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.
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.