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 13-year-old Indonesian boy who experienced successful living-related renal transplantation (LRRT) in 2017 (his 50-year-old father was his kidney donor) has been living with normal graft function. He underwent hemodialysis (HD) in 2014 after being diagnosed with end-stage renal disease (ESRD) secondary to bilateral renal hypoplasia. He was prepared for LRRT in March 2015; however, two months prior to the procedure he was infected with the hepatitis A virus (HAV). The HAV infection subsequently resolved, and LRRT preparations proceeded. Unfortunately, seven days prior to the scheduled LRRT procedure, there was a sudden significant rise in alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, resulting in cancellation of the procedure. The rise in ALT and AST levels was later revealed to be caused by HCV seroconversion (). The patient was always hemodialyzed with a single-use dialyzer, and there was no history of blood transfusions or family history of viral hepatitis; however, there was an HCV outbreak in our pediatric dialysis unit in 2015.\nIn April 2015, his liver function markers rose (AST 498 U/L, ALT 816 U/L, Gamma-Glutamyltransferase (GGT) 170 U/L) and he was subsequently diagnosed with HCV infection (viral load 3.75 × 105 IU/mL, 5.57 log IU/mL of serum HCV RNA) (). HCV RNA genotype testing was conducted using hybridization probe (The Versant HCV Genotype 2.0 Assay (LiPA), Siemens), which revealed HCV genotype 1a. A 7.3-kPa liver stiffness was observed with transient elastography (fibroscan), which was categorized as F1-F2 (mild–moderate liver fibrosis) ().\nHe received interferon-based therapy with ribavirin post-HD once a week since September 2015. Six months after treatment initiation, the HCV was undetected and his liver function normalized. However, 10 months after treatment initiation, he had HCV virological breakthrough, suggested by HCV RNA of 1.28 × 104 IU/mL (4.11 Log IU/mL), leading to cessation of interferon therapy.\nPlans for LRRT were continued and HCV treatment was set up to be given a year post LRRT when stable renal graft function was achieved. In September 2017, LRRT was conducted. One year post-LRRT, graft function was normal; thus, treatment with DAAs for chronic HCV infection was commenced. Owing to a lack of evidence regarding treatment safety with DAAs in pediatrics, we arranged a thorough discussion with the Hospital Ethics Committee to obtain parental consent. In December 2018, he began receiving sofosbuvir/daclatasvir for 12 weeks. Evaluation immediately after (March 2019), at 12 weeks (June 2019), and at 24 weeks (October 2019) following treatment cessation showed no HCV recurrence (). Adverse effects, such as mild fever, fatigue, musculoskeletal pain, decreased appetite, itching and nasal congestion, were not found during treatment with DAAs.