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 twenty-four-year-old Irish male with a background history of congenital deafness, intellectual impairment and repair of a posterior urethral valve initially presented to the paediatric nephrology services with nephrotic syndrome. A renal biopsy revealed secondary focal segmental glomerulosclerosis and significant tubuleinterstitial fibrosis. Following introduction of Renin-Angiotensin-Aldosterone system blockade, his proteinuria was controlled.\nDespite this, his chronic kidney disease progressed. Ten years later, he was approaching end-stage kidney disease. A Tenckhoff catheter was inserted without complication. Six weeks later, PD training was initiated. A bicarbonate/lactate buffered solution was used to avoid infusion pain, which he would be unable to verbalise. The following months were complicated by dialysis-associated pericarditis that resolved with intensive haemodialysis for a number of weeks. His baseline PD prescription consisted of seven cycles of two litre exchanges with 1.36% dextrose solution. He was also prescribed an icodextrin-based daytime dwell.\nFive months later, he was admitted with clinical and radiological evidence of a large, rightsided pleural effusion with pleural thickening. The exact duration of the effusion was unclear as he was unable to verbalise symptoms. It was thought to have developed over weeks given the apparent absence of symptoms and the degree of pleural thickening. A chest radiograph four months earlier showed normal lung fields.\nHe was afebrile and systemically well. His serum biochemistry and haematology were unchanged and his inflammatory markers were not raised. ECG and echo were normal. A diagnostic pleural aspirate was performed under ultrasound guidance. This yielded serous fluid and also identified numerous loculations within the collection.\nThe pleural fluid biochemistry was atypical for that seen with pleuroperitoneal leak (). However, as the patient was so well clinically, and numerous pleural fluid cultures were sterile, it was felt that the effusion was not related to infection. It was also felt that the effusion was not due to volume overload given the degree of loculation within the effusion and the absence of other clinical signs of volume overload. The low pleural fluid glucose and high lactate dehydrogenase (LDH) were difficult to interpret as the sampled fluid was walled off within a loculation, probably for many weeks. A clinical diagnosis of pleuroperitoneal leak was made and PD was discontinued.\nThe effusion did not resolve with drainage of the peritoneal cavity, and a chest drain was inserted. This drained minimal serous fluid due to the highly loculated nature of the effusion. A second drain was inserted and intrapleural alteplase administered. This drain became dislodged and was replaced by a third drain with further intrapleural alteplase administration. At this point, however, a chest radiograph confirmed persistence of the large, loculated effusion with a small pneumothorax and a thick pleural rind.\nVideo-assisted thorascopic surgery with decortication was performed. A rapid postoperative recovery ensued and the postoperative chest drains were removed without event. A chest radiograph six weeks later showed a well-expanded right lung, without effusion or pleural abnormality. HD is ongoing without complication.