Evidence map›Paper›PMID 33190567›Full record

ReviewJournal of the American Heart Association2020

Glucose Metabolism in the Kidney: Neurohormonal Activation and Heart Failure Development.

Edoardo Gronda, Mariell Jessup, Massimo Iacoviello, Alberto Palazzuoli, Claudio Napoli

Open access · goldAbstract readReview
In one paragraph

Review in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
5.8field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 88 citations in OpenAlex.

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  16. [Preliminary Investigation of the Molecular Mechanism of Empagliflozin Suppressing Gastric Cancer Through Mammalian Target of Rapamycin].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023
    Article
  17. Neurohumoral Activation in Heart Failure.International journal of molecular sciences · 2023
    Review
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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

5 authors at 5 institutions in 2 countries.

Edoardo GrondaProgramma Cardiorenale U.O.C. Nefrologia Dialisi e Trapianto Renale dell'Adulto Dipartimento di Medicina e Specialità Mediche Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico Milan Italy.
Mariell JessupAmerican Heart Association Dallas TX.
Massimo IacovielloSC Cardiologia Dipartimento delle Scienze Mediche e Chirurgiche AOU Policlinico Riuniti di FoggiaUniversità degli Studi di Foggia Foggia Italy.
Alberto PalazzuoliDivisione di Malattie Cardiovascolari Dipartimento di Medicina Interna Università di Siena Italy.
Claudio NapoliClinical Department of Internal Medicine and Specialistics Department of Advanced Medical and Surgical Sciences Università della Campania "Luigi Vanvitelli" Naples Italy.
American Heart Association · USFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITUniversity of Campania "Luigi Vanvitelli" · ITUniversity of Foggia · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver is not the exclusive site of glucose production in humans in the postabsorptive state. Robust data support that the kidney is capable of gluconeogenesis and studies have demonstrated that renal glucose production can increase systemic glucose production. The kidney has a role in maintaining glucose body balance, not only as an organ for gluconeogenesis but by using glucose as a metabolic substrate. The kidneys reabsorb filtered glucose through the sodium-glucose cotransporters sodium-glucose cotransporter (SGLT) 1 and SGLT2, which are localized on the brush border membrane of the early proximal tubule with immune detection of their expression in the tubularized Bowman capsule. In patients with diabetes mellitus, the renal maximum glucose reabsorptive capacity, and the threshold for glucose passage into the urine, are higher and contribute to the hyperglycemic state. The administration of SGLT2 inhibitors to patients with diabetes mellitus enhances sodium and glucose excretion, leading to a reduction of the glycosuria threshold and tubular maximal transport of glucose. The net effects of SGLT2 inhibition are to drive a reduction in plasma glucose levels, improving insulin secretion and sensitivity. The benefit of SGLT2 inhibitors goes beyond glycemic control, since inhibition of renal glucose reabsorption affects blood pressure and improves the hemodynamic profile and the tubule glomerular feedback. This action acts to rebalance the dense macula response by restoring adenosine production and restraining renin-angiotensin-aldosterone activation. By improving renal and cardiovascular function, we explain the impressive reduction in adverse outcomes associated with heart failure supporting the current clinical perspective.

Indexed as

GluconeogenesisGlucoseHeart FailureHumansKidneySodium-Glucose Transporter 2 InhibitorsSodium-Glucose Transport ProteinsGlucoseSodium-Glucose Transporter 2 InhibitorsSodium-Glucose Transport Proteinscardiovascular diseaseheart failuresodium‐glucose cotransporter‐2 inhibitorstype 2 diabetes mellitus

Identifiers

PMID33190567
PMCPMC7763788
OpenAlexW3098382417

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.