ArticleJournal of nephrology2024
Outcomes of acute kidney injury continuum in children.
Article in Journal of nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- TIMP-2 and IGFBP7 for the differentiation of functional and intrinsic pediatric acute kidney injury.Pediatric research · 2026Article
- Kidney health in VACTERL association: structural vulnerability and surveillance.Childhood kidney diseases · 2026Article
- Pediatric Chronic Kidney Disease During Pandemic Conditions-A Single-Center Experience.Journal of clinical medicine · 2025Article
- The relevance of acute kidney injury in dehydrated children.Frontiers in pediatrics · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute kidney injury (AKI) is associated with high morbidity and mortality. The continuum of kidney damage after an AKI episode is poorly explored in the paediatric population.
methodsWe performed a retrospective cohort study on 2346 children with AKI from a tertiary care hospital in Romania over a 9-year period. The main objective was to evaluate the impact of AKI duration on mortality and the risk of new-onset chronic kidney disease (CKD).
resultsOut of 2346 AKI patients, transient AKI was present in 655 patients (27.9%), persistent AKI in 1009 children (43%) and acute kidney disease in 682 patients (29.1%). In contrast to transient AKI, children who developed acute kidney disease were younger, with a higher degree of anaemia, lower number of platelets, higher procalcitonin, higher LDH, higher GGT, higher urea and higher serum creatinine levels. The pre-renal cause of AKI was the leading cause regardless of AKI duration. As kidney injury progressed over time, there was an increasing incidence of the intrinsic causes of AKI (11.1% in transient AKI, 13.2% in persistent AKI and 22.6% in acute kidney disease). Acute kidney disease patients had the highest mortality rate (16.42%), followed by transient AKI (14.66%) and persistent AKI (9.81%). Overall mortality increased in the presence of renal microvascular alterations, acute tubular necrosis, lower haemoglobin, serum proteins and platelets, and higher procalcitonin levels.
conclusionsThe continuum of AKI expressed as acute kidney disease resulted in an increased risk of new-onset CKD. CKD was influenced by the intrinsic cause of AKI and not by AKI severity.
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