ArticleHypertension (Dallas, Tex. : 1979)2014
Critical blood pressure threshold dependence of hypertensive injury and repair in a malignant nephrosclerosis model.
Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Associations of Long-Term Blood Pressure Burden and Variability With Kidney Function Decline.Journal of clinical hypertension (Greenwich, Conn.) · 2026Article
- Kidney-limited thrombotic microangiopathy caused by relative hypertension in a hemodynamically vulnerable kidney allograft, mimicking malignant hypertension.CEN case reports · 2026Article
- Animal models of hypertension and concurrent organs injury.Animal models and experimental medicine · 2025Review
- Acute Increase of Renal Perfusion Pressure Causes Rapid Activation of mTORC1 (Mechanistic Target Of Rapamycin Complex 1) and Leukocyte Infiltration.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Emerging Insights Into Chronic Renal Disease Pathogenesis in Hypertension From Human and Animal Genomic Studies.Hypertension (Dallas, Tex. : 1979) · 2021Review
- RNA sequencing reveals induction of specific renal inflammatory pathways in a rat model of malignant hypertension.Journal of molecular medicine (Berlin, Germany) · 2021Article
- BP Fluctuations and the Real-Time Dynamics of Renal Blood Flow Responses in Conscious Rats.Journal of the American Society of Nephrology : JASN · 2020Article
- Ischaemic stroke and pre-eclampsia in the third trimester of pregnancy: a diagnostic and therapeutic challenge.BMJ case reports · 2019Article
- Posterior reversible encephalopathy syndrome in stroke-prone spontaneously hypertensive rats on high-salt diet.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Animal Models of Hypertension: A Scientific Statement From the American Heart Association.Hypertension (Dallas, Tex. : 1979) · 2019Review
- Microvascular rarefaction and hypertension in the impaired recovery and progression of kidney disease following AKI in preexisting CKD states.American journal of physiology. Renal physiology · 2018Article
- Genetic Susceptibility to Hypertension-Induced Renal Injury.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Hypertensive Kidney Injury and the Progression of Chronic Kidney Disease.Hypertension (Dallas, Tex. : 1979) · 2017Review
- Progression of Chronic Kidney Disease After Acute Kidney Injury: Role of Self-Perpetuating Versus Hemodynamic-Induced Fibrosis.Hypertension (Dallas, Tex. : 1979) · 2016Article
- From malignant hypertension to hypertension-MOD: a modern definition for an old but still dangerous emergency.Journal of human hypertension · 2016Review
- Hemodynamic basis for the limited renal injury in rats with angiotensin II-induced hypertension.American journal of physiology. Renal physiology · 2015Article
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Authors and funding
6 authors.
Funding
Abstract
Most patients with essential hypertension do not exhibit substantial renal damage. Renal autoregulation by preventing glomerular transmission of systemic pressures has been postulated to mediate this resistance. Conversely, malignant nephrosclerosis (MN) has been postulated to develop when severe hypertension exceeds a critical ceiling. If the concept is valid, even modest blood pressure (BP) reductions to below this threshold regardless of antihypertensive class (1) should prevent MN and (2) lead to the healing of the already developed MN lesions. Both predicates were tested using BP radiotelemetry in the stroke-prone spontaneously hypertensive rats receiving 1% NaCl as drinking fluid for 4 weeks. Severe hypertension (final 2 weeks average systolic BP, >200 mm Hg) and MN (histological damage score 36±5; n=27) developed in the untreated stroke-prone spontaneously hypertensive rats but were prevented by all antihypertensive classes (enalapril [n=15], amlodipine [n=13], or a hydralazine/hydrochlorothiazide combination [n=15]) if the final 2-week systolic BP remained <190 mm Hg. More impressively, modest systolic BP reductions to 160 to 180 mm Hg (hydralazine/hydrochlorothiazide regimen) initiated at ≈4 weeks in additional untreated rats after MN had already developed (injury score 35±4 in the right kidney removed before therapy) led to a striking resolution of the vascular and glomerular MN injury over 2 to 3 weeks (post-therapy left kidney injury score 9±2, P<0.0001; n=27). Proteinuria also declined rapidly from 122±9.5 mg/24 hours before therapy to 20.5±3.6 mg 1 week later. These data clearly demonstrate the barotrauma-mediated pathogenesis of MN and the striking capacity for spontaneous and rapid repair of hypertensive kidney damage if new injury is prevented.
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