ReviewBiology2023
Renal Microcirculation Injury as the Main Cause of Ischemic Acute Kidney Injury Development.
Review in Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Current status and advances in ultrasound evaluation of neovascularization within carotid artery plaques: a systematic review.Cardiovascular ultrasound · 2025Pooled it
- Beyond the numbers: hypotension, algorithms, and the elusive promise of renal protection.Annals of translational medicine · 2026Article
- Naringenin protects against renal ischemia-reperfusion injury following unilateral nephrectomy via modulation of oxidative stress and kisspeptin expression.International urology and nephrology · 2026Article
- Predictive value of monocyte-to-high-density lipoprotein cholesterol ratio for acute kidney injury following coronary artery bypass grafting.BMC cardiovascular disorders · 2026Article
- Recent advances in stimuli-responsive nanomaterials for the treatment of acute kidney injury.Journal of nanobiotechnology · 2026Review
- Natural compounds targeting inflammatory signaling and cell adhesion molecules in ischemic acute kidney injury.Archives of pharmacal research · 2026Review
- Cellular microenvironment of erythropoietin-producing cells in hypoxic and injured mouse kidneys.Experimental physiology · 2026Article
- Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Nephrosclerosis-Related Histopathological Findings by Cortical Region From a Japanese Community-Based Study.Kidney medicine · 2026Article
- Renal-tubular-mitochondrial sequentially targeted nanoagent breaks the vicious cycle of oxidative stress and mtDNA-driven inflammation in acute kidney injury therapy.Journal of nanobiotechnology · 2026Article
- Mitochondrial Dysfunction in Acute Kidney Injury: Intersections Between Chemotherapy and Novel Cancer Immunotherapies.Biomolecules · 2026Review
- Targeting the renin-angiotensin system in sepsis-associated AKI: from pathophysiology to precision medicine.Frontiers in immunology · 2026Review
- Prerenal acute kidney injury diagnosed by urinary indices in a COVID-19 patient: A critical care case report.IDCases · 2026Article
- Optimal strategies for umbilical cord mesenchymal stem cell-derived exosomes in acute kidney injury: a network meta-analysis in rat models.Frontiers in cell and developmental biology · 2026Review
- Kidneys on the Frontline: Nephrologists Tackling the Wilds of Acute Kidney Injury in Trauma Patients-From Pathophysiology to Early Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- COVID-19 associated acute kidney injury.Infectious diseases & immunity · 2025Review
- Prostaglandin E2 receptor EP4 activation induces tolerogenic dendritic cells to mitigate ischemic acute kidney injury.Scientific reports · 2025Article
- Bilateral Renal Infarcts Due to Blunt Trauma in a Healthy Young Female Patient: A Case Report.Cureus · 2025Article
- Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.The Journal of clinical investigation · 2025Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) can result from multiple factors. The main cause is reduced renal perfusion. Kidneys are susceptible to ischemia due to the anatomy of microcirculation that wraps around the renal tubules-peritubular capillary (PTC) network. Cortical and medullary superficial tubules have a large share in transport and require the supply of oxygen for ATP production, while it is the cortex that receives almost 100% of the blood flowing through the kidneys and the medulla only accounts for 5-10% of it. This difference makes the tubules present in the superficial layer of the medulla very susceptible to ischemia. Impaired blood flow causes damage to the endothelium, with an increase in its prothrombotic and pro-adhesive properties. This causes congestion in the microcirculation of the renal medulla. The next stage is the migration of pericytes with the disintegration of these vessels. The phenomenon of destruction of small vessels is called peritubular rarefaction, attributed as the main cause of further irreversible changes in the damaged kidney leading to the development of chronic kidney disease. In this article, we will present the characteristic structure of renal microcirculation, its regulation, and the mechanism of damage in acute ischemia, and we will try to find methods of prevention with particular emphasis on the inhibition of the renin-angiotensin-aldosterone system.
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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 Socratic graph.