Evidence map›Paper›PMID 25927597›Full record

ArticlePloS one2015

Effect of Sodium-Glucose Cotransport Inhibition on Polycystic Kidney Disease Progression in PCK Rats.

Sarika Kapoor, Daniel Rodriguez, Meliana Riwanto, Ilka Edenhofer, Stephan Segerer, Katharyn Mitchell, Rudolf P Wüthrich

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 11% 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, 57 citations in OpenAlex.

  1. Trial
  2. Article
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  4. SGLT2 inhibition for patients with ADPKD - closing the evidence gap.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    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

7 authors at 2 institutions in 1 country.

Sarika KapoorDivision of Nephrology, University Hospital, Zürich, Switzerland; Institute of Physiology, University of Zürich, Zürich, Switzerland.
Daniel RodriguezDivision of Nephrology, University Hospital, Zürich, Switzerland; Institute of Physiology, University of Zürich, Zürich, Switzerland.
Meliana RiwantoDivision of Nephrology, University Hospital, Zürich, Switzerland; Institute of Physiology, University of Zürich, Zürich, Switzerland.
Ilka EdenhoferDivision of Nephrology, University Hospital, Zürich, Switzerland; Institute of Physiology, University of Zürich, Zürich, Switzerland.
Stephan SegererDivision of Nephrology, University Hospital, Zürich, Switzerland; Institute of Physiology, University of Zürich, Zürich, Switzerland.
Katharyn MitchellClinic for Equine Internal Medicine, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
Rudolf P WüthrichDivision of Nephrology, University Hospital, Zürich, Switzerland; Institute of Physiology, University of Zürich, Zürich, Switzerland.
University of Zurich · CHUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sodium-glucose-cotransporter-2 (SGLT2) inhibitor dapagliflozin (DAPA) induces glucosuria and osmotic diuresis via inhibition of renal glucose reabsorption. Since increased diuresis retards the progression of polycystic kidney disease (PKD), we investigated the effect of DAPA in the PCK rat model of PKD. DAPA (10 mg/kg/d) or vehicle was administered by gavage to 6 week old male PCK rats (n=9 per group). Renal function, albuminuria, kidney weight and cyst volume were assessed after 6 weeks of treatment. Treatment with DAPA markedly increased glucose excretion (23.6 ± 4.3 vs 0.3 ± 0.1 mmol/d) and urine output (57.3 ± 6.8 vs 19.3 ± 0.8 ml/d). DAPA-treated PCK rats had higher clearances for creatinine (3.1 ± 0.1 vs 2.6 ± 0.2 ml/min) and BUN (1.7 ± 0.1 vs 1.2 ± 0.1 ml/min) after 3 weeks, and developed a 4-fold increase in albuminuria. Ultrasound imaging and histological analysis revealed a higher cyst volume and a 23% higher total kidney weight after 6 weeks of DAPA treatment. At week 6 the renal cAMP content was similar between DAPA and vehicle, and staining for Ki67 did not reveal an increase in cell proliferation. In conclusion, the inhibition of glucose reabsorption with the SGLT2-specific inhibitor DAPA caused osmotic diuresis, hyperfiltration, albuminuria and an increase in cyst volume in PCK rats. The mechanisms which link glucosuria to hyperfiltration, albuminuria and enhanced cyst volume in PCK rats remain to be elucidated.

Indexed as

AlbuminuriaAnimalsBenzhydryl CompoundsBiopsyBody WeightCell ProliferationCyclic AMPDisease Models, AnimalDisease ProgressionDiuresisElectrolytesEpithelial CellsGlucosidesKidneyKidney Function TestsMaleBenzhydryl CompoundsCyclic AMPdapagliflozinElectrolytesGlucosidesSodium-Glucose Transport Proteins

Identifiers

PMID25927597
PMCPMC4416041
OpenAlexW2081094339

What OpenQuestion holds

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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.