ArticleJournal of the American Society of Nephrology : JASN2012
Aberrant tubuloglomerular feedback and HIF-1α confer resistance to ischemia after subtotal nephrectomy.
Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Restoration of afferent arteriolar autoregulatory behavior in ischemia-reperfusion injury in rat kidneys.American journal of physiology. Renal physiology · 2021Article
- Hypoxia-Inducible Factor and Oxygen Biology in the Kidney.Kidney360 · 2020Review
- Pathophysiology of unilateral ischemia-reperfusion injury: importance of renal counterbalance and implications for the AKI-CKD transition.American journal of physiology. Renal physiology · 2020Article
- Gut-derived uremic toxin handling in vivo requires OAT-mediated tubular secretion in chronic kidney disease.JCI insight · 2020Article
- Nitric oxide mediates anomalous tubuloglomerular feedback in rats fed high-NaCl diet after subtotal nephrectomy.American journal of physiology. Renal physiology · 2019Article
- Differential Impact of Dietary Branched Chain and Aromatic Amino Acids on Chronic Kidney Disease Progression in Rats.Frontiers in physiology · 2019Article
- Mechanisms of Organ Dysfunction in Sepsis.Critical care clinics · 2018Review
- Hypoxia-inducible factor-1α activation improves renal oxygenation and mitochondrial function in early chronic kidney disease.American journal of physiology. Renal physiology · 2017Article
- Renal Oxygenation and Hemodynamics in Kidney Injury.Nephron · 2017Review
- Renal Oxygenation in the Pathophysiology of Chronic Kidney Disease.Frontiers in physiology · 2017Review
- Renal Hemodynamics in AKI: In Search of New Treatment Targets.Journal of the American Society of Nephrology : JASN · 2016Article
- Interactions between HIF-1α and AMPK in the regulation of cellular hypoxia adaptation in chronic kidney disease.American journal of physiology. Renal physiology · 2015Article
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Severe renal mass reduction impairs recovery and promotes fibrosis after AKI.Journal of the American Society of Nephrology : JASN · 2014Article
- Heme oxygenase-1 and acute kidney injury.Current opinion in nephrology and hypertension · 2014Review
- Angiogenesis and hypoxia in the kidney.Nature reviews. Nephrology · 2013Review
- Renal oxygenation and haemodynamics in acute kidney injury and chronic kidney disease.Clinical and experimental pharmacology & physiology · 2013Review
- Metabolic control of renin secretion.Pflugers Archiv : European journal of physiology · 2013Review
- Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Nephron loss in a diseased kidney invokes adaptations in the remaining nephrons. Whether and how these adaptations condition the response of the kidney to injury is not known. We examined the susceptibility of the kidney after subtotal (5/6th) nephrectomy (STN) to ischemic injury in rats. GFR in STN kidneys did not significantly change after ischemia reperfusion (IR), whereas GFR fell by 70% after IR in unilateral nephrectomy controls. In micropuncture experiments, single-nephron GFR responses mirrored the whole-kidney responses: in STN, single-nephron GFR decreased by 7% after IR compared with 28% in controls. Furthermore, we found that tubuloglomerular feedback, a mechanism that links proximal tubular injury to a fall in GFR, was inoperative in STN but was normal in controls. Restoration of normal feedback in STN attenuated the functional resistance to IR. In addition to the functional resilience, the morphology of the kidney was better preserved in STN. In STN kidneys, the S3 segment of the proximal tubule, normally injured after ischemia, constitutively expressed hypoxia-inducible factor-1α (HIF-1α), which is cytoprotective in ischemia. Inducing HIF before IR improved GFR in control animals, and inhibiting the HIF target heme-oxygenase-1 before IR reduced GFR in STN animals. Taken together, these data suggest that fewer functioning nephrons in a diseased kidney do not increase the susceptibility to injury, but rather, hemodynamic and molecular adaptations in the remnant nephrons precondition them against ischemic injury.
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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.