scholarly journals Molecular Mechanisms of the Acute Kidney Injury to Chronic Kidney Disease Transition: An Updated View

2019 ◽  
Vol 20 (19) ◽  
pp. 4941 ◽  
Author(s):  
Francesco Guzzi ◽  
Luigi Cirillo ◽  
Rosa Maria Roperto ◽  
Paola Romagnani ◽  
Elena Lazzeri
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Kidney Injury ◽  
Small Population ◽  
Acute Injury ◽  
Tubular Necrosis ◽  
Kidney Disease Progression ◽  
Renal Progenitors

Increasing evidence has demonstrated the bidirectional link between acute kidney injury (AKI) and chronic kidney disease (CKD) such that, in the clinical setting, the new concept of a unified syndrome has been proposed. The pathophysiological reasons, along with the cellular and molecular mechanisms, behind the ability of a single, acute, apparently self-limiting event to drive chronic kidney disease progression are yet to be explained. This acute injury could promote progression to chronic disease through different pathways involving the endothelium, the inflammatory response and the development of fibrosis. The interplay among endothelial cells, macrophages and other immune cells, pericytes and fibroblasts often converge in the tubular epithelial cells that play a central role. Recent evidence has strengthened this concept by demonstrating that injured tubules respond to acute tubular necrosis through two main mechanisms: The polyploidization of tubular cells and the proliferation of a small population of self-renewing renal progenitors. This alternative pathophysiological interpretation could better characterize functional recovery after AKI.

scholarly journals Low-dose hydralazine prevents fibrosis in a murine model of acute kidney injury–to–chronic kidney disease progression

2017 ◽  
Vol 91 (1) ◽  
pp. 157-176 ◽  
Author(s):  
Björn Tampe ◽  
Ulrike Steinle ◽  
Désirée Tampe ◽  
Julienne L. Carstens ◽  
Peter Korsten ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Disease Progression ◽  
Murine Model ◽  
Low Dose ◽  
Kidney Injury ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression

scholarly journals Vitamin D Deficiency Aggravates Chronic Kidney Disease Progression after Ischemic Acute Kidney Injury

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107228 ◽  
Author(s):  
Janaína Garcia Gonçalves ◽  
Ana Carolina de Bragança ◽  
Daniele Canale ◽  
Maria Heloisa Massola Shimizu ◽  
Talita Rojas Sanches ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Disease Progression ◽  
Vitamin D Deficiency ◽  
Kidney Injury ◽  
Chronic Kidney Disease Progression ◽  
Kidney Disease Progression ◽  
Ischemic Acute Kidney Injury

scholarly journals Orai1: A New Therapeutic Target for the Acute Kidney Injury-to-Chronic Kidney Disease Transition

Nephron ◽  
2021 ◽  
pp. 1-4
Author(s):  
David P. Basile ◽  
Jason A. Collett
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Acute Injury ◽  
Chronic Kidney Injury ◽  
Sustained Increase

This review focuses on the potential mediation in the acute kidney injury (AKI)-to-chronic kidney disease (CKD) transition by lymphocytes. We highlight evidence that lymphocytes, particularly Th17 cells, modulate the severity of both acute injury and chronic kidney disease. Th17 cells are strongly influenced by the activity of the store-operated Ca<sup>2+</sup>channel Orai1, which is upregulated on lymphocytes in animal models of AKI. Inhibition of this channel attenuates both acute and chronic kidney injury in rodent models. In addition, Oria1+ cells are increased in peripheral blood of patients with AKI. Similarly, peripheral blood cells manifest an early and sustained increase in Orai1 expression in a rat model of ischemia/reperfusion, suggesting that blood cell Orai1 may represent a marker informing potential Th17 activity in the setting of AKI or the AKI-to-CKD transition.

scholarly journals Huaier Extract Attenuates Acute Kidney Injury to Chronic Kidney Disease Transition by Inhibiting Endoplasmic Reticulum Stress and Apoptosis via miR-1271 Upregulation

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Jing-Ying Zhao ◽  
Yu-Bin Wu
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury

Endoplasmic reticulum stress (ERS) is strongly associated with acute kidney injury (AKI) to chronic kidney disease (CKD) transition. Huaier extract (HE) protects against kidney injury; albeit, the underlying mechanism is unknown. We hypothesized that HE reduces kidney injury by inhibiting ERS. In this study, using an AKI-CKD mouse model of ischemia-reperfusion injury (IRI), we evaluated the effect of HE on AKI-CKD transition. We also explored the underlying molecular mechanisms in this animal model and in the HK-2 human kidney cell line. The results showed that HE treatment improved the renal function, demonstrated by a significant decrease in serum creatinine levels after IRI. HE appreciably reduced the degree of kidney injury and fibrosis and restored the expression of the microRNA miR-1271 after IRI. Furthermore, HE reduced the expression of ERS markers glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) and inhibited apoptosis in the IRI group. This in vivo effect was supported by in vitro results in which HE inhibited apoptosis and decreased the expression of CHOP and GRP78 induced by ERS. We demonstrated that CHOP is a target of miR-1271. In conclusion, HE reduces kidney injury, probably by inhibiting apoptosis and decreasing the expression of GRP78 and CHOP via miR-1271 upregulation.

Extended Mortality and Chronic Kidney Disease After Septic Acute Kidney Injury

2018 ◽  
Vol 35 (6) ◽  
pp. 527-535 ◽  
Author(s):  
Horng-Ruey Chua ◽  
Weng-Kin Wong ◽  
Venetia Huiling Ong ◽  
Dipika Agrawal ◽  
Anantharaman Vathsala ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Simplified Acute Physiology Score ◽  
Cardiac Events ◽  
Ckd Progression ◽  
Septic Acute Kidney Injury ◽  
Adverse Cardiac Events ◽  
Kidney Disease Progression

Purpose: To evaluate 1-year mortality in patients with septic acute kidney injury (AKI) and to determine association between initial AKI recovery patterns ( reversal within 5 days, beyond 5 days but recovery, or nonrecovery) and chronic kidney disease (CKD) progression. Methods: Prospective observational study, with retrospective evaluation of initial nonconsenters, of critically ill patients with septic AKI. Results: We studied 207 patients (age, mean [SD]: 64 [16] years, 39% males), of which 56 (27%), 18 (9%), and 9 (4%) died in intensive care unit (ICU), post-ICU in hospital, and posthospitalization, respectively. Infections (including pneumonia) and major adverse cardiac events accounted for 64% and 12% of deaths, respectively. Factors independently associated with 1-year mortality include older age, ischemic heart disease, higher Simplified Acute Physiology Score II, central nervous system or musculoskeletal primary infections, higher daily fluid balance (FB), and frusemide administration during ICU stay (all P < .05). Among 63 patients receiving renal replacement therapy (RRT), hospital mortality was higher with cumulative median FB >8 L versus ≤8 L at RRT initiation (57% vs 24%; P = .009); there was trend for less ICU- and RRT-free days at day 28 in patients with higher FB pre-RRT ( P = NS). Chronic kidney disease progression over 1 year developed in 21%, 30%, and 79% of 105 initial survivors with AKI reversal, recovery, and nonrecovery, respectively ( P < .001). Acute kidney injury nonrecovery during hospitalization independently predicted CKD progression ( P = .001). Conclusions: Patients with septic AKI had 40% 1-year mortality, mainly associated with infections. High FB and frusemide administration were modifiable risk factors. Risk of CKD progression is high especially with initial AKI nonrecovery.

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