Renal ischaemia-reperfusion injury

Weight, S. C.; Bell, P. R. F.; Nicholson, Michael L.

doi:10.1046/j.1365-2168.1996.02182.x

Cited by 118 publications

(94 citation statements)

References 118 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, the kidney may behave somewhat differently in ischemia-reperfusion injury. While neutrophils are recognized to play a significant role in ischemia-reperfusion injury in many different extrarenal organs, their role in the kidney is still debated or even negated [4, 36, 37]. Not unexpectedly, monocytes/macrophages do not seem to play a crucial role in our model.…”

Section: Discussionmentioning

confidence: 70%

“…Subsequent organ reperfusion may further aggravate ischemic cell damage [2]. Reperfusion with oxygenated blood is accompanied by synthesis and release of reactive oxygen species (ROS) and other inflammatory mediators by leukocytes and parenchymal cells such as endothelium [2, 3, 4, 5]. Cytotoxic ROS play a key role in the pathogenesis of ischemia-reperfusion injury causing adverse effects like lipid peroxidation and mitochondrial damage [1, 2, 5].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Renal Matrix Metalloproteinase Activity Is Unaffected by Experimental Ischemia-Reperfusion Injury and Matrix Metalloproteinase Inhibition Does Not Alter Outcome of Renal Function

Ziswiler¹,

Daniel²,

Franz³

et al. 2001

Nephron Exp Nephrol

View full text Add to dashboard Cite

Background: Ischemia-reperfusion injury can lead to organ damage, such as delayed graft function in kidney transplantation. Reactive oxygen species that play a key role in this disorder may directly activate latent matrix metalloproteinases (MMP). In the kidney, little is known about the role of MMP in ischemia-reperfusion. Therefore, the aim of our study was to analyze activity/expression of MMP and to assess their functional role by the use of the MMP inhibitor BB-94 (Batimastat). Methods: Renal ischemia was induced by left renal pedicle occlusion for 60 min, preceded by right nephrectomy. Thirty-two female Sprague-Dawley rats were analyzed: sham-operated rats (n = 8), treated sham-operated rats (n = 4), ischemic rats (n = 12), and treated ischemic rats (n = 8). Batimastat therapy (30 mg/kg body weight/day) was initiated 2 days prior to induction of ischemia. Animals were sacrificed 12 h (n = 8) and 24 h (n = 24) after ischemia for analyses of MMP activity/expression and of plasma creatinine levels. Results: We found no evidence for an alteration in the activity or expression of MMP as a result of renal ischemia-reperfusion. Importantly, plasma creatinine levels significantly increased to a mean of 374 ± 61 µmol/l in ischemic rats after 24 h, almost identical to the BB-94-treated ischemic rats (384 ± 36 µmol/l). The creatinine levels in sham-operated rats remained within normal limits. Conclusion: MMP play no role during the early phase of experimental renal ischemia-reperfusion injury.

show abstract

Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Renal Matrix Metalloproteinase Activity Is Unaffected by Experimental Ischemia-Reperfusion Injury and Matrix Metalloproteinase Inhibition Does Not Alter Outcome of Renal Function

Ziswiler¹,

Daniel²,

Franz³

et al. 2001

Nephron Exp Nephrol

View full text Add to dashboard Cite

show abstract

“…35 Indeed, clinical and experimental studies have shown that I/R injury is mediated by ROS. [36][37][38] It has been demonstrated that ROS-mediated cellular damage occurs when oxygen is supplied to the tissue by reperfusion and tissue detoxification capacity is deficient for ROS formation. 39 Hence, oxidation of cell protein and membrane lipid peroxidation causes cell death and damage of DNA helix.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of sitagliptin against renal ischemia reperfusion injury in rats

Nuransoy¹,

Beytur²,

Polat

et al. 2015

Renal Failure

View full text Add to dashboard Cite

This study was designed to investigate the protective effects of sitagliptin on renal damage induced by renal ischemia reperfusion (I/R) in rats. For this, rats were randomly divided into four groups (n ¼ 8): (1) sham group, in which the rats only underwent right nephrectomy; (2) right nephrectomy and left kidney ischemia (1 h) and reperfusion (24 h) group (I/R); (3) 5 mg/kg sitagliptin administrated group, per-oral once a day for two weeks; (4) 5 mg/kg sitagliptin administrated group, per-oral once a day for two weeks before left kidney I/R (n ¼ 8). Sitagliptin-treated rats that underwent renal I/R demonstrated significant decrease in the serum urea nitrogen and creatinine and also, lipid peroxidation, total oxidant status and malondialdehyde level in the renal tissue when compared to the renal I/R group. Additionally, reduced glutathione, glutathione peroxidase, superoxide dismutase, catalase and total antioxidative capacity were significantly increased after renal I/R in sitagliptin-treated rats. Our histopathological findings were in accordance with these biochemical results. In sum, in the current study all of our results indicated that sitagliptin treatment ameliorated renal damage induced by renal I/R in rats.

