ArticleInternational journal of hypertension2013
Renal tissue oxygenation in essential hypertension and chronic kidney disease.
Article in International journal of hypertension, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Multiparametric MR Imaging for Evaluating Renal Function and Microstructure.Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine · 2026Review
- Chronic Stress Induces Sex-Specific Renal Mitochondrial Dysfunction in Mice.Function (Oxford, England) · 2025Article
- MR T2* Map to Predict Worsening Hypertension Control: A Preliminary Study.Life (Basel, Switzerland) · 2025Article
- Article
- Non-invasive evaluation of renal structure and function of healthy individuals with multiparametric MRI: Effects of sex and age.Scientific reports · 2019Article
- Angiotensin II-induced hypertension in rats is only transiently accompanied by lower renal oxygenation.Scientific reports · 2018Article
- Renal tissue oxygenation in children with chronic kidney disease due to vesicoureteral reflux.Pediatric nephrology (Berlin, Germany) · 2016Article
- Contrast-induced nephropathy following angiography and cardiac interventions.Heart (British Cardiac Society) · 2016Article
- Magnetic Resonance Imaging-Derived Renal Oxygenation and Perfusion During Continuous, Steady-State Angiotensin-II Infusion in Healthy Humans.Journal of the American Heart Association · 2016Article
- Analysis of differentially expressed genes in cold-exposed mice to investigate the potential causes of cold-induced hypertension.Experimental and therapeutic medicine · 2014Article
- Assessing intrarenal nonperfusion and vascular leakage in acute kidney injury with multinuclear (1) H/(19) F MRI and perfluorocarbon nanoparticles.Magnetic resonance in medicine · 2014Article
- Perfluorocarbon nanoparticles for physiological and molecular imaging and therapy.Advances in chronic kidney disease · 2013Review
- Blockade of the renin-angiotensin system in hypertensive patients with atherosclerotic renal artery stenosis.Current hypertension reports · 2013Review
- Impact of cardiovascular organ damage on cortical renal perfusion in patients with chronic renal failure.BioMed research international · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Animal studies suggest that renal tissue hypoxia plays an important role in the development of renal damage in hypertension and renal diseases, yet human data were scarce due to the lack of noninvasive methods. Over the last decade, blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI), detecting deoxyhemoglobin in hypoxic renal tissue, has become a powerful tool to assess kidney oxygenation noninvasively in humans. This paper provides an overview of BOLD-MRI studies performed in patients suffering from essential hypertension or chronic kidney disease (CKD). In line with animal studies, acute changes in cortical and medullary oxygenation have been observed after the administration of medication (furosemide, blockers of the renin-angiotensin system) or alterations in sodium intake in these patient groups, underlining the important role of renal sodium handling in kidney oxygenation. In contrast, no BOLD-MRI studies have convincingly demonstrated that renal oxygenation is chronically reduced in essential hypertension or in CKD or chronically altered after long-term medication intake. More studies are required to clarify this discrepancy and to further unravel the role of renal oxygenation in the development and progression of essential hypertension and CKD in humans.
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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 OpenQuestion graph.