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.
A 14-year-old Indonesian girl who experienced successful live-unrelated renal transplantation from a 21-year-old donor in April 2017 has been living with normal graft function. In November 2014 she was diagnosed with ESRD secondary to nephrotic syndrome and started regular HD via single-use dialyzer. She had a history of repeated blood transfusions but no family history of viral hepatitis.\nShe was diagnosed with HCV infection with a high viral load (2.69 × 106 IU/mL, 6.43 log IU/mL of serum HCV RNA) and rising liver function markers (AST 180 U/L, ALT 133 IU/L, GGT 142 U/L) in September 2015 (). HCV RNA genotype testing was conducted using hybridization probe (The Versant HCV Genotype 2.0 Assay (LiPA), Siemens), revealing HCV genotype 1a. A 4.8-kPa liver stiffness was observed with transient elastography (fibroscan), which was categorized as F0-F1 (mild liver fibrosis) ().\nShe began receiving pegylated interferon and ribavirin in October 2015 prior to renal transplantation. Ten months later (August 2016), real-time PCR still showed the presence of HCV RNA (2.56 × 106 IU/mL, 5.41 Log IU/mL). In addition, she experienced thrombocytopenia—which is a side effect of interferon—resulting in termination of treatment.\nIn April 2017, she received kidney transplantation. At two months post-transplantation, she was diagnosed with post-transplant diabetes mellitus (PTDM), which manifested as a spontaneous inguinal abscess (10 × 3 × 0.5 cm), hyperglycemia (617 mg/dL), and ketonemia without acidosis. This PTDM is believed to be associated with her status as HCV-infected KTR, in addition to the side effect of tacrolimus–corticosteroid combination. PTDM resolved after tapering off methylprednisolone and seven months of insulin therapy.\nAt 20 months post-renal transplantation, graft function was normal; thus, treatment of HCV infection with DAAs was initiated. Since data about the treatment safety with DAAs in pediatrics are limited, we obtained parental consent after arranging meticulous discussion with the Hospital Ethics Committee. She started receiving sofosbuvir/daclatasvir in December 2018. HCV RNA with real-time PCR immediately after, at 12 weeks, and at 24 weeks after treatment initiation showed no HCV RNA (). There were no adverse effects during treatment with DAAs.