ArticleThe Journal of clinical investigation2018
Renal immune surveillance and dipeptidase-1 contribute to contrast-induced acute kidney injury.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 104 citations in OpenAlex.
- Methylmalonic acid as a ferroptosis-derived danger signal: activation of the PI3K-NF-κB pathway drives M1 macrophage polarization in renal ischemia-reperfusion injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Uromodulin p.His36Tyr promotes macrophage pyroptosis via App-Cd74 signaling to drive renal inflammation in ADTKD.Nature communications · 2026Article
- SGLT2 Inhibitors Mitigate Contrast-Induced Acute Kidney Injury in Diabetes: Clinical and Experimental Evidence.International journal of molecular sciences · 2026Article
- NLRP3 inflammasome in acute kidney injury: molecular mechanisms, post-translational regulation, and immunotherapeutic potential.Frontiers in immunology · 2026Review
- Crosstalk between macrophages and adjacent cells in AKI to CKD transition.Renal failure · 2025Review
- It is not only fluids: the impact of hydration protocols used for the prevention of contrast nephropathy on renal oxygenation.Renal failure · 2025Review
- Dimethyl fumarate ameliorated pyroptosis in contrast-induced acute renal injury by regulating endoplasmic reticulum stress and JAK2-STAT3 pathway.Renal failure · 2025Article
- Preoperative systemic immune-inflammation index as a predictor of contrast-induced acute kidney injury in coronary artery disease: a multicenter cohort study.Renal failure · 2025Article
- Beyond Blood Pressure: Emerging Pathways and Precision Approaches in Hypertension-Induced Kidney Damage.International journal of molecular sciences · 2025Review
- Integrated single-cell transcriptomic map of pig kidney cells across various periods and anatomical sites.Zoological research · 2025Article
- Irisin-mediated muscle-renal crosstalk as a protective mechanism against contrast-induced acute kidney injury via cGAS-STING signalling inhibition.Clinical and translational medicine · 2025Article
- Predictive Significance of the Monocyte-to-High-Density Lipoprotein Cholesterol Ratio in Post-Percutaneous Coronary Intervention Contrast-Induced Nephropathy Among Patients with Coronary Artery Disease.Journal of inflammation research · 2025Article
- N-acetylcysteine in Kidney Disease: Molecular Mechanisms, Pharmacokinetics, and Clinical Effectiveness.Kidney international reports · 2024Review
- Patient Preferences and Priorities for the Design of an Acute Kidney Injury Prevention Trial: Findings from a Consensus Workshop.Kidney360 · 2024Article
- Review
- Unveiling the Mysteries of Contrast-Induced Acute Kidney Injury: New Horizons in Pathogenesis and Prevention.Toxics · 2024Review
- Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics.Cell death discovery · 2024Review
- JQ1 attenuates contrast-induced acute kidney injury through the upregulation of autophagy and inhibition of inflammation.International urology and nephrology · 2024Article
- Signal pathways involved in contrast-induced acute kidney injury.Frontiers in physiology · 2024Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiographic contrast agents cause acute kidney injury (AKI), yet the underlying pathogenesis is poorly understood. Nod-like receptor pyrin containing 3-deficient (Nlrp3-deficient) mice displayed reduced epithelial cell injury and inflammation in the kidney in a model of contrast-induced AKI (CI-AKI). Unexpectedly, contrast agents directly induced tubular epithelial cell death in vitro that was not dependent on Nlrp3. Rather, contrast agents activated the canonical Nlrp3 inflammasome in macrophages. Intravital microscopy revealed diatrizoate (DTA) uptake within minutes in perivascular CX3CR1+ resident phagocytes in the kidney. Following rapid filtration into the tubular luminal space, DTA was reabsorbed and concentrated in tubular epithelial cells via the brush border enzyme dipeptidase-1 in volume-depleted but not euvolemic mice. LysM-GFP+ macrophages recruited to the kidney interstitial space ingested contrast material transported from the urine via direct interactions with tubules. CI-AKI was dependent on resident renal phagocytes, IL-1, leukocyte recruitment, and dipeptidase-1. Levels of the inflammasome-related urinary biomarkers IL-18 and caspase-1 were increased immediately following contrast administration in patients undergoing coronary angiography, consistent with the acute renal effects observed in mice. Taken together, these data show that CI-AKI is a multistep process that involves immune surveillance by resident and infiltrating renal phagocytes, Nlrp3-dependent inflammation, and the tubular reabsorption of contrast via dipeptidase-1.
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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.