Effect of captopril treatment on recuperation from ischemia/reperfusion-induced acute renal injury

Abstract

At the acute stage of renal ischemia/reperfusion-induced AKI, ACE inhibition substantially contributed to the amelioration of acute injury by improving renal function, inhibiting systemic and intrarenal angiotensin-II, attenuating intrarenal inflammation and preserving renal tissue structure. Later on, at the post-reperfusion stage, most of the beneficial effects of captopril administration on the recuperating post-ischemic kidney were no longer evident. Concurrently, ACE inhibition exacerbated intrarenal hypoxia and accelerated oxidative stress, indicating that renal adaptation to some consequences of ischemia does require bioavailability of RAS components.

Biomarkers of AKI

“…An unexplored area is the potential therapeutic benefit of shunting the RAS pathway from activation of angiotensin II receptor type 1 by angiotensin II to activation of the Mas receptor by angiotensin 1-7. Pretreatment with angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aliskiren has been shown to mitigate renal ischemia-reperfusion injury in experimental models, primarily by reduction in postreperfusion inflammation (66)(67)(68). Additionally, one study reported a reduction in the severity of AKI at 48 hours postreperfusion when captopril was continuously administered through an intraperitoneal osmotic micropump implanted immediately after renal ischemia-reperfusion injury.…”

Adenovirus-Mediated Over-Expression of Nrf2 Within Mesenchymal Stem Cells (MSCs) Protected Rats Against Acute Kidney Injury

“…[6][7][8] The pathogenesis of AKI is complex, however, it has been shown that ischemia/reperfusion triggers AKI, mainly via aggravating stresses, inflammation and activation of renin-angiotensin system (RAS). 9 Hypoxia, serum deprivation and oxidative stress are important factors in the pathogenesis of AKI. [10][11][12] As mentioned before, MSC transplantation could treat AKI; however, the most important problem with the application of MSCs for the treatment is their low survival rate in such a stressful microenvironment.…”

Protective effect of theophylline on renal functions in experimental pneumoperitoneum model

“…34 In another study, cystatin-C levels were found higher in rats where ischemia was formed experimentally compared to the control group and the group receiving treatment. 35 In our study, cystatin-C values were determined to be significantly lower in pneumoperitoneum + theophylline group. These our results show similarity to the studies performed previously in the literature.…”