Evidence map›Paper›PMID 23803592›Full record

ReviewJournal of human hypertension2014

Hypertension and kidneys: unraveling complex molecular mechanisms underlying hypertensive renal damage.

S Mennuni, S Rubattu, G Pierelli, G Tocci, C Fofi, M Volpe

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of human hypertension, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 5 pooled it
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

152 citing papers in PubMed, 5 syntheses or guidelines pooled it, 295 citations in OpenAlex.

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92 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

S MennuniDepartment of Clinical and Molecular Medicine, School of Medicine and Psychology, University Sapienza of Rome, Ospedale S. Andrea, Rome, Italy.
S Rubattu1] Department of Clinical and Molecular Medicine, School of Medicine and Psychology, University Sapienza of Rome, Ospedale S. Andrea, Rome, Italy [2] IRCCS Neuromed, Pozzilli, Italy.
G PierelliDepartment of Clinical and Molecular Medicine, School of Medicine and Psychology, University Sapienza of Rome, Ospedale S. Andrea, Rome, Italy.
G TocciIRCCS Neuromed, Pozzilli, Italy.
C FofiNephrology and Dialysis Unit, School of Medicine and Psychology, University Sapienza of Rome, Ospedale S. Andrea, Rome, Italy.
M Volpe1] Department of Clinical and Molecular Medicine, School of Medicine and Psychology, University Sapienza of Rome, Ospedale S. Andrea, Rome, Italy [2] IRCCS Neuromed, Pozzilli, Italy.
Azienda Ospedaliera Sant'Andrea · ITIstituto Neurologico Mediterraneo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney damage represents a frequent event in the course of hypertension, ranging from a benign to a malignant form of nephropathy depending on several factors, that is, individual susceptibility, degree of hypertension, type of etiology and underlying kidney disease. Multiple mechanisms are involved in determination of kidney glomerular, tubular and interstitial injuries in hypertension. The present review article discusses relevant contributory molecular mechanisms underpinning the promotion of hypertensive renal damage, such as the renin-angiotensin-aldosterone system (RAAS), oxidative stress, endothelial dysfunction, and genetic and epigenetic determinants. We highlighted major pathways involved in the progression of inflammation and fibrosis leading to glomerular sclerosis, tubular atrophy and interstitial fibrosis, thus providing a state of the art review of the pathogenetic background useful for a better understanding of current and future therapeutic strategies toward hypertensive nephropathy. An adequate control of high blood pressure, obtained through an appropriate therapeutic intervention, still represents the key strategy to achieve a satisfactory control of renal damage in hypertension. In this regard, we reviewed the impact of currently available antihypertensive pharmacological treatment on kidney damage, with particular regard to RAAS inhibitors. Notably, recent findings underscored the ability of the kidneys to regenerate and to repair tissue injuries through the differentiation of resident embryonic stem cells. Pharmacological modulation of the renal endogenous reparative process (that is, with angiotensin-converting enzyme inhibitors and AT1 angiotensin II receptor blockers), as well as future therapeutic strategies targeted to the renopoietic system, offers interesting perspectives for the management of hypertensive nephropathy.

Indexed as

Blood PressureAnimalsAntihypertensive AgentsEndothelium, VascularGenetic Predisposition to DiseaseHumansHypertensionInflammation MediatorsKidneyKidney DiseasesOxidative StressPrognosisRenin-Angiotensin SystemRisk FactorsSignal TransductionAntihypertensive AgentsInflammation Mediators

Identifiers

PMID23803592
OpenAlexW2072277203

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.