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How does colistin-induced nephropathy develop and can it be treated?
Gulsum Ozkan1, Sukru Ulusoy, Asim Orem
1Department of Nephrology, Karadeniz Technical University, School of Medicine, Trabzon, Turkey. gulsumozkan78@hotmail.com
Antimicrobial Agents and Chemotherapy
|May 1, 2013
Summary
Colistin antibiotic use causes kidney damage by increasing apoptosis and specific protein expressions. Grape seed proanthocyanidin extract (GSPE) offers a protective effect against this colistin-induced nephropathy.
Area of Science:
- Nephrology
- Pharmacology
- Molecular Biology
Background:
- Colistin is a vital antibiotic for multidrug-resistant Gram-negative infections.
- Colistin's nephrotoxicity previously led to its suspension, but its use has resumed.
- The mechanisms underlying colistin-induced kidney damage remain unclear, with no effective treatments available.
Purpose of the Study:
- To investigate the roles of caspase-mediated apoptosis, caspase 1, calpain 1, inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) in colistin nephrotoxicity.
- To evaluate the renoprotective potential of grape seed proanthocyanidin extract (GSPE) against colistin-induced kidney injury.
Main Methods:
- Induction of colistin-associated nephropathy in rats via intraperitoneal administration.
- Measurement of blood urea nitrogen (BUN) and creatinine levels.
- Histopathological examination and immunohistochemical staining for apoptosis markers (TUNEL), caspase 1 and 3, calpain 1, iNOS, and eNOS.
Main Results:
- Colistin administration significantly increased BUN, creatinine, histopathological damage, and expression of TUNEL, caspase 1 and 3, calpain 1, iNOS, and eNOS.
- Co-administration of GSPE significantly reduced BUN, creatinine, histopathological damage, and the expression of these markers compared to the colistin-only group.
Conclusions:
- Caspase-mediated apoptosis, iNOS, caspase 1, and calpain 1 are implicated in the pathogenesis of colistin-associated nephropathy.
- Grape seed proanthocyanidin extract (GSPE) demonstrates a significant renoprotective effect against colistin-induced kidney injury by modulating these pathways.
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