ArticleScientific reports2016
Wnt4 is a novel biomarker for the early detection of kidney tubular injury after ischemia/reperfusion injury.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Local Surgicel/rhBMP-7 delivery is associated with renal repair responses after surgically induced acute kidney injury.Frontiers in medicine · 2026Article
- Pulsed ultrasound targeted to the spleen mitigates against kidney injury and promotes kidney repair.American journal of physiology. Renal physiology · 2025Article
- Comprehensive strategy for identifying extracellular vesicle surface proteins as biomarkers for chronic kidney disease.Frontiers in physiology · 2024Review
- Gray level co-occurrence matrix and wavelet analyses reveal discrete changes in proximal tubule cell nuclei after mild acute kidney injury.Scientific reports · 2023Article
- Roles and action mechanisms of WNT4 in cell differentiation and human diseases: a review.Cell death discovery · 2021Review
- Wnt4 is significantly upregulated during the early phases of cisplatin-induced acute kidney injury.Scientific reports · 2018Observational
- The hormetic functions of Wnt pathways in tubular injury.Pflugers Archiv : European journal of physiology · 2017Review
- Multiple Mechanisms are Involved in Salt-Sensitive Hypertension-Induced Renal Injury and Interstitial Fibrosis.Scientific reports · 2017Article
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Authors and funding
13 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Earlier intervention after acute kidney injury would promote better outcomes. Our previous study found that Wnt proteins are promptly upregulated after ischemic kidney injury. Thus, we assessed whether Wnt4 could be an early and sensitive biomarker of tubular injury. We subjected mice to bilateral ischemia/reperfusion injury (IRI). Kidney and urinary Wnt4 expression showed an early increase at 3 hours and increased further at 24 hours post-IRI and was closely correlated with histopathological alterations. Serum creatinine slightly increased at 6 hours, indicating that it was less sensitive than Wnt4 expression. These data were further confirmed by clinical study. Both kidney and urinary Wnt4 expression were significantly increased in patients diagnosed with biopsy-proven minimal change disease (MCD) with tubular injury, all of whom nevertheless had normal estimated glomerular filtration rate (eGFR) and serum creatinine. The increased Wnt4 expression also strongly correlated with histopathological alterations in these MCD patients. In conclusion, this is the first demonstration that increases in both kidney and urinary Wnt4 expression can be detected more sensitively and earlier than serum creatinine after kidney injury. In particular, urinary Wnt4 could be a potential noninvasive biomarker for the early detection of tubular injury.
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