ArticleBMC nephrology2013
Triggering of suicidal erythrocyte death by uremic toxin indoxyl sulfate.
Article in BMC nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 78 citations in OpenAlex.
- Current understanding of eryptosis: mechanisms, physiological functions, role in disease, pharmacological applications, and nomenclature recommendations.Cell death & disease · 2025Review
- Review
- Eryptosis in renal anemia: mechanisms, clinical implications, and therapeutic targeting.Frontiers in pharmacology · 2025Review
- Influence of Inflammation on Red Blood Cell Lifespan in Peritoneal Dialysis Patients.Journal of clinical medicine · 2024Article
- Review
- The Role of the Gut Microbiota in Complications among Hemodialysis Patients.Microorganisms · 2024Review
- Stimulation of Calcium/NOS/CK1α Signaling by Cedrol Triggers Eryptosis and Hemolysis in Red Blood Cells.Yonago acta medica · 2024Article
- Iron Metabolism and Inflammatory Mediators in Patients with Renal Dysfunction.International journal of molecular sciences · 2024Review
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Effect of roxadustat on red blood cell lifespan in patients with long-term haemodialysis: a single-centre, prospective, single-arm study.Clinical kidney journal · 2023Article
- The Effect of Synbiotic Supplementation on Uremic Toxins, Oxidative Stress, and Inflammation in Hemodialysis Patients-Results of an Uncontrolled Prospective Single-Arm Study.Medicina (Kaunas, Lithuania) · 2023Article
- Eryptosis in Patients with Chronic Kidney Disease: A Possible Relationship with Oxidative Stress and Inflammatory Markers.Journal of clinical medicine · 2022Article
- Research progress on the relationship between IS and kidney disease and its complications.International urology and nephrology · 2022Review
- In Vitro Induction of Eryptosis by Uremic Toxins and Inflammation Mediators in Healthy Red Blood Cells.Journal of clinical medicine · 2022Article
- Indoxyl sulfate impairsExperimental biology and medicine (Maywood, N.J.) · 2022Article
- Indoxyl Sulfate Induces Oxidative Changes in Plasma and Hemolysate.Molecules (Basel, Switzerland) · 2022Article
- Is there an association between the plasma levels of uremic toxins from gut microbiota and anemia in patients on hemodialysis?International urology and nephrology · 2022Article
- Hemodiafiltration improves red blood cell lifespan in patients with end-stage renal disease.Seminars in dialysis · 2022Article
- Red blood cell lifespan in long-term hemodialysis patients treated with roxadustat or recombinant human erythropoietin.Renal failure · 2021Observational
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnemia in end stage renal disease is attributed to impaired erythrocyte formation due to erythropoietin and iron deficiency. On the other hand, end stage renal disease enhances eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and phosphatidylserine-exposure at the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca(2+)-activity ([Ca(2+)]i) and by ceramide, which sensitizes erythrocytes to [Ca2+]i. Mechanisms triggering eryptosis in endstage renal disease remained enigmatic. The present study explored the effect of indoxyl sulfate, an uremic toxin accumulated in blood of patients with chronic kidney disease.
methodsCell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, ceramide abundance by specific antibodies, hemolysis from hemoglobin release, and [Ca(2+)]i from Fluo3-fluorescence.
resultsA 48 hours exposure to indoxyl sulfate significantly increased [Ca(2+)]i (≥ 300 μM), significantly decreased forward scatter (≥ 300 μM) and significantly increased annexin-V-binding (≥ 50 μM). Indoxyl sulfate (150 μM) induced annexin-V-binding was virtually abolished in the nominal absence of extracellular Ca(2+). Indoxyl sulfate (150 μM) further enhanced ceramide abundance.
conclusionIndoxyl sulfate stimulates suicidal erythrocyte death or eryptosis, an effect in large part due to stimulation of extracellular Ca(2+)entry with subsequent stimulation of cell shrinkage and cell membrane scrambling.
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.