ArticleCritical care (London, England)2010
Protective effect of resin adsorption on septic plasma-induced tubular injury.
Article in Critical care (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 48 citations in OpenAlex.
- High-flux hemodialysis with polymethylmethacrylate membranes reduces soluble CD40L, a mediator of cardiovascular disease in uremia.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Trial
- High-volume hemofiltration does not protect human kidney endothelial and tubular epithelial cells from septic plasma-induced injury.Scientific reports · 2024Article
- Extracorporeal blood purification therapies for sepsis-associated acute kidney injury in critically ill patients: expert opinion from the SIAARTI-SIN joint commission.Journal of nephrology · 2023Article
- Article
- Review
- Acute Tubular Injury is Associated With Severe Traumatic Brain Injury: in Vitro Study on Human Tubular Epithelial Cells.Scientific reports · 2019Observational
- Exosomes and microvesicles in normal physiology, pathophysiology, and renal diseases.Pediatric nephrology (Berlin, Germany) · 2019Review
- Lipopolysaccharide Mediates the Destruction of Intercellular Tight Junction among Renal Tubular Epithelial Cells via RhoT1/SMAD-4/JAM-3 Pathway.International journal of medical sciences · 2018Article
- Hemoadsorption corrects hyperresistinemia and restores anti-bacterial neutrophil function.Intensive care medicine experimental · 2017Article
- The Role of Endotoxin in the Setting of Cardiorenal Syndrome Type 5.Cardiorenal medicine · 2017Review
- Extracellular vesicles in renal disease.Nature reviews. Nephrology · 2017Review
- Continuous Renal Replacement Therapy: Forty-year Anniversary.The International journal of artificial organs · 2017Article
- Cellular apoptosis in the cardiorenal axis.Heart failure reviews · 2016Review
- IMMUNE CELL PHENOTYPE AND FUNCTION IN SEPSIS.Shock (Augusta, Ga.) · 2016Review
- Effect of therapeutic plasma exchange on plasma levels and total removal of adipokines and inflammatory markers.BMC obesity · 2015Article
- Septic acute kidney injury: molecular mechanisms and the importance of stratification and targeting therapy.Critical care (London, England) · 2014Review
- Epithelial transport during septic acute kidney injury.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2014Review
- Heart-kidney crosstalk and role of humoral signaling in critical illness.Critical care (London, England) · 2014Review
- Monocytes, peripheral blood mononuclear cells, and THP-1 cells exhibit different cytokine expression patterns following stimulation with lipopolysaccharide.Mediators of inflammation · 2013Article
- Resveratrol-poor red wines modulate SIRT1 in human renal cells.Plant foods for human nutrition (Dordrecht, Netherlands) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionA pro-apoptotic effect of circulating mediators on renal tubular epithelial cells has been involved in the pathogenesis of sepsis-associated acute kidney injury (AKI). Adsorption techniques have been showed to efficiently remove inflammatory cytokines from plasma. The aim of this study was to evaluate the efficiency of the hydrophobic resin Amberchrom CG161 M to adsorb from septic plasma soluble mediators involved in tubular injury.
methodsWe enrolled in the study 10 critically ill patients with sepsis-associated AKI and we evaluated the effects of their plasma on granulocyte adhesion, apoptosis and functional alterations of cultured human kidney tubular epithelial cells. We established an in vitro model of plasma adsorption and we studied the protective effect of unselective removal of soluble mediators by the Amberchrom CG161 M resin on septic plasma-induced tubular cell injury.
resultsPlasma from septic patients induced granulocyte adhesion, apoptosis and altered polarity in tubular cells. Plasma adsorption significantly decreased these effects and abated the concentrations of several soluble mediators. The inhibition of granulocyte adhesion to tubular cells was associated with the down-regulation of ICAM-1 and CD40. Resin adsorption inhibited tubular cell apoptosis induced by septic plasma by down-regulating the activation of caspase-3, 8, 9 and of Fas/death receptor-mediated signalling pathways. The alteration of cell polarity, morphogenesis, protein reabsorption and the down-regulation of the tight junction molecule ZO-1, of the sodium transporter NHE3, of the glucose transporter GLUT-2 and of the endocytic receptor megalin all induced by septic plasma were significantly reduced by resin adsorption.
conclusionsSeptic plasma induced a direct injury of tubular cells by favouring granulocyte adhesion, by inducing cell apoptosis and by altering cell polarity and function. All these biological effects are related to the presence of circulating inflammatory mediators that can be efficiently removed by resin adsorption with a consequent limitation of tubular cell injury.
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.