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.
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.