show abstract

“…Renal ischemia, whether caused by shock or during surgery or transplantation, is a major cause of ARF, initiating a complex and interrelated sequence of events resulting in injury to and eventual death of renal cells [2]. The prognosis is complicated by the fact that reperfusion, although essential for the survival of ischemic renal tissue, causes additional damage (reperfusion injury) [3]which contributes to the renal dysfunction and injury associated with ischemia/reperfusion (I/R) of the kidney.…”

Section: Introductionmentioning

confidence: 99%

EUK-134 Reduces Renal Dysfunction and Injury Caused by Oxidative and Nitrosative Stress of the Kidney

et al. 2004

View full text Add to dashboard Cite

Background/Aims: Oxidative and nitrosative stress plays important roles in the pathogenesis of renal ischemia/reperfusion (I/R) injury. Here we investigate the effect of EUK-134, a synthetic superoxide dismutase and catalase mimetic, (i) on renal dysfunction and injury caused by I/R in vivo and (ii) on proximal tubular cell (PTC) injury and death caused by oxidative and nitrosative stress. Methods: Rats, subjected to bilateral renal ischemia (45 min) followed by reperfusion (6 h), were administered EUK-134 (0.3 and 3 mg/kg, i.v.) prior to and during reperfusion, after which biochemical and histological indicators of renal dysfunction and injury were measured. The expression of poly(ADP-ribose) (PAR) and inducible nitric oxide (NO) synthase (iNOS) and nitrotyrosine formation were determined immunohistochemically and used as indicators of oxidative and nitrosative stress. Primary cultures of rat PTCs, isolated and cultured from the kidney cortex, were incubated with hydrogen peroxide (H₂O₂; 1 mM for 2 h) in the presence of increasing concentrations of EUK-134 (1–100 µM) after which PTC injury and death were measured. The effects of EUK-134 on serum levels of NO in rats subjected to renal I/R or on NO production by PTCs incubated with interferon-γ (IFN-γ, 100 IU/ml) and bacterial lipopolysaccharide (LPS, 10 µg/ml) in combination for 24 h were also measured. Results: EUK-134 produced a significant reduction in renal dysfunction and injury caused by I/R. Specifically, serum creatinine levels, an indicator of renal dysfunction, were reduced from 227 ± 11 (n = 12, I/R only) to 146 ± 9 µM (n = 12, I/R +3 mg/kg EUK-134). Urinary N-acetyl-β-D-glucosaminidase activity, an indicator of tubular damage, was reduced from 42 ± 5 (n = 12, I/R only) to 22 ± 3 IU/l (n = 12, I/R +3 mg/kg EUK-134). EUK-134 significantly reduced renal injury caused by oxidative stress in vivo (reduction in PAR formation), and in vitro EUK-134 reduced PTC injury and death caused by H₂O₂. However, EUK-134 also reduced nitrosative stress caused by I/R in vivo (reduction of iNOS expression and nitrotyrosine formation), which was reflected by a significant reduction in serum NO levels in rats subjected to renal I/R. Specifically, serum NO levels were reduced from 57 ± 12 (n = 12, I/R only) to 23 ± 3 mM (n = 12, I/R +3 mg/kg EUK-134). In vitro, EUK-134 significantly reduced NO production by PTCs incubated with IFN-γ/LPS. Conclusion: We propose that EUK-134 reduces renal I/R injury not only via reduction of oxidative stress, but also by reducing nitrosative stress caused by renal I/R.

show abstract

Renal ischaemia-reperfusion injury

Cited by 118 publications

References 118 publications

Renal Matrix Metalloproteinase Activity Is Unaffected by Experimental Ischemia-Reperfusion Injury and Matrix Metalloproteinase Inhibition Does Not Alter Outcome of Renal Function

Renal Matrix Metalloproteinase Activity Is Unaffected by Experimental Ischemia-Reperfusion Injury and Matrix Metalloproteinase Inhibition Does Not Alter Outcome of Renal Function

Protective effect of sitagliptin against renal ischemia reperfusion injury in rats

EUK-134 Reduces Renal Dysfunction and Injury Caused by Oxidative and Nitrosative Stress of the Kidney

Contact Info

Product

Resources

About