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In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury

Hosohata, Keiko ; Jin, Denan ; Takai, Shinji

International journal of molecular sciences, 2021-10, Vol.22 (21), p.11448 [Periódico revisado por pares]

Switzerland: MDPI AG

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Título:
In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
Autor: Hosohata, Keiko ; Jin, Denan ; Takai, Shinji
Assuntos: Acute Kidney Injury - metabolism ; Acute Kidney Injury - physiopathology ; Acute Kidney Injury - urine ; Amidohydrolases - metabolism ; Amidohydrolases - urine ; Animals ; Biomarkers ; Biomarkers - urine ; Creatinine ; Creatinine - analysis ; Creatinine - blood ; Early Diagnosis ; Glucosaminidase ; Hexosaminidases - metabolism ; Hexosaminidases - urine ; Hypoxia ; Immunofluorescence ; Ischemia ; Ischemia - metabolism ; ischemia-reperfusion ; Kidney - metabolism ; Kidneys ; Male ; Oxidative stress ; Oxidative Stress - physiology ; Protein expression ; Proteins ; Proximal tubules ; Rats ; Rats, Sprague-Dawley ; Renal artery ; renal tubular damage ; Reperfusion ; Reperfusion Injury - metabolism ; Reperfusion Injury - physiopathology ; Reperfusion Injury - urine ; Rodents ; sensitive biomarker ; Sepsis ; Urinary Tract - metabolism ; Urine
É parte de: International journal of molecular sciences, 2021-10, Vol.22 (21), p.11448
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
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Descrição: Oxidative stress plays an important role in the pathophysiology of acute kidney injury (AKI). Previously, we reported that vanin-1, which is involved in oxidative stress, is associated with renal tubular injury. This study was aimed to determine whether urinary vanin-1 is a biomarker for the early diagnosis of AKI in two experimental models: in vivo and in vitro. In a rat model of AKI, ischemic AKI was induced in uninephrectomized rats by clamping the left renal artery for 45 min and then reperfusing the kidney. On Day 1 after renal ischemia/reperfusion (I/R), serum creatinine (SCr) in I/R rats was higher than in sham-operated rats, but this did not reach significance. Urinary N-acetyl-β-D-glucosaminidase (NAG) exhibited a significant increase but decreased on Day 2 in I/R rats. In contrast, urinary vanin-1 significantly increased on Day 1 and remained at a significant high level on Day 2 in I/R rats. Renal vanin-1 protein decreased on Days 1 and 3. In line with these findings, immunofluorescence staining demonstrated that vanin-1 was attenuated in the renal proximal tubules of I/R rats. Our in vitro results confirmed that the supernatant from HK-2 cells under hypoxia/reoxygenation included significantly higher levels of vanin-1 as well as KIM-1 and NGAL. In conclusion, our results suggest that urinary vanin-1 might be a potential novel biomarker of AKI induced by I/R.
Editor: Switzerland: MDPI AG
Idioma: Inglês

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In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury

Hosohata, Keiko ; Jin, Denan ; Takai, Shinji

Switzerland: MDPI AG

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