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.
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.