Evidence map›Paper›PMID 40008354›Full record

ReviewClinical kidney journal2025

Kidney hemodynamic effects of sodium-glucose cotransporter 2 inhibitors in diabetes: physiology and clinical implications.

David León-Jiménez, Vikas S Sridhar, Manuel López-Mendoza, Rosalie A Scholtes, Roland E Schmieder, David Z I Cherney, Daniël H van Raalte, Francisco J Toro-Prieto, José Pablo Miramontes-González, Erik J M van Bommel

Abstract readReview
In one paragraph

Review in Clinical kidney journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Trial
  2. Review
  3. Antiproteinuric effect of SGLT2 inhibitors in non-diabetic glomerulopathies is dependent on body mass index.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Observational
  4. Article
  5. Article
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

10 authors.

David León-JiménezVascular Risk Unit, Internal Medicine Department, Virgen del Rocío University Hospital, University of Seville, Instituto de Biomedicina de Sevilla (IBIS), Seville, Spain.ORCID https://orcid.org/0000-0003-4343-045X
Vikas S SridharDivision of Nephrology, University Health Network, University of Toronto, Toronto, ON, Canada.
Manuel López-MendozaNephrology Department, Virgen del Rocío University Hospital, University of Seville, Spain.
Rosalie A ScholtesDiabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, VU University Medical Center, Amsterdam, The Netherlands.ORCID https://orcid.org/0000-0002-2794-2263
Roland E SchmiederDepartment of Internal Medicine, Nephrology and Hypertension, Friedrich-Alexander University Erlangen, Erlangen, Germany.
David Z I CherneyDivision of Nephrology, University Health Network, University of Toronto, Toronto, ON, Canada.
Daniël H van RaalteDiabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, VU University Medical Center, Amsterdam, The Netherlands.
Francisco J Toro-PrietoNephrology Department, Virgen del Rocío University Hospital, University of Seville, Spain.
José Pablo Miramontes-GonzálezInternal Medicine, Institute of Biomedical Research of Salamanca (IBSAL), Río Hortega University Hospital, Valladolid, Spain.
Erik J M van BommelDiabetes Center, Department of Internal Medicine, Amsterdam University Medical Centers, VU University Medical Center, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The progressive loss of kidney function in diabetes mellitus is partly attributable to the occurrence of glomerular hyperfiltration. Consequently, therapeutic interventions that lower intra-glomerular pressure are a cornerstone of treatment in diabetic kidney disease. Sodium-glucose cotransporter 2 (SGLT2) inhibitors consistently reduce glomerular filtration rate (GFR) and calculated intraglomerular pressures across studies. However, the net effect on arteriolar tone that leads to acute GFR declines may differ between cohorts. While pre-glomerular vasoconstriction appears to be the dominant mechanism responsible for GFR dipping in patients with type 1 diabetes (T1D) and glomerular hyperfiltration, other factors, including post-glomerular vasodilation, may contribute to the acute GFR decline in normofilterering individuals with T1D and type 2 diabetes. Regardless of the responsible mechanisms, acute changes in GFR are associated with long-term kidney function preservation-a relationship that may reflect an underlying protective decline in glomerular hypertension.

Indexed as

albuminuriaCKDdiabetic kidney diseaseproteinuriarenin–angiotensin system

Identifiers

PMID40008354
PMCPMC11852268

What OpenQuestion holds

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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.