Literature review of the mechanisms of acute kidney injury secondary to acute liver injury

Platt, Esther; Klootwijk, Enriko; Salama, Alan D.; Davidson, Brian R; Robertson, Francis P.

doi:10.5527/wjn.v11.i1.13

Cited by 5 publications

(6 citation statements)

References 99 publications

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“…Much work suggests that the kidney is susceptible to hypoxic injury and the injury can be caused after exposure to hypoxia (Platt et al, 2022). Hypoxic precondition induces injury in human renal tubular epithelial cells (Hosohata et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

Arginine‐methylated c‐Myc affects mitochondrial mitophagy in mouse acute kidney injury via Slc25a24

Liu,

et al. 2024

Journal Cellular Physiology

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The transcription factor methylated c‐Myc heterodimerizes with MAX to modulate gene expression, and plays an important role in energy metabolism in kidney injury but the exact mechanism remains unclear. Mitochondrial solute transporter Slc25a24 imports ATP into mitochondria and is central to energy metabolism. Gene Expression Omnibus data analysis reveals Slc25a24 and c‐Myc are consistently upregulated in all the acute kidney injury (AKI) cells. Pearson correlation analysis also shows that Slc25a24 and c‐Myc are strongly correlated (⍴ > 0.9). Mutant arginine methylated c‐Myc (R299A and R346A) reduced its combination with MAX when compared with the wild type of c‐Myc. On the other hand, the Slc25a24 levels were also correspondingly reduced, which induced the downregulation of ATP production. The results promoted reactive oxygen species (ROS) production and mitophagy generation. The study revealed that the c‐Myc overexpression manifested the most pronounced mitochondrial DNA depletion. Additionally, the varied levels of mitochondrial proteins like TIM23, TOM20, and PINK1 in each group, particularly the elevated levels of PINK1 in AKI model groups and lower levels of TIM23 and TOM20 in the c‐Myc overexpression group, suggest potential disruptions in mitochondrial dynamics and homeostasis, indicating enhanced mitophagy or mitochondrial loss. Therefore, arginine‐methylated c‐Myc affects mouse kidney injury by regulating mitochondrial ATP and ROS, and mitophagy via Slc25a24.

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Section: Introductionmentioning

confidence: 99%

Arginine‐methylated c‐Myc affects mitochondrial mitophagy in mouse acute kidney injury via Slc25a24

Liu,

et al. 2024

Journal Cellular Physiology

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“…Renal ischemia reperfusion injury (IRI) referred to the condition in which blood flow was interrupted and its recovery led to increased renal insufficiency and tissue damage. It was also the most common cause of acute kidney injury (AKI) resulting in death in patients with renal disease, with high morbidity and mortality [ 1 ]. As a complex disease, numerous changes in molecular characteristics happened during IRI.…”

Section: Introductionmentioning

confidence: 99%

Identification of renal ischemia reperfusion injury-characteristic genes, pathways and immunological micro-environment features through bioinformatics approaches

Lv,

Fan,

et al. 2024

Aging

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Background: Biomarkers and pathways associated with renal ischemia reperfusion injury (IRI) had not been well unveiled. This study was intended to investigate and summarize the regulatory networks for related hub genes. Besides, the immunological micro-environment features were evaluated and the correlations between immune cells and hub genes were also explored. Methods: GSE98622 containing mouse samples with multiple IRI stages and controls was collected from the GEO database. Differentially expressed genes (DEGs) were recognized by the R package limma, and the GO and KEGG analyses were conducted by DAVID. Gene set variation analysis (GSVA) and weighted gene coexpression network analysis (WGCNA) had been implemented to uncover changed pathways and gene modules related to IRI. Besides the known pathways such as apoptosis pathway, metabolic pathway, and cell cycle pathways, some novel pathways were also discovered to be critical in IRI. A series of novel genes associated with IRI was also dug out. An IRI mouse model was constructed to validate the results. Results: The well-known IRI marker genes (Kim1 and Lcn2) and novel hub genes (Hbegf, Serpine2, Apbb1ip, Trip13, Atf3, and Ncaph) had been proved by the quantitative real-time polymerase chain reaction (qRT-PCR). Thereafter, miRNAs targeted to the dysregulated genes were predicted and the miRNA-target network was constructed. Furthermore, the immune infiltration for these samples was predicted and the results showed that macrophages infiltrated to the injured kidney to affect the tissue repair or fibrosis. Hub genes were significantly positively or negatively correlated with the macrophage abundance indicating they played a crucial role in macrophage infiltration. Conclusions: Consequently, the pathways, hub genes, miRNAs, and the immune microenvironment may explain the mechanism of IRI and might be the potential targets for IRI treatments.

