Physiopathology of acute renal failure during sepsis

Regueira, Tomás; Andresen, Max; Mercado, Marcelo; Downey, Patricio

doi:10.1016/j.medine.2011.03.007

Cited by 21 publications

(23 citation statements)

References 99 publications

(59 reference statements)

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“…Renal mitochondrial dysfunction also occurs during the course of sepsis-induced AKI (6). Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is a member of the ALDH gene family, which is highly expressed in the heart, liver, kidney and muscle (7).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of ALDH2 expression aggravates renal injury in a rat sepsis syndrome model

Wang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is closely associated with organ injury. The aim of the present study was to investigate the change of ALDH2 expression in a rat model of sepsis-induced acute renal injury, and to observe the effect of ALDH2 inhibition on the kidney. A model of sepsis syndrome was established in Sprague-Dawley (SD) rats by cecal ligation and puncture (CLP). The rats were divided into sham, CLP and CLP + cyanamide (CYA, an ALDH2 inhibitor) groups. The hemodynamic parameters heart rate (HR) and mean arterial blood pressure (MABP) were measured. Plasma creatinine (CRE) and urea nitrogen (BUN) levels were measured using an automatic biochemical analyzer. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in the kidney tissue were measured. Histological changes of the kidney tissue were observed using hematoxylin and eosin staining and NF-κB p65 expression was observed by an immunohistochemical staining method. The expression of renal ALDH2 at the mRNA and protein levels was detected by reverse transcription-polymerase chain reaction and western blotting. In the CLP compared with the sham group after 24 h, the MABP was decreased, plasma CRE and BUN levels were elevated, the renal MDA level was increased and SOD activity was decreased. In addition, glomerular atrophy occurred, the renal protein expression of NF-κB p65 was increased, and the mRNA and protein expression levels of ALDH2 were decreased. In contrast with the CLP group, in the CLP + CYA group, the MABP and ALDH2 expression were further decreased while glomerular atrophy was aggravated. Furthermore, CRE, BUN, MDA levels and NF-κB p65 expression were further increased and SOD activity was further reduced. In this rat model of sepsis syndrome, the reduction of renal ALDH2 expression was accompanied by kidney injury. Inhibition of ALDH2 with CYA aggravated the renal injury, and was associated with the overproduction of reactive oxygen species and inflammatory reaction.

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Section: Introductionmentioning

confidence: 99%

Inhibition of ALDH2 expression aggravates renal injury in a rat sepsis syndrome model

Wang

et al. 2017

Experimental and Therapeutic Medicine

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“…AKI can cause permanent loss of kidney function [3], has a poor prognosis, and a high mortality rate (20% to 35%). When it is associated with hemodynamic alterations, mortality can increase up to 60% [4,5].…”

Section: Introductionmentioning

confidence: 99%

“…TNF-α promotes leukocyte infiltration, induces cell death and endothelial dysfunction, mediates remote organ injury, and activates an inflammatory cascade that results in further production of cytokines and chemokines. The pharmacologic modulation of TNF-α production has been a strategy in the attempt to prevent I/R injury [4].…”

Section: Introductionmentioning

confidence: 99%

Bupropion Cannot Reduce Acute Kidney Injury Due to Ischemia-Reperfusion

FJ¹,

AJ²,

JM³

et al. 2017

Clin Exp Pharmacol

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Bupropion can limit the increase of TNF-alpha, reducing the inflammatory response and injury due to IschemiaReperfusion (I/R) on tissues such as the bowel. Our objective was to evaluate bupropion as a preconditioning agent for ischemic acute kidney injury.Experiments were performed on female Wistar rats. Bupropion groups received 25 mg/kg 60 min before the maneuver. As a first step, 30 rats with a right nephrectomy were divided into 6 groups (n=5): sham 24, sham 48, bupropion 24, bupropion 48, ischemia-reperfusion 24 and ischemia-reperfusion 48. After 60 min of ischemia (except sham groups) 24 or 48 h of reperfusion was allowed. During a second step, 30 rats, with both kidneys conserved, were divided into 6 groups (n=5): sham 3, sham 72, bupropion 3, bupropion 72, ischemia-reperfusion 3, and ischemia-reperfusion 72 (IR72). Ischemia in these groups (except sham groups) was performed for 60 min only on the left kidney, and 3 or 72 h of reperfusion were allowed. Serum and histologic evaluations were done.After 48 h of reperfusion, all mono-renal rats that received bupropion died. Bupropion cannot avoid histological damage nor does it impact creatinine clearance, BUN, TNF-α or KIM-1 serum levels secondary to I/R. In conclusion: The pharmacologic preconditioning with Bupropion cannot improve the AKI evolution in rats with renal ischemiareperfusion injury.

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“…El síndrome de disfunción multiorgánica (SDOM) es la principal causa de muerte en los pacientes sépticos 2 , siendo la injuria renal aguda (IRA) la disfunción orgánica más precoz y frecuente durante la sepsis, y que se asocia con una mayor mortalidad 3 . Varios mecanismos han sido propuestos para explicar la génesis de la IRA en la sepsis, sin embargo, los procesos fisiopatológicos predominantes de la IRA durante la sepsis aún no son claros [4][5][6] . Clásicamente, la reducción en el flujo sanguíneo renal (FSR) se ha propuesto como el mecanismo más importante en la patogenia de la IRA 5 , sin embargo, la escasa presencia de necrosis reportada en tejido renal de pacientes que fallecen en sepsis con IRA hacen que la pérdida de flujo renal sea un proceso probablemente poco relevante 7,8 .…”

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