Distinct Pathophysiologic Mechanism of Septic Acute Kidney Injury – Role of Immune Suppression and Apoptosis

Lee, So‐Young; Jo, Sang-Kyung; Cho, Won-Yong; Kim, Hyoung Kyu

doi:10.1016/s0953-6205(11)60219-7

Cited by 29 publications

(51 citation statements)

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“…26 Interestingly, in a cecal ligation and puncture sepsis model, Treg depletion with PC61 protected mice from renal dysfunction and improved survival. 27 In summary, intrinsic Tregs protect from aseptic ischemic and nephrotoxic renal injury but may contribute to septic AKI.…”

Section: Role Of Intrinsic Tregs In Akimentioning

confidence: 99%

Regulatory T Cells in AKI

Kinsey

Sharma

Okusa

2013

Journal of the American Society of Nephrology

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Human AKI is manifested by inflammation, and an early feature in the pathogenesis is the accumulation of immune cells in the kidney. To understand the pathophysiology of AKI, results from animal models have shown a causal relation between the leukocyte activation and infiltration to the kidney after kidney ischemia-reperfusion. Blocking the activation or trafficking of proinflammatory leukocytes into the kidney preserves renal function and histologic integrity. In contrast, the anti-inflammatory lymphocytes called regulatory T cells have an intrinsic renal-protective function and may represent a novel therapeutic approach and/or target for pharmacological manipulation to ameliorate AKI. This review will highlight the recent insight gained into the role and mechanisms of regulatory T cells in AKI.

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Section: Role Of Intrinsic Tregs In Akimentioning

confidence: 99%

Regulatory T Cells in AKI

Kinsey

Sharma

Okusa

2013

Journal of the American Society of Nephrology

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“…Blocking interleukin-10 rescued septic mice from the development of AKI, whereas it had no effect in ischemia/reperfusion injury. 16 An important reason that the immunity is repressed in septic patients is the lymphocyte apoptosis. Septic patients are generally lymphopenic.…”

mentioning

confidence: 99%

Renal Cell Apoptosis and New Treatment Options in Sepsis-Induced Acute Kidney Injury

Koçkara

Kayataş

2012

Renal Failure

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Sepsis is a common and important cause of mortality in critically ill patients. Acute kidney injury (AKI) is one of the most important factors determining morbidity and mortality in the prognosis of sepsis. Recent studies have indicated that the pathogenetic mechanism in septic AKI is totally different from that in non-septic AKI. Our understanding of sepsisassociated AKI pathophysiology is shifting from renal vasoconstriction, ischemia, and acute tubular necrosis to heterogeneous vasodilation, hyperemia, and acute tubular apoptosis. Especially, apoptosis is gradually gaining importance in the understanding of the development of renal injury. The frequency of renal tubular apoptosis on biopsies of septic patients has been pointed out in recently published studies. Apoptosis can be triggered by ischemia, exogen toxins, or endogen mediators. It has been shown in some animal models that hyperglycemia, which is common in critically ill patients, causes apoptosis in renal tubular cells. New treatment options have emerged in the light of recent findings. Ghrelin that inhibits pro-inflammatory cytokines, caspase inhibitors that block the apoptotic pathway, and suppression of anti-inflammatory reactions are under study. Among the existing methods of treatment, usage of arginine, which is a vasopressor agent, ventilation with a low tidal volume, and hemofiltration methods cleaning toxic mediators from the circulation should be considered in the first place. Hyperglycemia treatment is of major importance, since, besides its antiinflammatory effect, it has a protective role on the kidney. Regarding pathogenesis, rates of morbidity and mortality are aimed to be reduced through the new agents of therapy that have been studied on.

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“…The pathogenesis of AKI results in increased oxidative stress, and renal tubular apoptosis and inflammation [28]. Currently, attention has been focused on discovering compounds of natural origins to protect against renal injury [29][30][31][32].…”

Section: Discussionmentioning

confidence: 99%

Icariin Improves Sepsis-Induced Mortality and Acute Kidney Injury

Xie¹,

Liu

Wang

et al. 2018

Pharmacology

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Objectives: Icariin (ICA) is a bioactive flavonoid with renal protective actions. This study investigated the effects of ICA on renal injury, inflammation, oxidative damage, apoptosis, and survival in a mouse model of cecal ligation and perforation (CLP)-induced sepsis. Methods: Sepsis was induced by CLP. Mice were treated with ICA (30 or 60 mg/kg) for 3 days before CLP. Renal functions, inflammatory responses, oxidative damage, histological changes, apoptosis, and vascular permeability were examined. The effects of ICA on CLP-induced expression of renal nuclear factor-κB (NF-κB), cleaved caspase-3, Bax, and Bcl-2 were evaluated. Results: Mice in the CLP group had a low survival rate and increases in blood urea nitrogen and creatinine levels, proinflammatory cytokine levels, oxidative damage, apoptosis, and vascular permeability. These renal changes were dramatically improved by ICA treatment, especially in the 60 mg/kg ICA group. The detection of molecules involved in the inflammation and apoptosis of the kidney indicated that ICA reduced expression of NF-κB, cleaved caspase-3, and Bax but enhanced expression of Bcl-2. Conclusion: ICA improves CLP-induced mortality and acute kidney injury by inhibiting renal oxidant damage, inflammatory responses, apoptosis, and vascular permeability.

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Distinct Pathophysiologic Mechanism of Septic Acute Kidney Injury – Role of Immune Suppression and Apoptosis

Cited by 29 publications

References 0 publications

Regulatory T Cells in AKI

Regulatory T Cells in AKI

Renal Cell Apoptosis and New Treatment Options in Sepsis-Induced Acute Kidney Injury

Icariin Improves Sepsis-Induced Mortality and Acute Kidney Injury

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