Evidence map›Paper›PMID 35812284›Full record

ArticleKidney international reports2022

Renal Autologous Cell Therapy to Stabilize Function in Diabetes-Related Chronic Kidney Disease: Corroboration of Mechanistic Action With Cell Marker Analysis.

Joseph Stavas, Guido Filler, Deepak Jain, John Ludlow, Joydeep Basu, Richard Payne, Emily Butler, Maria Díaz-González de Ferris, Tim Bertram

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Kidney international reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Joseph StavasProKidney, LLC, Raleigh, North Carolina, USA.
Guido FillerDepartments of Paediatrics, Medicine, Pathology and Laboratory Medicine, University of Western Ontario, London, Canada.
Deepak JainProKidney, LLC, Raleigh, North Carolina, USA.
John LudlowProKidney, LLC, Raleigh, North Carolina, USA.
Joydeep BasuProKidney, LLC, Raleigh, North Carolina, USA.
Richard PayneProKidney, LLC, Raleigh, North Carolina, USA.
Emily ButlerProKidney, LLC, Raleigh, North Carolina, USA.
Maria Díaz-González de FerrisDepartment of Pediatrics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Tim BertramProKidney, LLC, Raleigh, North Carolina, USA.
University of North Carolina at Chapel Hill · USWestern University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Chronic kidney disease (CKD) is a worldwide disease without cure. Selected renal cells (SRCs) can augment kidney function in animal models. This study correlates the phenotypical characteristics of autologous homologous SRCs (formulated product called Renal Autologous Cell Therapy [REACT]) injected into patients' kidneys with advanced type 2 diabetes-related CKD (D-CKD) to clinical and laboratory findings. Methods: A total of 22 adults with type 2 D-CKD underwent a kidney biopsy followed by 2 subcortical injections of SRCs, 7 ± 3 months apart. There were 2 patients who had only 1 injection. We compared annualized estimated glomerular filtration rate (eGFR) slopes pre- and post-REACT injection using the 2009 CKD-EPI formula for serum creatinine (sCr) and the 2012 CKD-EPI Creatinine-Cystatin C equation and report clinical/laboratory changes. Fluorescent Activated Cell Sorting (FACS) Analysis for renal progenitor lineages in REACT and donor vascular endothelial growth factor A (VEGF-A) analysis were performed. Longitudinal parameter changes were analyzed with longitudinal linear mixed effects model. Results: At baseline, the mean diabetes duration was 18.4 ± 8.80 years, glycated hemoglobin (Hgb) was 7.0 ± 1.05, and eGFR was 40.3 ± 9.35 ml/min per 1.73 m Conclusion: Our cell marker analysis suggests that SRCs may enable REACT to stabilize and improve kidney function, possibly halting type 2 D-CKD progression.

Indexed as

cell-based therapychronic kidney diseaseestimated glomerular filtration rateselected renal cellstype 2 diabetes mellitus

Identifiers

PMID35812284
PMCPMC9263255
OpenAlexW4224209880

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.