Urinary Plasminogen Activator Inhibitor-1: A Biomarker of Acute Tubular Injury
| العنوان: | Urinary Plasminogen Activator Inhibitor-1: A Biomarker of Acute Tubular Injury |
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| المؤلفون: | Alfredo G. Casanova, Adalberto Benito-Hernández, Víctor Blanco-Gozalo, Manuel Arias, Francisco J. López-Hernández, Maria Paniagua-Sancho, Yaremi Quiros, Consuelo Agüeros-Blanco, Sandra M. Sancho-Martínez, M.A. Ramos-Barron, C. Gómez-Alamillo |
| المصدر: | American Journal of Nephrology. 52:714-724 |
| بيانات النشر: | S. Karger AG, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Adult, Male, medicine.medical_specialty, Urinary system, Urology, Urine, urologic and male genital diseases, Excretion, chemistry.chemical_compound, Plasminogen Activator Inhibitor 1, Animals, Humans, Medicine, Rats, Wistar, Acute tubular necrosis, Aged, business.industry, Acute kidney injury, Acute Kidney Injury, Middle Aged, medicine.disease, Rats, Kidney Tubules, chemistry, Nephrology, Plasminogen activator inhibitor-1, Biomarker (medicine), Female, business, Plasminogen activator, Biomarkers |
| الوصف: | Introduction: Acute kidney injury (AKI) is a threatening, multiaetiological syndrome encompassing a variety of forms and damage patterns. AKI lacks sufficiently specific diagnostic tools to evaluate the distinct combination of pathophysiological events underlying each case, which limits personalized and optimized handling. Therefore, a pathophysiological diagnosis based on new urinary biomarkers is sought for practical (readiness and noninvasiveness) and conceptual reasons, as the urine is a direct product of the kidneys. However, biomarkers found in the urine may also have extrarenal origin, thus conveying pathophysiological information from other organs or tissues. Urinary plasminogen activator inhibitor-1 (PAI-1) has been associated to AKI, although its origin and traffic to the urine are not known. Methods: Herein, we studied the blood or renal origin of urinary PAI-1 (uPAI-1) in experimental AKI in Wistar rats, by means of the in situ renal perfusion method. For this purpose, urine was collected while the kidneys of rats with AKI showing increased uPAI-1 excretion, and controls, were in situ perfused with a saline solution. Results: Our results show that during perfusion, PAI-1 remained in the urine of AKI rats, suggesting that renal cells shed this protein directly to the urine. PAI-1 is also significantly increased in the urine of AKI patients. Its low correlation with other urinary markers such as NGAL or NAG suggests that PAI-1 provides complementary and distinct phenotypical information. Conclusion: In conclusion, uPAI-1 is a biomarker produced by damaged kidneys following AKI, whose precise pathophysiological meaning in AKI needs to be further investigated. |
| تدمد: | 1421-9670 0250-8095 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2e9fb609f820e86dbe46947f81fc78b5Test https://doi.org/10.1159/000518455Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....2e9fb609f820e86dbe46947f81fc78b5 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14219670 02508095 |
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