Search

Background: Chronic kidney disease (CKD) impacts long‐term morbidity in pediatric liver transplant (LT) recipients. The prevalence of estimated glomerular filtration rate (eGFR) < 90 mL/min/1.73 m2 (eGFR < 90) at our institution was 25% at 1 year post‐LT; thus, quality improvement (QI) project was initiated, aiming to decrease the prevalence of eGFR < 90 by at least 20% at 1 year‐post LT. Methods: Children post‐LT under 19 years from 2010 to 2018 were included. Three QI interventions were implemented starting 1/2016: documentation of blood pressure percentile (BP%) and eGFR, documentation of a kidney management plan if either was abnormal, and amlodipine initiation prior to hospital discharge after LT. We compared the prevalence of eGFR < 90 at 3, 12, and 24 months after LT in the pre‐ and post‐intervention period. Results: 68 patients in pre‐ and 42 in post‐intervention periods met inclusion criteria. Pre‐intervention BP%, eGFR, and kidney management plan were documented at 25%, 10%, and 22%, compared to 71%, 83%, and 71% post‐intervention, respectively. 22% of patients were started on amlodipine prior to discharge from LT in the pre‐ versus 74% in the post‐intervention period. Prevalence of eGFR < 90 at 3 m post‐LT was 19% in pre‐ versus 14% in the post‐intervention period (p =.31); at 12 months 24% versus 7% (p =.01) and at 24 months 16% versus 6% (p =.13), respectively. Significant non‐modifiable risk factors for eGFR < 90 were malignancy (RR = 4.5, p <.0001), metabolic disorder (RR = 2.6, p =.02), and age at transplant (7% increased risk per year of age, p =.007). Conclusion: By improving documentation of BP%, eGFR, and kidney management plan, the prevalence of eGFR < 90 was decreased by a relative 74% and 60% at 12 and 24 months post‐LT, respectively. [ABSTRACT FROM AUTHOR]

In areas of the world where human herpesvirus 8 (HHV‐8) is endemic, Kaposi sarcoma (KS) is a common SOT‐associated cancer. In the United States, where the virus is not prevalent, PTKS is rare, and there is little literature on pediatric PTKS. We present a North American female who underwent deceased donor, left lateral segment liver transplant for biliary atresia at age 11 months. The donor was a male with no known history of KS, originally from an HHV‐8‐endemic country. Three months after transplantation, the patient developed liver nodules and portal vein thrombosis. Analysis of needle biopsy established the diagnosis of KS and confirmed that the transformed cells were donor‐derived. HHV‐8 viremia was detected, and ganciclovir dosing (which had been started prophylactically) was increased. Immunosuppression was changed from tacrolimus to sirolimus. After further disease progression, 8 cycles of paclitaxel were administered. Under this treatment, her nodules regressed, HHV‐8 viremia resolved, and she had marked clinic improvement. Notably, the adult recipient of the right liver lobe from the same donor also developed PTKS. This is one of few pediatric PTKS cases described in the literature. It contributes to the mechanistic understanding of PTKS development, illustrating the risk posed by donors from HHV‐8‐endemic countries, as well as the potential for strong PTKS correlation between multiple recipients of organs from a single shared donor. [ABSTRACT FROM AUTHOR]