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 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.