ReviewCurrent hypertension reports2004
Hypertensive renal damage: insights from animal models and clinical relevance.
Review in Current hypertension reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 45 citations in OpenAlex.
- Beyond Blood Pressure: Emerging Pathways and Precision Approaches in Hypertension-Induced Kidney Damage.International journal of molecular sciences · 2025Review
- Podocytes from hypertensive and obese mice acquire an inflammatory, senescent, and aged phenotype.American journal of physiology. Renal physiology · 2024Article
- Sex differences in hypertension: lessons from spontaneously hypertensive rats (SHR).Clinical science (London, England : 1979) · 2021Review
- Restoration of afferent arteriolar autoregulatory behavior in ischemia-reperfusion injury in rat kidneys.American journal of physiology. Renal physiology · 2021Article
- Renal Perfusion Pressure Determines Infiltration of Leukocytes in the Kidney of Rats With Angiotensin II-Induced Hypertension.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Hypertensive Kidney Injury and the Progression of Chronic Kidney Disease.Hypertension (Dallas, Tex. : 1979) · 2017Review
- Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression.Journal of the American Society of Nephrology : JASN · 2015Review
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- P2 receptors in renal autoregulation.Current vascular pharmacology · 2014Review
- Afferent Arteriolar Responses to β,γ-methylene ATP and 20-HETE are not Blocked by ENaC Inhibition.Physiological reports · 2013Article
- Rethinking hypertensive kidney disease: arterionephrosclerosis as a genetic, metabolic, and inflammatory disorder.Current opinion in nephrology and hypertension · 2013Review
- Increased susceptibility to hypertensive renal disease in streptozotocin-treated diabetic rats is not modulated by salt intake.Diabetologia · 2012Article
- Role of blood pressure and the renin-angiotensin system in development of diabetic nephropathy (DN) in eNOS-/- db/db mice.American journal of physiology. Renal physiology · 2012Article
- Genetic polymorphism of ACE and the angiotensin II type1 receptor genes in children with chronic kidney disease.Journal of inflammation (London, England) · 2011Article
- Renal inflammation and elevated blood pressure in a mouse model of reduced {beta}-ENaC.American journal of physiology. Renal physiology · 2011Article
- Acute kidney injury: a springboard for progression in chronic kidney disease.American journal of physiology. Renal physiology · 2010Review
- Yes, no, maybe so: ENaC proteins as mediators of renal myogenic constriction.Hypertension (Dallas, Tex. : 1979) · 2009Article
- Angiotensin II regulation of renal vascular ENaC proteins.American journal of hypertension · 2009Article
- Lewis K. Dahl Memorial Lecture. Mysteries of renal autoregulation.Hypertension (Dallas, Tex. : 1979) · 2009Article
- Endothelial dysfunction and the development of renal injury in spontaneously hypertensive rats fed a high-fat diet.Hypertension (Dallas, Tex. : 1979) · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Investigations using chronic blood pressure (BP) radiotelemetry in conscious animals have provided substantial insights into the pathophysiology of hypertensive renal damage. Normal renal autoregulation protects the renal microvasculature from significant injury in most patients with primary hypertension, unless BP exceeds a certain threshold, when malignant nephrosclerosis develops. However, if autoregulation is impaired, as in chronic renal disease and/or diabetes models, the threshold for renal damage is lowered and glomerulosclerosis (GS) increases linearly with increasing BP. Modest BP reductions are predicted to prevent malignant nephrosclerosis, but prevention of GS in patients with diabetes and chronic renal disease requires that BP be lowered well into the normotensive range, as recognized in the currently recommended BP goals. When BP load is accurately assessed in these experimental models, renal protection is proportional to the achieved BP reductions, and there is little evidence of BP-independent protection, even with agents that block the renin-angiotensin system (RAS). Recent clinical data also suggest that achieving lower BP targets might be vastly more important than the choice of therapeutic regimens. Nevertheless, because aggressive diuretic use is usually necessary to achieve such BP goals, RAS blockade should be included as initial therapy both for antihypertensive synergy and to minimize the potassium and magnesium depletion associated with diuretics.
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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.