A 35-year-old Philipino female presented to our unit with advanced chronic kidney disease, secondary to medullary cystic kidney disease, which was diagnosed many years earlier in the Philipines. She had no significant heart disease. One year later, she was approaching end-stage kidney disease and a Tenckhoff catheter was inserted. Training for PD began four weeks later, using standard dextrose-based solutions.\nShe presented after four days of PD training with dyspnoea. She was otherwise well and was afebrile. Blood tests and ECG were unchanged. She had clinical evidence of a large, rightsided pleural effusion. This was confirmed on a chest radiograph (). A diagnostic aspirate was performed and yielded serous fluid. The pleural fluid biochemistry was consistent with a transudative process (). The high-pleural-fluid-serum-glucose ratio confirmed the clinical suspicion of a pleuroperitoneal leak.\nThe pleural effusion resolved over a number of days with conservative management and the maintenance of a dry peritoneal cavity. A follow-up chest radiograph was normal (). In accordance with patient preference, PD was discontinued. Haemodialysis (HD) access was established and HD is ongoing one year later.
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.