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Urinary kidney injury molecule-1 in renal disease
Kidney injury molecule-1 (KIM-1), a type l transmembrane glycoprotein, is recognized as a potential biomarker for detection of tubular injury in the main renal diseases. Urinary KIM-1 increases rapidly upon the tubular injury, and its levels are associated with the degree of tubular injury, intersti...
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Published in: | Clinica chimica acta 2018-12, Vol.487, p.15-21 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Kidney injury molecule-1 (KIM-1), a type l transmembrane glycoprotein, is recognized as a potential biomarker for detection of tubular injury in the main renal diseases. Urinary KIM-1 increases rapidly upon the tubular injury, and its levels are associated with the degree of tubular injury, interstitial fibrosis, and inflammation in the injured kidney. Currently, the investigation of kidney diseases is usually performed through the assessment of serum creatinine and urinary albumin. However, these biomarkers are limited for the early detection of changes in renal function. Besides, the tubular injury appears to precede glomerular damage in the pathophysiology of renal diseases. For these reasons, the search for sensitive, specific and non-invasive biomarkers is of interest. Therefore, the purpose of this article is to review the physiological mechanisms of KIM-1, as well to present clinical evidence about the association between elevated urinary KIM-1 levels and the main renal diseases such as chronic kidney disease, diabetic kidney disease, acute kidney injury, and IgA nephropathy.
•The KIM-1 expression is increased in tubular proximal tubule cells after injury.•Urinary KIM-1 is increased in renal diseases such as CKD, AKI, and IgA nephropathy.•Changes in urinary KIM-1 are observed before changes in serum creatinine.•Urinary KIM-1 presents value for the diagnosis and prognosis of the main renal diseases. |
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ISSN: | 0009-8981 1873-3492 |
DOI: | 10.1016/j.cca.2018.09.011 |