Erythrocyte superoxide dismutase as a biomarker of septic acute kidney injury

Costa, Nara Aline; Gut, Ana Lúcia; Azevedo, Paula Schmidt; Tanni, Suzana Erico; Cunha, Natália Baraldi; Magalhães, Eloá Siqueira; Silva, Graziela Biude; Polegato, Bertha Furlan; Zornoff, Leonardo A. M.; Paiva, Sérgio Alberto Rupp de; Balbi, André Luís; Ponce, Daniela; Minicucci, Marcos F.

doi:10.1186/s13613-016-0198-5

Cited by 22 publications

(21 citation statements)

References 37 publications

(41 reference statements)

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“…147 Erythrocyte superoxide dismutase 1 (SOD1) is the most abundant member of the family of antioxidant enzymes, representing approximately 90% of SODs. 148,149 It is a major defense against reactive oxygen species and primarily is intracellular, where it is found in the copper-zinc bound form. SOD1 long has been known to be involved in ischemic AKI in animal models because its administration to rats combined with sucrose reduced histologic and functional lesions.…”

Section: Q26mentioning

confidence: 99%

“…151 More recently, SOD1 activity in erythrocytes has been shown to be associated with septic AKI in critically ill patients, although the diagnostic performance was weak (AUC, 0.69). 149 Semaphorin-3A is a 89-kDa secreted protein with short-range context-dependent chemorepulsive and chemoattractive properties. Initially described in the context of axon guidance, it later became clear that semaphorin-3A also plays a role in vascular growth, angiogenesis, and immune cell regulation.…”

Section: Q26mentioning

confidence: 99%

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Proteomics and Metabolomics for AKI Diagnosis

Marx

Metzger

Pejchinovski

et al. 2018

Seminars in Nephrology

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Acute kidney injury (AKI) is a severe and frequent condition in hospitalized patients. Currently, no efficient therapy of AKI is available. Therefore, efforts focus on early prevention and potentially early initiation of renal replacement therapy to improve the outcome in AKI. The detection of AKI in hospitalized patients implies the need for early, accurate, robust, and easily accessible biomarkers of AKI evolution and outcome prediction because only a narrow window exists to implement the earlier-described measures. Even more challenging is the multifactorial origin of AKI and the fact that the changes of molecular expression induced by AKI are difficult to distinguish from those of the diseases associated or causing AKI as shock or sepsis. During the past decade, a considerable number of protein biomarkers for AKI have been described and we expect from recent advances in the field of omics technologies that this number will increase further in the future and be extended to other sorts of biomolecules, such as RNAs, lipids, and metabolites. However, most of these biomarkers are poorly defined by their AKI-associated molecular context. In this review, we describe the state-of-the-art tissue and biofluid proteomic and metabolomic technologies and new bioinformatics approaches for proteomic and metabolomic pathway and molecular interaction analysis. In the second part of the review, we focus on AKI-associated proteomic and metabolomic biomarkers and briefly outline their pathophysiological context in AKI.

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Section: Q26mentioning

confidence: 99%

Section: Q26mentioning

confidence: 99%

Proteomics and Metabolomics for AKI Diagnosis

Marx

Metzger

Pejchinovski

et al. 2018

Seminars in Nephrology

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“…In a number of studies, urine L-FABP has been able to reliably predict the occurrence of AKI and death in ICU patients [64]. Recently, Costa et al found that erythrocyte superoxide dismutase (SOD1) activity could play a role as an early marker of septic AKI and could be seen as a new research avenue in the field of biomarker in AKI [67]. …”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and Acute Kidney Injury in Critical Illness: Pathophysiologic Mechanisms—Biomarkers—Interventions, and Future Perspectives

Pavlakou

Liakopoulos

Eleftheriadis

et al. 2017

Oxidative Medicine and Cellular Longevity

107

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Acute kidney injury (AKI) is a multifactorial entity that occurs in a variety of clinical settings. Although AKI is not a usual reason for intensive care unit (ICU) admission, it often complicates critically ill patients' clinical course requiring renal replacement therapy progressing sometimes to end-stage renal disease and increasing mortality. The causes of AKI in the group of ICU patients are further complicated from damaged metabolic state, systemic inflammation, sepsis, and hemodynamic dysregulations, leading to an imbalance that generates oxidative stress response. Abundant experimental and to a less extent clinical data support the important role of oxidative stress-related mechanisms in the injury phase of AKI. The purpose of this article is to present the main pathophysiologic mechanisms of AKI in ICU patients focusing on the different aspects of oxidative stress generation, the available evidence of interventional measures for AKI prevention, biomarkers used in a clinical setting, and future perspectives in oxidative stress regulation.

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“…This prospective observational clinical study, was a subanalysis of a previous study of our group that analyzed oxidative stress markers as early predictors of septic shock mortality and SAKI development [18]. We included patients admitted to the Intensive Care Unit (ICU) of our institution with the diagnosis of septic shock, from May 2014 to June 2015.…”

Section: Study Populationmentioning

confidence: 99%

Evaluation of peptidylarginine deiminase 4 concentration and PADI4 polymorphisms in sepsis-induced acute kidney injury

Costa¹,

Polegato²,

Pereira³

et al. 2019

Preprint

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Background: The influence of PAD4 concentration and its polymorphisms in SAKI development are poorly evaluated. Thus, the aim of this study is to evaluate the PAD 4 concentration and PADI4 polymorphisms, as predictors of AKI development, need for renal replacement therapy (RRT), and mortality in patients with septic shock. Methods: We included all individuals aged ≥ 18 years, with the diagnosis of septic shock at ICU admission. Blood samples were taken within the first 24 hours of the patient’s admission to determine serum PAD4 concentration and its polymorphism PADI4 (rs11203367) and (rs874881). Patients were followed during their ICU stay and the development of SAKI was evaluated. Among the patients in whom SAKI developed, mortality and need for RRT were also evaluated. Results: 99 patients were included in the analysis. SAKI developed in approximately 51.5% of patients during the ICU stay; of these, 21.5% required RRT and 80% died. There was no difference between PAD4 concentration (p = 0.116) and its polymorphisms rs11203367 (p = 0.910) and rs874881 (p = 0.769) in patients in whom SAKI did or did not develop. However, PAD4 had a positive correlation with plasma urea concentration (r = 0.269 and p = 0.007) and creatinine (r = 0.284 and p = 0.004). The PAD4 concentration and PADI4 polymorphisms were also not associated with RRT and with mortality in patients with SAKI. Conclusion: PAD4 concentration and its polymorphisms were not associated with SAKI development, the need for RRT, or mortality in patients with septic shock. However, PAD4 concentrations were associated with creatinine and urea levels in these patients.

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Erythrocyte superoxide dismutase as a biomarker of septic acute kidney injury

Cited by 22 publications

References 37 publications

Proteomics and Metabolomics for AKI Diagnosis

Proteomics and Metabolomics for AKI Diagnosis

Oxidative Stress and Acute Kidney Injury in Critical Illness: Pathophysiologic Mechanisms—Biomarkers—Interventions, and Future Perspectives

Evaluation of peptidylarginine deiminase 4 concentration and PADI4 polymorphisms in sepsis-induced acute kidney injury

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