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.
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.