The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Tubular kidney injury molecule‐1 (KIM‐1) in human renal disease
Open accessAbstract
KIM‐1, a transmembrane tubular protein with unknown function, is undetectable in normal kidneys, but is markedly induced in experimental renal injury. The KIM‐1 ectodomain is cleaved, detectable in urine, and reflects renal damage. KIM‐1 expression in human renal biopsies and its correlation with urinary KIM‐1 (uKIM‐1) is unknown. In biopsies from various renal diseases ( n = 102) and controls ( n = 7), the fraction of KIM‐1 positive tubules and different renal damage parameters were scored. Double labelling was performed for KIM‐1 with macrophages (M Ø ), α‐smooth muscle actin (α‐SMA), proximal (aquaporin‐1) and distal (E‐cadherin) tubular markers and a dedifferentiation marker (vimentin). uKIM‐1 at the time of biopsy ( n = 53) was measured by ELISA. Renal KIM‐1 was significantly increased in all diseases versus controls ( p < 0.05), except minimal change. KIM‐1 was primarily expressed at the luminal side of dedifferentiated proximal tubules, in areas with fibrosis (α‐SMA) and inflammation (M Ø ). Independent of the disease, renal KIM‐1 correlated positively with renal damage, negatively with renal function, but not with proteinuria. uKIM‐1 was increased in renal patients versus controls ( p < 0.001), including minimal change, and correlated positively with tissue KIM‐1 and M Ø , negatively with renal function, but not with proteinuria. In conclusion, KIM‐1 is upregulated in renal disease and is associated with renal fibrosis and inflammation. uKIM‐1 is also associated with inflammation and renal function, and reflects tissue KIM‐1, indicating that it can be used as a non‐invasive biomarker in renal disease. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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Kidney Injury Molecule-1 (KIM-1): A novel biomarker for human renal proximal tubule injury
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Self-citationChronic kidney disease: the global challenge
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Kidney injury molecule-1: a tissue and urinary biomarker for nephrotoxicant-induced renal injury
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Mechanisms of progression and regression of renal lesions of chronic nephropathies and diabetes
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Pathophysiology of proteinuria
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TIM-4 is the ligand for TIM-1, and the TIM-1–TIM-4 interaction regulates T cell proliferation
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Diagnosis, Epidemiology and Outcomes of Acute Kidney Injury
Waikar, S. S., Liu, K. D., & Chertow, G. M. (2008) · Clinical Journal of the American Society of Nephrology · doi:10.2215/cjn.05191107 · Cited by 533
Biomarkers in acute kidney injury – pathophysiological basis and clinical performance
Schrezenmeier, E. V., Barasch, J., Budde, K., Westhoff, T., & Schmidt‐Ott, K. M. (2017) · Acta Physiologica · doi:10.1111/apha.12764 · Cited by 401
Tanase, D. M., Gosav, E. M., Radu, S., Costea, C. F., Ciocoiu, M., Carauleanu, A., Lacatusu, C. M., Maranduca, M. A., Floria, M., & Rezus, C. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20205238 · Cited by 191
Schreiber, S., Bueche, C. Z., Garz, C., & Braun, H. (2013) · Experimental & Translational Stroke Medicine · doi:10.1186/2040-7378-5-4 · Cited by 144
Metadata
- Authors
- van Timmeren, M., van den Heuvel, M., Bailly, V, Bakker, S., van Goor, H., & Stegeman, C.
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2007-05-11
- Volume
- 212
- Issue
- 2
- Pages
- 209-217
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- OpenAlex
- W2039499065
- Cited by
- 481
- References
- 23
- FWCI
- 12.13
- Type
- journal article
- Language
- en
- Open access
- bronze
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