ArticleScientific reports2021
Biomarkers of persistent renal vulnerability after acute kidney injury recovery.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Resolution of drug-induced acute kidney injury: mechanistic assessment to guide patient care.Intensive care medicine · 2026Article
- Serial Combination of Toxic and Ischemic Renal Damages Causes Subsequent Chronic, Irreversible, and Progressive Renal Disease in Rats.International journal of molecular sciences · 2025Article
- Urinary proteomics reveals biological processes related to acute kidney injury in Bothrops atrox envenomings.PLoS neglected tropical diseases · 2024Article
- Identification of Pre-Renal and Intrinsic Acute Kidney Injury by Anamnestic and Biochemical Criteria: Distinct Association with Urinary Injury Biomarkers.International journal of molecular sciences · 2023Article
- Cellular and Functional Biomarkers of Renal Injury and Disease.Current opinion in toxicology · 2022Article
- Diagnosis of Cardiac Surgery-Associated Acute Kidney Injury: State of the Art and Perspectives.Journal of clinical medicine · 2022Review
- Update on prognosis driven classification of pediatric AKI.Frontiers in pediatrics · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a risk factor for new AKI episodes, chronic kidney disease, cardiovascular events and death, as renal repair may be deficient and maladaptive, and activate proinflammatory and profibrotic signals. AKI and AKI recovery definitions are based on changes in plasma creatinine, a parameter mostly associated to glomerular filtration, but largely uncoupled from renal tissue damage. The evolution of structural and functional repair has been incompletely described. We thus aimed at identifying subclinical sequelae persisting after recovery from cisplatin-induced AKI in rats. Compared to controls, after plasma creatinine recovery, post-AKI kidneys showed histological alterations and attendant susceptibility to new AKI episodes. Tubular function (assessed by the furosemide stress test, FST) also remained affected. Lingering parenchymal and functional subclinical alterations were paralleled by tapering, but abnormally high levels of urinary albumin, transferrin, insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinases-2 (TIMP-2) and, especially, the [TIMP-2]*[IGFBP7] product. As subclinical surrogates of incomplete renal recovery, the FST and the urinary [TIMP-2]*[IGFBP7] product provide two potential diagnostic tools to monitor the sequelae and kidney vulnerability after the apparent recovery from AKI.
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Registered trials
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