Abstract
Chrysin or mannitol for treatment of acute kidney injury: Evidence for pharmacokinetic interaction
Highlights
Acute kidney injury (AKI) is a major problematic clinical situation worldwide especially in hospitalized patients as it confers to high mortality rate up to 17% in ICU cases (Santos and Monteiro, 2015)
The renoprotective effect of chrysin was comparable to mannitol; the combination of both drugs resulted in weak protection against renal injury and showed a decrease in PK parameters Cmax and area under the plasma concentrationtime curve as compared to chrysin alone
Oral pretreatment with chrysin (50 mg/kg) for 21 consecutive days resulted in a significant reduction of serum lactate dehydrogenase (LDH) and creatinine levels to be 60.08% and 74.36% as compared to renal I/R rats, respectively
Summary
Acute kidney injury (AKI) is a major problematic clinical situation worldwide especially in hospitalized patients as it confers to high mortality rate up to 17% in ICU cases (Santos and Monteiro, 2015). Ischemic injury has been reported to contribute to about 80%–90% of the etiology of AKI and accounts for more than 50% of mortality cases as a result of ischemia-reperfusion (I/R) (Bonventre and Yang, 2011). Duration of ischemia affects the severity of I/R injury, and further, during the reperfusion phase, additional damage is caused due to reinstitution of essential blood flow to the ischemic tissue (Kennedy and Erlich, 2008). Cellular mechanisms including the high generation rate of reactive oxygen species (ROS), endothelial cell injury, and apoptosis are implicated in the pathogenesis of early phases of renal I/R injury (Bonventre and Weinberg, 2003). There is accumulating evidence that I/R injury results in an inflammatory disease, as manifested by the infiltration of leucocytes, upregulation of chemotactic factors by endothelial cells, and generation of proinflammatory mediators by renal tubular epithelial cells (Ysebaert et al, 2004)
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