ArticleClinical and experimental nephrology2015
An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions.
Article in Clinical and experimental nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Combination of biomarkers for diagnosis of acute kidney injury after cardiopulmonary bypass.Renal failure · 2015Trial
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- Macula densa nitric oxide synthase 1β restoration by kidney alkalization enhances renal graft outcomes.American journal of physiology. Renal physiology · 2025Article
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- 5-Hydroxytryptamine 1F Receptor Agonist Lasmiditan Differentially Regulates Successful Repair and Failed Repair Genes in a Mouse Model of Acute Kidney Injury.ACS pharmacology & translational science · 2024Article
- The Value of Urinary NGAL, KIM-1, and IL-18 Measurements in the Early Detection of Kidney Injury in Oncologic Patients Treated with Cisplatin-Based Chemotherapy.International journal of molecular sciences · 2024Article
- Perturbations in podocyte transcriptome and biological pathways induced by FSGS associated circulating factors.Annals of translational medicine · 2023Article
- Snapshots of nascent RNA reveal cell- and stimulus-specific responses to acute kidney injury.JCI insight · 2022Article
- Innate Bacteriostatic Mechanisms Defend the Urinary Tract.Annual review of physiology · 2022Review
- A Mixture of Pure, Isolated Polyphenols Worsens the Insulin Resistance and Induces Kidney and Liver Fibrosis Markers in Diet-Induced Obese Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Reduced urinary excretion of neutrophil gelatinase-associated lipocalin as a risk factor for recurrence of febrile urinary tract infection in children.Pediatric nephrology (Berlin, Germany) · 2021Article
- Rule Out Acute Kidney Injury in the Emergency Department With a Urinary Dipstick.Kidney international reports · 2020Article
- Macrophage-Derived Iron-Bound Lipocalin-2 Correlates with Renal Recovery Markers Following Sepsis-Induced Kidney Damage.International journal of molecular sciences · 2020Article
- Genetically Modified Mesenchymal Stromal/Stem Cells: Application in Critical Illness.Stem cell reviews and reports · 2020Review
- Molecular nephrology: types of acute tubular injury.Nature reviews. Nephrology · 2019Review
- Differential gene expression analysis reveals novel genes and pathways in pediatric septic shock patients.Scientific reports · 2019Article
- Clinical efficacy of sublingual immunotherapy is associated with restoration of steady-state serum lipocalin 2 after SLIT: a pilot study.The World Allergy Organization journal · 2018Article
- Obesity-promoting and anti-thermogenic effects of neutrophil gelatinase-associated lipocalin in mice.Scientific reports · 2017Article
- A Dormant Microbial Component in the Development of Preeclampsia.Frontiers in medicine · 2016Review
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLipocalin 2 (LCN2 or neutrophil gelatinase-associated lipocalin) is a secretory protein discovered from neutrophils, which accumulates in the blood and urine during acute kidney injury (AKI) and in the blood by bacterial infection. Little is known about the tissue source and molecular forms of this protein under normal and pathophysiologic conditions.
methodsBy sandwich ELISA, serum and urinary LCN2 levels were measured in 36 patients with hematologic malignancies who transiently became neutropenic by stem cell transplantation (SCT). To evaluate contribution of neutrophil-derived LCN2 in the physiologic blood LCN2 concentrations, we examined CCAAT/enhancer-binding protein ε (C/EBPε) knockout mice, which lack mature neutrophils.
resultsIn patients without AKI and bacterial infection, at 1 week after SCT, the median blood neutrophil counts became zero and serum LCN2 levels were decreased by 76 ± 6 % (p < 0.01), but urinary LCN2 levels were not altered. During neutropenic conditions, bacterial infection caused only a modest rise of serum LCN2 but AKI produced a marked rise of serum and urinary LCN2 levels. Serum LCN2 concentrations in C/EBPε knockout mice were reduced by 66 ± 11 % compared to wild-type mice (p < 0.05). Blood LCN2 existed predominantly in high molecular weight forms (>100 kDa), while urinary LCN2 was mainly in low molecular weight forms.
conclusionOur findings suggest that neutrophils are the major source of circulating LCN2 in normal and infected conditions, whereas blood and urinary LCN2 mainly derive from the kidney during AKI, and that the molecular forms and regulation of blood and urinary LCN2 are clearly distinct.
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