Paradigmenwechsel im Verständnis der akuten Nierenschädigung bei chronischer Leberinsuffizienz: Von der Pathophysiologie zur Definition von Krankheitsentitäten

Scurt, Florian G; Bose, Katrin; Canbay, Ali; Mertens, Peter R.; Chatzikyrkou, Christos

doi:10.1055/a-1088-1582

Cited by 8 publications

(2 citation statements)

References 104 publications

(83 reference statements)

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“…Not only the comorbidities associated with MAFLD, such as DM, obesity, and hypertension, but also pathophysiological processes‐induced by MAFLD, liver fibrosis, and liver cirrhosis, respectively—can lead both directly to parenchymal changes (e.g., bile acid nephropathy, ischemic tubular epithelial cell necrosis, and glomerulonephritis associated with hepatitis B and C)—defined as non‐hepatorenal syndrome—acute kidney injury (non‐HRS‐AKI) or non‐hepatorenal syndrome—CKD (non‐HRS‐CKD)—as well as indirectly via vasodilation in the splanchnic area, causing cardiac dysfunction and adrenal insufficiency as well as chronic inflammation and thus worsening renal function (hepatorenal syndrome—acute kidney injury [HRS‐AKI], hepatorenal syndrome—non acute kidney injury [HRS‐NAKI]) 129–132 . A more detailed explanation of the pathomechanisms mentioned here is beyond the scope of this review, and the reader is referred to the excellent reviews by Davenport et al and Velez et al 130,132 …”

Section: Mechanisms Of Renal Injury In Concomitant Diseases Of Metsmentioning

confidence: 99%

Association of metabolic syndrome and chronic kidney disease

Scurt,

Ganz,

Herzog

et al. 2023

Obesity Reviews

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SummaryThe prevalence of kidney disease is increasing rapidly worldwide, reflecting rising rates of obesity, diabetes, and associated metabolic syndrome (MetS). Chronic kidney disease and related comorbidities such as obesity, diabetes, and hypertension place a significant financial burden on healthcare systems. Despite the widespread use of RAAS inhibitors, intensive blood pressure and glycemic control, and newer therapeutic options consisting of sodium/glucose cotransporter‐2 (SGLT‐2) inhibitors or glucagon‐like peptide‐1 (GLP‐1) receptor agonists, a significant risk of progression to end‐stage renal disease remains in the high‐risk obese and diabetic population. The MetS is a cluster of cardiovascular risk factors that adversely affect the development and progression of chronic kidney failure. According to the criteria of the World Health Organization, it is defined by visceral adiposity, impaired glucose tolerance or insulin resistance, atherogenic dyslipidemia, raised blood pressure, and microalbuminuria with a albumin‐to‐creatinine ratio ≥30 mg/g. At molecular level MetS is marked by a proinflammatory state and increased oxidative stress leading to various pathophysiological changes causing endothelial dysfunction and a hypercoagulable state. Because the kidney is a highly vascularized organ, it is especially susceptible for those microvascular changes. Therefore, the MetS and its individual components are associated with the premature development, acceleration, and progression of chronic kidney disease. Therefore, it is becoming increasingly important to elucidate the underlying mechanisms of MetS‐associated chronic kidney disease in order to develop new strategies for preventing and slowing the progression of renal disease. In this review, we will elucidate (i) the renal structural, hemodynamic, and metabolic changes that occur in obesity and obesity‐related kidney injury; (ii) the clinicopathological characteristics of obesity‐related kidney injury, primarily focusing on obesity‐associated glomerulopathy; (iii) the potential additional factors or predisposing factors that may turn patients more susceptible to renal structural or functional compensatory failure and subsequent injury.

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Section: Mechanisms Of Renal Injury In Concomitant Diseases Of Metsmentioning

confidence: 99%

Association of metabolic syndrome and chronic kidney disease

Scurt,

Ganz,

Herzog

et al. 2023

Obesity Reviews

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“…Studies have shown that there is intrarenal/renal interstitial hypoxia in the kidneys. Hypoxia can lead to abnormal metabolism, biochemical disorders, structural and functional impairments of renal tubular epithelial cells, induce inflammatory reactions, and generate oxygen free radicals, which can cause, aggravate, or amplify the pathological changes of the kidney caused by chronic hypoxic injury [8,9]. Therefore, ischemia and hypoxia play a very important role in the occurrence and development of kidney disease.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of SP1 restores autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway

et al. 2021

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Background Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. SP1, a well-known transcription factor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes. However, the underlying mechanism of SP1 in these pathological processes remain largely unknown. Methods An in vitro HK-2 cells with anoxia-reoxygenation injury model (In vitro simulated ischemic injury disease) and an in vivo rat renal ischemia-reperfusion injury model were used in this study. The expression levels of SP1, miR-205 and PTEN were detected by RT-qPCR, and the protein expression levels of SP1, p62, PTEN, AKT, p-AKT, LC3II, LC3I and Beclin-1 were assayed by western blot. Cell proliferation was assessed by MTT assay, and the cell apoptosis was detected by flow cytometry. The secretions of IL-6 and TNF-α were detected by ELISA. The targeted relationship between miR-205 and PTEN was confirmed by dual luciferase report assay. The expression and positioning of LC-3 were observed by immunofluorescence staining. TUNEL staining was used to detect cell apoptosis and immunohistochemical analysis was used to evaluate the expression of SP1 in renal tissue after ischemia-reperfusion injury in rats. Results The expression of PTEN was upregulated while SP1 and miR-205 were downregulated in renal ischemia-reperfusion injury. Overexpression of SP1 protected renal tubule cell against injury induced by ischemia-reperfusion via miR-205/PTEN/Akt pathway mediated autophagy. Overexpression of SP1 attenuated renal ischemia-reperfusion injury in rats. Conclusions SP1 overexpression restored autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

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