Evidence mapPaperPMID 35409276Full record

ReviewInternational journal of molecular sciences2022

A Shared Nephroprotective Mechanism for Renin-Angiotensin-System Inhibitors, Sodium-Glucose Co-Transporter 2 Inhibitors, and Vasopressin Receptor Antagonists: Immunology Meets Hemodynamics.

Giovanna Capolongo, Giovambattista Capasso, Davide Viggiano

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Pillar Risk-Based Treatment for Chronic Kidney Disease in People With Type 2 Diabetes: A Narrative Review.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Review
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  6. Article
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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

3 authors at 1 institution in 1 country.

Giovanna CapolongoDepartment of Translational Medical Sciences, University of Campania "L. Vanvitelli", 80138 Naples, Italy.
Giovambattista CapassoDepartment of Translational Medical Sciences, University of Campania "L. Vanvitelli", 80138 Naples, Italy.
Davide ViggianoDepartment of Translational Medical Sciences, University of Campania "L. Vanvitelli", 80138 Naples, Italy.ORCID 0000-0002-2425-6057
University of Campania "Luigi Vanvitelli" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major paradigm in nephrology states that the loss of filtration function over a long time is driven by a persistent hyperfiltration state of surviving nephrons. This hyperfiltration may derive from circulating immunological factors. However, some clue about the hemodynamic effects of these factors derives from the effects of so-called nephroprotective drugs. Thirty years after the introduction of Renin-Angiotensin-system inhibitors (RASi) into clinical practice, two new families of nephroprotective drugs have been identified: the sodium-glucose cotransporter 2 inhibitors (SGLT2i) and the vasopressin receptor antagonists (VRA). Even though the molecular targets of the three-drug classes are very different, they share the reduction in the glomerular filtration rate (GFR) at the beginning of the therapy, which is usually considered an adverse effect. Therefore, we hypothesize that acute GFR decline is a prerequisite to obtaining nephroprotection with all these drugs. In this study, we reanalyze evidence that RASi, SGLT2i, and VRA reduce the eGFR at the onset of therapy. Afterward, we evaluate whether the extent of eGFR reduction correlates with their long-term efficacy. The results suggest that the extent of initial eGFR decline predicts the nephroprotective efficacy in the long run. Therefore, we propose that RASi, SGLT2i, and VRA delay kidney disease progression by controlling maladaptive glomerular hyperfiltration resulting from circulating immunological factors. Further studies are needed to verify their combined effects.

Indexed as

Sodium-Glucose Transporter 2 InhibitorsAntidiuretic Hormone Receptor AntagonistsAntihypertensive AgentsGlomerular Filtration RateHumansRenin-Angiotensin SystemAntidiuretic Hormone Receptor AntagonistsAntihypertensive AgentsSodium-Glucose Transporter 2 Inhibitorschronic kidney diseaseGFRRASiSGLT2ivaptans

Identifiers

PMID35409276
PMCPMC8999762
OpenAlexW4223466718

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.