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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Acute kidney injury (AKI) is a common complication in paediatric pneumonia, particularly in cases caused by Streptococcus pneumoniae due to the additional risk of haemolytic uraemic syndrome. However, data on the progression of AKI in this population remain limited. This study aimed to determine the incidence of AKI in children with severe pneumococcal pneumonia requiring critical care, identify factors associated with its development, and evaluate the progression of renal injury.
We retrospectively reviewed children admitted to the paediatric intensive care unit (PICU) with severe community-acquired pneumonia due to Streptococcus pneumoniae between July 2013 and December 2024. The primary outcome was the development of AKI within the first 7 days, while acute kidney disease (AKD) was defined as persistent kidney dysfunction from day 7 to 90 days after AKI onset, both determined using the KDIGO serum creatinine criteria.
A total of 69 patients (32 boys, 46%) with a median age of 5.3 years were included. Twenty-five patients (36%) developed AKI in the first week: stage 1 (n=11, 16%), stage 2 (n=6, 9%), and stage 3 (n=8, 12%). Five patients with stage 3 AKI required CKRT. Severe AKI (stage 2-3) was associated with lower serum sodium, white cell and platelet counts, ad higher C-reactive protein on admission (Table 1). During the first week, patients with stage 3 AKI had lower haemoglobin nadir (5.3 vs. 8.6 g/dL, p = 0.024), lower platelet nadir (13 vs. 223 × 10⁹/L, p <0.001), and higher peak serum bilirubin (84 vs. 9 umol/L, p = 0.001), consistent with the biochemical features of haemolytic uraemic syndrome. ALT levels were not significantly different (p = 0.388).
Among patients with AKI (n = 25), 11 (44%) developed AKD. The majority of these patients (23/25, 92%) had recovered kidney function during admission, with longer recovery time observed in higher AKI stages (Figure 1). There was no mortality in this cohort. Patients with severe AKI (stage 2-3) had prolonged PICU stay (19.2 vs. 8.1 days, p = 0.003) and hospital stay (40.0 vs. 21.1 days, p = 0.001).
Among patients with stage 3 AKI, 6 (75%) developed AKD. Renal function normalised at a median of 7.2 days (IQR 5.3, 19.1) in 7 of 8 patients. After a median follow-up of 5.7 years (IQR 2.0, 8.4), two patients (25%) with stage 3 AKI developed chronic kidney disease (CKD) with proteinuria.
Approximately one-third of children with severe Streptococcus pneumoniae pneumonia developed AKI, and 20% of those required CKRT. High-grade AKI was associated with hyponatraemia and cytopenia. Nearly half of patients with AKI developed AKD, but most achieved renal recovery before discharge, with recovery time dependent on AKI stage. One-quarter of stage 3 AKI patients progressed to CKD during long-term follow-up.