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“…Though the mechanism of kidney injury (KI) in ALF is often attributed to kidney hypoperfusion this area remains understudied 7,8 . Several key differences in KI associated with ALF compared to hepatorenal syndrome (HRS) have been reported, including high urinary sodium and features of glomerular injury such as hematuria and proteinuria 9–11 . A better understanding of KI in the setting of ALF is crucial because the specific pathophysiology of KI in patients with liver disease can influence the likelihood of kidney recovery 12 …”

Section: Introductionmentioning

confidence: 99%

“…7,8 Several key differences in KI associated with ALF compared to hepatorenal syndrome (HRS) have been reported, including high urinary sodium and features of glomerular injury such as hematuria and proteinuria. [9][10][11] A better understanding of KI in the setting of ALF is crucial because the specific pathophysiology of KI in patients with liver disease can influence the likelihood of kidney recovery. 12 It is well established that both AKI and chronic kidney disease (CKD) in cirrhosis is increasingly prevalent and associated with increased mortality and post-liver transplant end-stage kidney disease (ESKD).…”

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confidence: 99%

Kidney injury and status 1 liver transplantation: Outcomes, kidney function, and listing for kidney transplantation

Cloonan

Westphal

et al. 2023

Clinical Transplantation

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Background Effects of kidney injury (KI) at the time of liver transplantation (LT) for acute liver failure (ALF) remain poorly described. We hypothesized that patients with ALF and KI who undergo LT have persistent post‐transplant KI, inferior survival, and increased rate of kidney transplantation (KT). Methods The US Scientific Registry of Transplant Recipients database was queried for patients transplanted with status 1 listing for LT between 2002 and 2021. KI was defined as estimated glomerular filtration rate (eGFR) ≤ 30 mL/min/1.73 m2 or dialysis in the week prior to LT. Outcomes evaluated were post‐LT eGFR, listing for subsequent KT, and overall survival (OS) after LT. Results A total of 2984 patients underwent LT for ALF with 1241 (41.6%) having KI. KI patients had lower eGFR at 6 months post‐LT (57.8 vs. 68.7, p < .001) that persisted out to 5 years (59.9 vs. 69.7, p < .001). KI patients were more likely to be listed for KT (4.3% vs. 1.9%, p < .001) and undergo listing sooner after LT (.8 vs. 3.7 years, p < .001). Patients without KI had higher adjusted post‐transplant OS compared to those with KI (HR .75, p < .001). Conclusion KI in the setting of ALF portends a worse prognosis for both kidney recovery and OS.

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Literature review of the mechanisms of acute kidney injury secondary to acute liver injury

Cited by 5 publications

References 99 publications

Arginine‐methylated c‐Myc affects mitochondrial mitophagy in mouse acute kidney injury via Slc25a24

Arginine‐methylated c‐Myc affects mitochondrial mitophagy in mouse acute kidney injury via Slc25a24

Identification of renal ischemia reperfusion injury-characteristic genes, pathways and immunological micro-environment features through bioinformatics approaches

Kidney injury and status 1 liver transplantation: Outcomes, kidney function, and listing for kidney transplantation

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