A 9-year-old Indonesian boy on CAPD was admitted to the emergency unit of our center due to dyspnea, swelling, and increased body weight. There was no fever, cough, or chest pain. Two years previously, he was diagnosed with end-stage renal disease (ESRD) secondary to bilateral renal hypoplasia; since then, he had been receiving CAPD comprising five cycles of 1-L exchanges with 1.5% dextrose-based solution for 22 months. Furthermore, he had no medical history of heart disease, peritonitis, hernia, thoracic and abdominal trauma, pneumonia, or thoracic and abdominal surgery, except for Tenckhoff catheter insertion. During the previous 3 days, his body weight had increased by 4 kg (12%), and he experienced ultrafiltration failure because although PD fluid at 1 L per cycle was being infused as usual, the effluent drainage was only approximately 0.6 L per cycle.\nPhysical examination revealed a respiratory rate of 34 breaths/min, heart rate of 120 beats/min, and blood pressure of 147/86 mm Hg. Oxygen saturation was 92% with nasal oxygen at 2 L/min. Auscultation of the lungs revealed diminished vesicular sounds in the right chest wall. Cardiac findings were normal. Arterial blood gas analysis results were as follows: pH: 7.467, pCO2: 4.51 kPa, pO2: 22.52 kPa, bicarbonate: 24.8 mmol/L, and base deficit: 2 mmol/L. His hemoglobin level was 131 g/L, albumin level was 34.6 g/L, BUN level was 7.08 mmol/L, and creatinine level was 840.33 µmol/L. Chest radiograph revealed right pleural effusion and bilateral pulmonary infiltrates (Fig. ). The chest tube drained 500 mL of transudative fluid. A comparison of serum, pleural fluid, and peritoneal fluid parameters has been presented in Table .\nAfter the excessive pleural fluid was completely removed, PD was continued via an installed chest tube (Fig. ). Intravenous cefotaxime was administered to treat pneumonia that occurred as an additional complication. Recurrent pleural effusion was subsequently found along with ultrafiltration failure. Pleural fluid culture did not show any microbial growth. Hydrothorax secondary to PPF was suspected, and PD was suspended from the 8th day of hospitalization. Hemodialysis (HD) was subsequently initiated.\nCT peritoneography was performed on the 9th day using 300 mg/mL of iohexol contrast agent immersed in PD fluid. Serial examinations at 30 and 180 min after administering the contrast agent showed excessive fluid in the right pleural cavity (Fig. ). PPF in the right posterolateral side was suspected.\nThe patient underwent VATS on the 20th day of hospitalization; however, no fistula was detected in the right chest cavity. Instead, adhesions between the parietal and visceral pleura with septated appearance were observed (Fig. ). Pleurodesis was performed using 20 mL of bleomycin for the right diaphragm. Following this, pleural effusion of the right lung resolved (Fig. ), and the patient underwent regular HD for 10 weeks. Subsequently, PD was gradually initiated until achieving 1 L of 1.5% dextrose-based dialysate solution with five daily exchanges. A 3-year follow-up showed normal PD without any recurrence of hydrothorax (Fig. ).
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.