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. ).
An 80-year-old gentleman on treatment with PD was admitted with increasing dyspnea and progressive reduction in ultrafiltration volumes over the previous week. His end-stage kidney disease was secondary to hypertension; he had also previously had a left nephrectomy for cancer. His comorbidities included systemic hypertension, stroke, glaucoma, prostatic hypertrophy, and osteoarthritis. He had started PD 3 months prior to admission. During the previous 2 weeks, he had switched from CAPD with daytime exchanges to nocturnal cycler-assisted automated peritoneal dialysis (APD).\nOn initial assessment, he was tachypneic and hypoxic. The jugular venous pressure was elevated; there was also peripheral edema. On auscultation, he had reduced breath sounds over the right lower hemithorax, with dullness on percussion. His electrocardiogram (ECG) and initial blood tests were unremarkable. The chest X-ray showed a large right pleural effusion ().\nTherapeutic thoracentesis was performed. 3 litres of fluid were drained; his clinical status improved markedly. A repeat chest X-ray showed complete resolution of pleural effusion ().\nBiochemical analysis of pleural fluid showed high concentrations of sugar and creatinine, and negligible protein, consistent with peritoneal dialysate fluid ().\nTreatment was changed temporarily to hemodialysis via a tunneled central venous catheter. He underwent video-assisted thoracoscopic surgery and talc pleurodesis, which he tolerated well. At the time of the procedure, most pleural fluids had been drained. There was no fresh drainage of fluid into the pleural space. Some pleural thickening was described.\n4 weeks later, PD was recommenced, in CAPD mode, with small fill volumes and avoidance of nightly dwells. He subsequently tolerated CAPD without complications and was recommenced on APD. Hemodialysis was successfully discontinued.