated by infusing dialysate. She had no other systemic symptoms. She was seven kg above her dry weight and had clinical evidence of a rightsided pleural effusion and pedal oedema. Her electrocardiogram (ECG) and routine blood tests were unchanged. As she appeared volume overloaded, she had three litres of isolated ultrafiltration, using her central venous catheter. Her diuretic regime was maximized and she was discharged.\nDespite these interventions, she presented several days later with worsening dyspnoea. A chest radiograph confirmed a large rightsided pleural effusion. Again, she had 3 litres of isolated ultrafiltration. With this, she developed bad cramping. Therapeutic thoracocentesis was performed, with the removal of 1.2 litres of serous fluid. This led to marked clinical and radiological resolution of the pleural effusion.\nAlthough the initial presumed diagnosis was volume overload, the high pleural fluid glucose relative to the serum glucose confirmed the presence of a pleuroperitoneal leak (). In accordance with patient preference, PD was discontinued and the Tenckhoff catheter was removed. HD is ongoing without complication.