High Dose of N-Acetylcystein Prevents Acute Kidney Injury in Chronic Kidney Disease Patients Undergoing Myocardial Revascularization

Santana–Santos, Eduesley; Gowdak, Luís Henrique Wolff; Gaiotto, Fábio Antônio; Puig, Luiz Bóro; Hajjar, Ludhmila Abrahão; Zeferino, S; Drager, Luciano F.; Shimizu, Maria Heloísa Massola; Bortolotto, Luiz Aparecido; Lima, José Jayme Galvão de

doi:10.1016/j.athoracsur.2014.01.056

Cited by 40 publications

(33 citation statements)

References 41 publications

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“…Santana-Santos et al [74] recently published results of a small, single-center RCT of high-dose NAC (150 mg/kg, then 50 mg/kg infusion over 6 hours) in 70 patients with Stage 3 or 4 CKD undergoing CABG surgery with or without CPB. The primary end point was AKI defined by AKIN criteria.…”

Section: N-acetylcysteinementioning

confidence: 97%

Acute kidney injury in cardiac surgery

Gaffney

Sladen

2015

Current Opinion in Anaesthesiology

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Section: N-acetylcysteinementioning

confidence: 97%

Acute kidney injury in cardiac surgery

Gaffney

Sladen

2015

Current Opinion in Anaesthesiology

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“…These findings are consistent with human clinical trials investigating NAC pre-treatment against AKI, including contrast-induced nephropathy (Kay et al, 2003), and cardiovascular bypass surgeries (Santana-Santos et al, 2014).…”

Section: Discussionsupporting

confidence: 80%

“…NAC was the only antioxidant that showed benefit in vitro. NAC has also been used in human trials for preventing hospital acquired AKI (Kay et al, 2003;Santana-Santos et al, 2014).…”

Section: General Cell Antioxidants Can Enhance Progressive Kidney Patmentioning

confidence: 99%

“…NAC was the only antioxidant that showed benefit in vitro. NAC has also been used in human trials for preventing hospital acquired AKI (Kay et al, 2003;Santana-Santos et al, 2014).Treatment of PTE cells in vitro with NAC during oxidative stress inhibited oxidative stress-induced apoptosis, senescence and restored the proliferative capacity of PTE cells. In vivo, the protective effects of NAC were maintained in the early response to IR-induced AKI, however proved deleterious long-term.…”

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confidence: 99%

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Identification of potential mediators of oxidative damage and targets for novel treatments for chronic kidney disease

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Chronic kidney disease (CKD) is a common and serious problem causing a significant burden to healthcare systems and, most importantly, the affected individual. Despite this, few successful treatments exist for CKD. Understanding the pathophysiological features that are common to chronic kidney pathologies is vital to identify targets for treatment. Oxidative stress has been implicated in all chronic diseases, acting via highly conserved pathways of disease progression.However, evidence to date shows limited benefit of antioxidants as therapies for CKD patients, suggesting a need to better identify the pathways that are stimulated.This thesis focuses on the role of oxidative stress, the regulation of mitochondrial homeostasis, the action of antioxidant compounds, and the disruption of oxidant signalling networks in chronic kidney pathologies (reviewed in Chapter 1). The aims of this project were to: (1) to use an in vitro model of oxidative stress-induced kidney injury to determine how a failure in balance between oxidative stress and oxidant control causes the cellular characteristics of CKD, then to determine whether exogenous antioxidants can prevent and restore renal cell bioenergetics and reduce cell injury; (2) to use an in vivo model of oxidative stress-induced kidney injury with molecular and metabolic imaging to measure potential biomarkers identified in Aim 1, in association with changes in kidney structure and function, and determine whether treatment with an antioxidant therapy modulates kidney disease pathology; and (3) to explore the links between biomarkers of oxidative stress and clinical characteristics of CKD in patients to determine whether a lifestyle intervention in conjunction with standard nephrology care improve systemic oxidative stress and whether this influences kidney function. The renal specific in vitro, in vivo, and clinical models and the methods used are explained in Chapter 2.Chapter 3 reports the separate and cumulative effects of oxidative stress, mitochondrial dysfunction and cell senescence in promoting loss of renal cells in an in vitro model of kidney disease. The results demonstrate that oxidative stress and cell senescence cause mitochondrial destabilization and kidney tubular epithelial cell loss. This may contribute to the development of cellular and tissue atrophy seen in CKD.Chapter 4 further defines the role of mitochondrial alterations as a consequence of a specificallyimpaired oxidant signalling regulatory mechanism, namely, peroxisome proliferator-activated receptor-gamma (PPARγ)-regulated mitochondrial biogenesis. Oxidative stress promoted mitochondrial destabilisation in kidney proximal tubular epithelial cells, in association with ii increased PPARγ Serine 112 phosphorylation. Despite their positive effects in other tissues, PPARγ agonists failed to protect proximal tubular epithelial (PTE) cells, and appear to be detrimental to kidney PTE cell health when oxidative stress induces the cell damage.Chapter 5 examined mediators of oxidative stress in an in...

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“…Santana-Santos et al [14] showed that the incidence of kidney injury was reduced with NAC in CABG. They investigated two independent markers of kidney injury, namely cystatin C and neutrophil gelatinase associated lipocalin (NGAL).…”

Section: Discussionmentioning

confidence: 99%

N-acetylcysteine Versus Dopamine to Prevent Acute Kidney Injury After Cardiac Surgery In Patients with Pre-existing Moderate Renal Insufficiency

Şavluk

Güzelmeriç

Yavuz

et al. 2015

Journal of Cardiothoracic and Vascular Anesthesia

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Objective: Acute kidney injury after cardiac surgery is associated with mortality and morbidity. Therefore, strategies to prevent acute kidney injury are very important. The aim of this placebo-controlled randomized double-blind study was to compare the prophylactic efficacy of N-Acetylcysteine and dopamine administration in patients with pre-existing moderate renal insufficiency who were undergoing cardiopulmonary bypass.Methods: This study included 135 patients with pre-existing moderate renal insufficiency who were scheduled for coronary artery bypass grafting surgery. Serum creatinine and GFR were recorded preoperatively and on the first and second postoperative days.Results: On the first and second postoperative days, the drugs used showed statistically significant differences among the creatinine groups (P<0.001). According to Tukey's HSD, on the first and second PO, the creatinine of Group N, D and P were significantly different (P<0.001). On the first and second PO, the used drugs showed statistically significant differences among the effects of eGFR (P<0.001). According to Tukey's HSD on the first postoperative day, the average eGFR score of Group N compared to D and P were significantly difference (P<0.001). On the second postoperative day, the eGFR of Group N and D showed no difference (P=0.37), but P showed a difference (P<0.001).Conclusion: We found that the prophylactic use of intravenous N-Acetylcysteine had a protective effect on renal function, whereas the application of renal dose dopamine did not have a protective effect in patients with pre-existing moderate renal failure.

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High Dose of N-Acetylcystein Prevents Acute Kidney Injury in Chronic Kidney Disease Patients Undergoing Myocardial Revascularization

Cited by 40 publications

References 41 publications

Acute kidney injury in cardiac surgery

Acute kidney injury in cardiac surgery

Identification of potential mediators of oxidative damage and targets for novel treatments for chronic kidney disease

N-acetylcysteine Versus Dopamine to Prevent Acute Kidney Injury After Cardiac Surgery In Patients with Pre-existing Moderate Renal Insufficiency

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