ReviewNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2013
'Biologic memory' in response to acute kidney injury: cytoresistance, toll-like receptor hyper-responsiveness and the onset of progressive renal disease.
Review in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed.
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- The Role of Mitochondrial Dysfunction in Sepsis-Associated Acute Kidney Injury: A Narrative Review.Drug design, development and therapy · 2025Review
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Update on persistent acute kidney injury in critical illnesses.Clinical kidney journal · 2023Review
- Sepsis-associated acute kidney injury: consensus report of the 28th Acute Disease Quality Initiative workgroup.Nature reviews. Nephrology · 2023Review
- Oxidant- induced preconditioning: A pharmacologic approach for triggering renal 'self defense'.Physiological reports · 2022Review
- The Hippo pathway and its correlation with acute kidney injury.Zoological research · 2022Review
- Epigenetic memory contributing to the pathogenesis of AKI-to-CKD transition.Frontiers in molecular biosciences · 2022Review
- DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation.iScience · 2021Article
- Metabolic Reprogramming and Host Tolerance: A Novel Concept to Understand Sepsis-Associated AKI.Journal of clinical medicine · 2021Review
- Anaesthesia-Induced Transcriptomic Changes in the Context of Renal Ischemia Uncovered by the Use of a Novel Clamping Device.International journal of molecular sciences · 2021Article
- The dysregulation of metabolic pathways and induction of the pentose phosphate pathway in renal ischaemia-reperfusion injury.The Journal of pathology · 2021Article
- Inhibition of aerobic glycolysis alleviates sepsis‑induced acute kidney injury by promoting lactate/Sirtuin 3/AMPK‑regulated autophagy.International journal of molecular medicine · 2021Article
- Pathophysiology of unilateral ischemia-reperfusion injury: importance of renal counterbalance and implications for the AKI-CKD transition.American journal of physiology. Renal physiology · 2020Article
- Impact on Outcomes across KDIGO-2012 AKI Criteria According to Baseline Renal Function.Journal of clinical medicine · 2019Article
- Mitochondria in Sepsis-Induced AKI.Journal of the American Society of Nephrology : JASN · 2019Review
- Kidney and Brain, an Unbroken Chain.American journal of respiratory and critical care medicine · 2017Article
- Between chromatin and SNPs: genetic variability and the susceptibility to acute kidney injury.Critical care (London, England) · 2017Article
- Beneficial Effects ofJournal of the American Society of Nephrology : JASN · 2017Article
- Metabolic reprogramming and tolerance during sepsis-induced AKI.Nature reviews. Nephrology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Following the induction of ischemic or toxin-mediated acute kidney injury (AKI), cellular adaptations occur that 're-program' how the kidney responds to future superimposed insults. This re-programming is not simply a short-lived phenomenon; rather it can persist for many weeks, implying that a state of 'biologic memory' has emerged. These changes can be both adaptive and maladaptive in nature and they can co-exist in time. A beneficial adaptation is the emergence of acquired cytoresistance, whereby a number of physiologic responses develop that serve to protect the kidney against further ischemic or nephrotoxic attack. Conversely, some changes are maladaptive, such as a predisposition to Gram-negative or Gram-positive bacteremia due to a renal tubular up-regulation of toll-like receptor responses. This latter change culminates in exaggerated cytokine production, and with efflux into the systemic circulation, extra-renal tissue injury can result (so-called 'organ cross talk'). Another maladaptive response is a persistent up-regulation of pro-inflammatory, pro-fibrotic and vasoconstrictive genes, culminating in progressive renal injury and ultimately end-stage renal failure. The mechanisms by which this biologic re-programming, or biologic memory, is imparted remain subjects for considerable debate. However, injury-induced, and stable, epigenetic remodeling at pro-inflammatory/pro-fibrotic genes seems likely to be involved. The goal of this editorial is to highlight that the so-called 'maintenance phase' of acute renal failure is not a static one, somewhere between injury induction and the onset of repair. Rather, this period is one in which the induction of 'biologic memory' can ultimately impact renal functional recovery, extra-renal injury and the possible transition of AKI into chronic, progressive renal disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.