ArticlePhysiological reports2022
Renal injury in cardiorenal syndrome type 1 is mediated by albumin.
Article in Physiological reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 6 citations in OpenAlex.
- Perioperative albumin versus other fluids to prevent cardiac surgery-associated kidney injury: a systematic review and meta-analysis of randomized trials.Critical care science · 2026Pooled it
- Alterations in the Plasma Protein Expression Pattern in Congenital Analbuminemia-A Systematic Review.Biomolecules · 2023Pooled it
- Kidney cell response to acute cardiorenal and isolated kidney ischemia-reperfusion injury.Physiological genomics · 2025Article
- Diagnostic value and utility of commonly used biomarkers of cardiac and renal function in cardiorenal syndromes: a narrative review.Biochemia medica · 2023Review
- From heart failure and kidney dysfunction to cardiorenal syndrome: TMAO may be a bridge.Frontiers in pharmacology · 2023Review
- Renal injury in cardiorenal syndrome type 1 is mediated by albumin.Physiological reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Cardiorenal syndrome type 1 (CRS-1) acute kidney injury (AKI) is a critical complication of acute cardiovascular disease but is poorly understood. AKI induces acute albuminuria. As chronic albuminuria is associated with worsening kidney disease and albumin has been implicated in tubular epithelial injury, we investigated whether albumin participates in CRS-1, and whether CRS-1 alters renal albumin handling. We report the role of albumin in in vivo and in vitro CRS-1 models. An established translational model, cardiac arrest and cardiopulmonary resuscitation (CA/CPR) induced severe acute albuminuria which correlated with tubular epithelial cell death. In vivo microscopy demonstrated CA/CPR-induced glomerular filtration of exogenous albumin, while administration of exogenous albumin after CA/CPR worsened AKI compared to iso-oncotic control. Increased albumin signal was observed in the proximal tubules of CA/CPR mice compared to sham. Comparison of albumin flux from tubular lumen to epithelial cells revealed saturated albumin transport within minutes of albumin injection after CA/CPR. In vitro, HK2 cells (human kidney tubular epithelial cells), exposed to oxygen-glucose deprivation were injured by albumin in a dose dependent fashion. This interference was unchanged by the tubular endocytic receptor megalin. In conclusion, CRS-1 alters albumin filtration and tubular uptake, leading to increased tubular exposure to albumin, which is injurious to tubular epithelial cells, worsening AKI. Our findings shed light on the pathophysiology of renal albumin and may guide interventions such as albumin resuscitation to improve CRS-1 outcomes. This investigation may have important translational relevance for patients that receive exogenous albumin as part of their CRS-1 treatment regimen.
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Registered trials
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