Long-term Sequelae from Acute Kidney Injury: Potential Mechanisms for the Observed Poor Renal Outcomes

Varrier, Matt; Forni, Lui G.; Ostermann, Marlies

doi:10.1007/978-3-319-13761-2_28

Cited by 2 publications

(2 citation statements)

References 74 publications

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“…This is independent of renal-function recovery, based on routinely used parameters such as serum-creatinine (SCr) levels or estimated glomerular filtration rate (eGFR) (9). Further to this, AKI is an important contributor towards development of Chronic Kidney Disease (CKD) (10). AKI-related treatment cost is significant; in the United Kingdom (UK) alone, AKI-treatment costs £620 million annually (11).…”

Section: Introductionmentioning

confidence: 99%

Pre-operative Functional Cardiovascular Reserve Is Associated with Acute Kidney Injury after Intervention

Saratzis

Shakespeare

Jones

et al. 2017

European Journal of Vascular and Endovascular Surgery

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What this paper addsThe impact of cardiovascular reserve on acute kidney injury (AKI) after endovascular surgery remains unclear, mostly due to the difficulties in assessing cardiovascular reserve. We are still unsure whether AKI is related mostly to pre-existing occult co-morbidities, such as cardiovascular disease, or procedure-related parameters. Hence, developing an adequate renoprotective strategy is not an easy task. In this analysis, we have shown that development of AKI after intervention is associated with pre-operative cardiovascular reserve, independent of other risk-factors and procedural parameters. This offers insight in what drives AKI development after endovascular intervention and where/how preventative measures should focus.

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Section: Introductionmentioning

confidence: 99%

Pre-operative Functional Cardiovascular Reserve Is Associated with Acute Kidney Injury after Intervention

Saratzis

Shakespeare

Jones

et al. 2017

European Journal of Vascular and Endovascular Surgery

View full text Add to dashboard Cite

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“…Effectively controlling the pathogenesis of CKD, such as chronic glomerulonephritis, diabetic nephropathy, lupus nephritis, hypertensive nephropathy, and interstitial nephritis, has a clearly protective effect on delaying the progress of CKD. Recently, many studies have indicated that AKI could also induce CKD [16][17][18][19][20][21]. Patients with mild to moderate AKI often experience "adaptive repair" with repaired kidney function, while patients with severe AKI often bear "maladaptive repair" resulting in reduced kidney function.…”

Section: Discussionmentioning

confidence: 99%

Indoleamine-2,3-Dioxygenase Activates Wnt/β-Catenin Inducing Kidney Fibrosis after Acute Kidney Injury

et al. 2021

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Introduction: As disorder of tryptophan metabolism is common in CKD, the rate-limiting enzyme of tryptophan, indoleamine-2,3-dioxygenase (IDO), has been reported to be involved in CKD, while the accurate mechanism remains unknown. This study was designed to explore correlations between IDO and kidney fibrosis after ischemia-reperfusion injury (IRI). Methods: Wild-type (WT) mice and IDO knockout (IDO−/−) mice were divided into the sham group and acute kidney injury (AKI) group. Mice in the sham group underwent dorsal incision and exposure of renal pedicle without clamping renal artery, while mice in the AKI group received unique renal artery IRI, and the contralateral kidney was removed at day 13 after IRI. Blood and IRI kidneys were collected at day 14. Kidney function was analyzed by measuring serum Cr and BUN. Morphology was analyzed by tissue periodic acid-Schiff (PAS) staining and Masson staining. Further, fibrosis markers and Wnt/β-catenin pathway proteins were determined by Western blot. Prostaglandin E2 (PGE2) was administrated for 2 weeks after the IRI mice model was established to observe whether it ameliorates kidney fibrosis after IRI. Results: WT AKI mice revealed elevated expression of IDO compared with WT sham mice. Kidney function of IDO−/− AKI mice showed better than that of WT AKI mice. PAS staining exhibited less loss of tubular epithelial cells and atrophy tubules in IDO−/− AKI mice. Furthermore, kidney fibrosis areas and the expressions of fibrosis markers, including α-SMA, fibronectin, and vimentin, were increased in WT AKI mice. In addition, GSK-3β and β-catenin were significantly declined in IDO−/− AKI mice. On top of that, PGE2 administration revealed inhibited IDO expression and that reducing GSK-3β and β-catenin resulting in lower expressions of α-SMA, fibronectin, and vimentin in WT AKI mice. Conclusions: IRI could increase IDO expression to activate Wnt/β-catenin pathway resulting kidney fibrosis. PGE2 could ameliorate kidney fibrosis via inhibiting IDO expression.

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Long-term Sequelae from Acute Kidney Injury: Potential Mechanisms for the Observed Poor Renal Outcomes

Abstract: This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2015 and co-published as a series in Critical Care. Other articles in the series can be found online at

Cited by 2 publications

References 74 publications

Pre-operative Functional Cardiovascular Reserve Is Associated with Acute Kidney Injury after Intervention

Pre-operative Functional Cardiovascular Reserve Is Associated with Acute Kidney Injury after Intervention

Indoleamine-2,3-Dioxygenase Activates Wnt/β-Catenin Inducing Kidney Fibrosis after Acute Kidney Injury

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