Acute renal failure potentiates methylmalonate-induced oxidative stress in brain and kidney of rats

Schuck, Patrícia Fernanda; Alves, Letícia Biscaino; Pettenuzzo, Letícia Ferreira; Felisberto, Francine; Rodrigues, L B; Freitas, Bruna Waddington de; Petronilho, Fabrícia; Dal‐Pizzol, Felipe; Streck, Emílio L.; Ferreira, Gustavo C.

doi:10.3109/10715762.2012.762771

Cited by 17 publications

(9 citation statements)

References 55 publications

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“…Moreover, the exchange of methylmalonic acid for α‐ketoglutarate seems to deplete mitochondria from α‐ketoglutarate, but this could not be confirmed in vivo . In addition, a methylmalonic acid‐induced increase of lipid and protein peroxidation and decrease of superoxide dismutase activity was observed in rat brain and kidney tissue, which was further amplified by the induction of renal failure …”

Section: Effects Of Accumulating Toxic Metabolitesmentioning

confidence: 98%

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Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

Haijes

Hasselt

Jans

et al. 2019

J of Inher Metab Disea

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Despite realizing increased survival rates for propionic acidemia (PA) and methylmalonic acidemia (MMA) patients, the current therapeutic regimen is inadequate for preventing or treating the devastating complications that still can occur. The elucidation of pathophysiology of these complications allows us to evaluate and rethink treatment strategies. In this review we display and discuss potential therapy targets and we give a systematic overview on current, experimental and unexplored treatment strategies in order to provide insight in what we have to offer PA and MMA patients, now and in the future. Evidence on the effectiveness of treatment strategies is often scarce, since none were tested in randomized clinical trials. This raises concerns, since even the current consensus on best practice treatment for PA and MMA is not without controversy. To attain substantial improvements in overall outcome, gene, mRNA or enzyme replacement therapy is most promising since permanent reduction of toxic metabolites allows for a less strict therapeutic regime. Hereby, both mitochondrial‐associated and therapy induced complications can theoretically be prevented. However, the road from bench to bedside is long, as it is challenging to design a drug that is delivered to the mitochondria of all tissues that require enzymatic activity, including the brain, without inducing any off‐target effects. To improve survival rate and quality of life of PA and MMA patients, there is a need for systematic (re‐)evaluation of accepted and potential treatment strategies, so that we can better determine who will benefit when and how from which treatment strategy.

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Section: Effects Of Accumulating Toxic Metabolitesmentioning

confidence: 98%

“…46 In addition, a methylmalonic acid-induced increase of lipid and protein peroxidation and decrease of superoxide dismutase activity was observed in rat brain 47 and kidney tissue, which was further amplified by the induction of renal failure. 48…”

Section: Methylmalonic Acidmentioning

confidence: 99%

Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

Haijes

Hasselt

Jans

et al. 2019

J of Inher Metab Disea

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“…At present, the subjects of ischemia-reperfusion injury after CA in animal experiments were mostly brain [6] and heart [7], but AKI was also associated with poor outcome [8]. Nevertheless, several studies have found that AKI may have an impact on neurological recovery [9,10]. Therefore, it is equally important to study AKI after CA and CPR, and the occurrence of AKI in CA rats have not been well-studied.…”

Section: Introductionmentioning

confidence: 99%

The incidence of acute kidney injury following cardiac arrest and cardiopulmonary resuscitation in a rat model

Zheng

et al. 2019

Renal Failure

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Objective : In the current study, we investigated the incidence of acute kidney injury (AKI) induced by cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) and whether such an AKI can recover spontaneously in rats. Methods: We used transesophageal alternating current stimulation to establish 7 min of CA rat model followed by conventional CPR. The experimental rats were randomly divided into three groups ( n = 20 per group) according to the different time points after restoration spontaneous circulation (ROSC): the ROSC 24 h, ROSC 48 h, and ROSC 72 h group. The diagnosis of rat AKI refers to the 2012 KDIGO adult AKI diagnostic criteria. The severity of AKI quantified by the serum creatinine (SCR), blood urea nitrogen (BUN) levels and histological features of renal tissue. Results: The incidence rates of AKI in ROSC 24 h, ROSC 48 h, and ROSC 72 h group were 65%, 45%, and 42.9%. Moreover, the values of SCR and BUN were highest at ROSC 24 h, and then gradually decreased with the time of ROSC. The histological changes of the renal tissues such as glomerular collapse, renal tubular cell swelling, and inflammatory cell infiltration had also observed. Conclusion: The incidence of AKI in rats was high after suffering from CA and CPR, but renal function improved with the prolongation of ROSC time, indicating the ability of the kidney to self-repair.

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“…Finally, AKI may have an impact on neurological recovery. In an experimental model of renal injury, AKI was found to contribute to the inflammatory injury in the hippocampus, altered blood–brain barrier permeability and potentiated oxidative stress in the cerebral tissue [ 15 , 16 ]. Patients with AKI also have a higher incidence of stroke and cognitive disorders than patients without AKI [ 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

Acute kidney injury after cardiac arrest

et al. 2015

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IntroductionThe aim of this study was to evaluate the incidence and determinants of AKI in a large cohort of cardiac arrest patients.MethodsWe reviewed all patients admitted, for at least 48 hours, to our Dept. of Intensive Care after CA between January 2008 and October 2012. AKI was defined as oligo-anuria (daily urine output <0.5 ml/kg/h) and/or an increase in serum creatinine (≥0.3 mg/dl from admission value within 48 hours or a 1.5 time from baseline level). Demographics, comorbidities, CA details, and ICU interventions were recorded. Neurological outcome was assessed at 3 months using the Cerebral Performance Category scale (CPC 1–2 = favorable outcome; 3–5 = poor outcome).ResultsA total of 199 patients were included, 85 (43%) of whom developed AKI during the ICU stay. Independent predictors of AKI development were older age, chronic renal disease, higher dose of epinephrine, in-hospital CA, presence of shock during the ICU stay, a low creatinine clearance (CrCl) on admission and a high cumulative fluid balance at 48 hours. Patients with AKI had higher hospital mortality (55/85 vs. 57/114, p = 0.04), but AKI was not an independent predictor of poor 3-month neurological outcome.ConclusionsAKI occurred in more than 40% of patients after CA. These patients had more severe hemodynamic impairment and needed more aggressive ICU therapy; however the development of AKI did not influence neurological recovery.

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Acute renal failure potentiates methylmalonate-induced oxidative stress in brain and kidney of rats

Cited by 17 publications

References 55 publications

Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

The incidence of acute kidney injury following cardiac arrest and cardiopulmonary resuscitation in a rat model

Acute kidney injury after cardiac arrest

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