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.
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.