A 33-year-old Caucasian woman with end-stage renal failure secondary to systemic lupus erythematosus started PD in December 2008. She had previously been treated with PD without complication 17 years before, in the context of acute kidney injury, from which she recovered. Exact details of PD were unavailable, but it was recalled to be of short duration and probably of small fill volume. The patient denied any history of traumatic injury to the chest or diaphragmatic surgery.\nA Tenckhoff catheter was inserted 28 days before commencement of PD without complication. Her first exchange revealed asymptomatic slightly cloudy dialysate with 210 white cells [82% polymorphonuclear cells] and negative growth and was treated as culture-negative PD peritonitis.\nOne week later, she presented with sudden onset of dyspnea associated with right pleuritic chest pain. Chest X-ray (Figure ) showed right pleural effusion.\nThoracentesis was performed for symptomatic relief. Pleural fluid biochemistry results were consistent with transudate, according to Light's criteria (Table ). Culture of pleural aspirate showed no evidence of infection. Clinically, no evidence of lupus flare or nephrotic syndrome was noted.\nPleural fluid biochemistry results were consistent with PD-related hydrothorax. An effusion reaccumulated with further PD treatment. It was unclear whether poor dialysis (uremia) or ultrafiltration was contributing to the effusion. Tc-99 m DTPA scintigraphy was performed to confirm pleuroperitoneal leakage, showing prompt (within 15 minutes) appearance of tracer in the pleural space on the right side with no evidence of tracer entering the left hemithorax (Figure ). Thus, the etiology of hydrothorax likely was due to congenital diaphragmatic defects, exacerbated by persistently elevated intraabdominal pressure from PD.\nThe patient was temporarily transferred to hemodialysis via a tunneled line and underwent right video-assisted thoracoscopic surgery and talc pleurodesis. An intraoperative methylene blue test failed to identify the pleuroperitoneal defect. Two months after the procedure, she successfully recommenced PD without reoccurrence of hydrothorax.
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.