ArticleKidney international2016
Combined iron sucrose and protoporphyrin treatment protects against ischemic and toxin-mediated acute renal failure.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- RBT-1, a "preconditioning" agent, mitigates syndecan-1 shedding in patients undergoing "on pump" cardiac surgery and following experimental AKI.Physiological reports · 2025Trial
- Patient reported outcome measures and cardiovascular outcomes following high dose modern intravenous iron in non-dialysis dependent chronic kidney disease: secondary analysis of ExplorIRON-CKD.Scientific reports · 2023Trial
- The NRF2 stimulating agent, tin protoporphyrin, activates protective cytokine pathways in healthy human subjects and in patients with chronic kidney disease.Physiological reports · 2020Trial
- A pH-responsive ultrasmall Fe-kaempferol nanoplatform ameliorates acute kidney injury by enhancing efferocytosis and metabolic reprogramming.Journal of nanobiotechnology · 2026Article
- Veverimer, a Nonabsorbed Gastrointestinal Tract HCl Binder, Decreases Renal Ammoniagenesis and Mitigates Nephrotoxic Serum Nephritis.Kidney360 · 2025Article
- ISL1-overexpressing BMSCs attenuate renal ischemia-reperfusion injury by suppressing apoptosis and oxidative stress through the paracrine action.Cellular and molecular life sciences : CMLS · 2024Article
- Effects of RBT-1 on preconditioning response biomarkers in patients undergoing coronary artery bypass graft or heart valve surgery: a multicentre, double-blind, randomised, placebo-controlled phase 2 trial.EClinicalMedicine · 2024Article
- Animal models of kidney iron overload and ferroptosis: a review of the literature.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Review
- Heme Proteins and Kidney Injury: Beyond Rhabdomyolysis.Kidney360 · 2022Review
- Oxidant- induced preconditioning: A pharmacologic approach for triggering renal 'self defense'.Physiological reports · 2022Review
- Early loss of glutathione -s- transferase (GST) activity during diverse forms of acute renal tubular injury.Physiological reports · 2022Article
- Renal hypoxia-HIF-PHD-EPO signaling in transition metal nephrotoxicity: friend or foe?Archives of toxicology · 2022Review
- Modulation of gentamicin-induced acute kidney injury by myo-inositol oxygenase via the ROS/ALOX-12/12-HETE/GPR31 signaling pathway.JCI insight · 2022Article
- Article
- New insights into the role of heme oxygenase-1 in acute kidney injury.Kidney research and clinical practice · 2020Review
- The multifaceted role of iron in renal health and disease.Nature reviews. Nephrology · 2020Review
- Serum alpha 1-antitrypsin predicts severe acute kidney injury after cardiac surgery.Journal of thoracic disease · 2019Article
- Overview of iron metabolism in health and disease.Hemodialysis international. International Symposium on Home Hemodialysis · 2017Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Tissue preconditioning, whereby various short-term stressors initiate organ resistance to subsequent injury, is well recognized. However, clinical preconditioning of the kidney for protection against acute kidney injury (AKI) has not been established. Here we tested whether a pro-oxidant agent, iron sucrose, combined with a protoporphyrin (Sn protoporphyrin), can induce preconditioning and protect against acute renal failure. Mice were pretreated with iron sucrose, protoporphyrin, cyanocobalamin, iron sucrose and protoporphyrin, or iron sucrose and cyanocobalamin. Eighteen hours later, ischemic, maleate, or glycerol models of AKI were induced, and its severity was assessed the following day (blood urea nitrogen, plasma creatinine concentrations; post-ischemic histology). Agent impact on cytoprotective gene expression (heme oxygenase 1, hepcidin, haptoglobin, hemopexin, α1-antitrypsin, α1-microglobulin, IL-10) was assessed as renal mRNA and protein levels. AKI-associated myocardial injury was gauged by plasma troponin I levels. Combination agent administration upregulated multiple cytoprotective genes and, unlike single agent administration, conferred marked protection against each tested model of acute renal failure. Heme oxygenase was shown to be a marked contributor to this cytoprotective effect. Preconditioning also blunted AKI-induced cardiac troponin release. Thus, iron sucrose and protoporphyrin administration can upregulate diverse cytoprotective genes and protect against acute renal failure. Associated cardiac protection implies potential relevance to both AKI and its associated adverse downstream effects.
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