ArticleMetabolic brain disease2018
Oxidative stress in the brain caused by acute kidney injury.
Article in Metabolic brain disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Brain-derived extracellular vesicles circUsp32 polarized macrophages causing acute kidney injury after traumatic brain injury.Science advances · 2025Article
- A second act for spironolactone: cognitive benefits in renal dysfunction - a critical review.Metabolic brain disease · 2025Review
- Mitigating Remote Organ-Induced Brain Injury in Renal Ischemia-Reperfusion: The Role of Oleuropein in Inhibiting Oxidative Stress, Inflammation, Ferroptosis, and Apoptosis in Male Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Nanoselenium attenuates renal ischemia-reperfusion injury in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Central Auditory Processing Impairment in Renal Failure.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2024Article
- The effects of CORM3 or NaHS on the oxidative stress caused by chronic kidney disease in rats: potential interaction between CO and HMetabolic brain disease · 2023Article
- Butylphthalide improves brain damage induced by renal ischemia-reperfusion injury rats through Nrf2/HO-1 and NOD2/MAPK/NF-κB pathways.Renal failure · 2023Article
- Associations among Alzheimer disease, depressive disorder, and risk of end-stage kidney disease in elderly people.Kidney research and clinical practice · 2022Article
- Impact of Chronic Kidney Disease on Brain Structure and Function.Frontiers in neurology · 2022Review
- Accelerated lipid peroxidation in a rat model of gentamicin nephrotoxicity.Experimental and therapeutic medicine · 2021Article
- Acute kidney injury.Nature reviews. Disease primers · 2021Review
- S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression.Molecular medicine reports · 2021Article
- Ameliorative effects of hydrogen sulfide (NaHS) on chronic kidney disease-induced brain dysfunction in rats: implication on role of nitric oxide (NO) signaling.Metabolic brain disease · 2018Article
- Molecular Mechanisms Involved in Oxidative Stress-Associated Liver Injury Induced by Chinese Herbal Medicine: An Experimental Evidence-Based Literature Review and Network Pharmacology Study.International journal of molecular sciences · 2018Review
- The influence of renal ischemia-reperfusion injury on remote organs: The histological brain changes in male and female rats.Brain circulationArticle
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uremic encephalopathy is a severe complication of renal failure. The underlying pathogenesis is unknown although several mechanisms have been suggested. Renal failure causes oxidative stress leading to cardiovascular complications. It has been suggested as the potential mediator of uremic encephalopathy as well, but it is largely unknown whether brain tissue itself undergoes oxidative damage in uremia. The aim of our experiment was to analyze oxidative stress markers in different brain regions in an animal model of acute kidney injury (AKI). AKI was induced by ischemia-reperfusion injury in male Wistar rats. Urine was collected in metabolic cages after 24 h. Samples of plasma and several brain regions were collected after 48 h. Markers of lipid peroxidation, protein oxidation and total antioxidant capacity were assessed. Renal failure was confirmed by high plasma creatinine, urea and urinary albumin to creatinine ratio. Our data confirmed increased systemic oxidative stress in the AKI group with plasma concentrations of markers of oxidative damage being twice as high compared to the sham-operated control group. No effect was seen in the urine. In the hippocampus, lipid and protein oxidation was higher, while antioxidant capacity was lower in the rats with AKI. Lipid oxidation markers in the frontal cortex were higher by 33%. No differences to controls were found in the cerebellum and hypothalamus. In conclusion, our results indicate that AKI leads to oxidative stress in the brain, especially in the hippocampus and in the frontal cortex. This kidney-brain crosstalk mediated by increased oxidative stress might explain some of the symptoms of uremic encephalopathy. The causes and consequences of oxidative damage observed in the brain during AKI remain to be elucidated.
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