Evidence map›Paper›PMID 37098380›Full record

ArticleKidney international2023

Kidney medullary sodium chloride concentrations induce neutrophil and monocyte extracellular DNA traps that defend against pyelonephritis in vivo.

Adrian Goldspink, Jessica Schmitz, Olena Babyak, Nicolas Brauns, Julia Milleck, Anne M Breloh, Susanne V Fleig, Katarzyna Jobin, Lisa Schwarz, Hermann Haller and 4 more

Abstract read
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In one paragraph

Article in Kidney international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.0field-weighted citation impact, top 13% 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, 12 citations in OpenAlex.

  1. Monocyte Chemokines Enhance Atherosclerotic Plaque Necrosis After Bacterial Kidney Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. LDL receptor promotes urinary tract infection by α-hemolysin-producingProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Immune defenses in the urinary tract.Trends in immunology · 2023
    Review
  8. Article
  9. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 1 country.

Adrian GoldspinkNephrology Section, First Medical Clinic, University Clinic and Rheinische Friedrich-Wilhelms Universität Bonn, Bonn, Germany.
Jessica SchmitzNephropathology Unit, Institute for Pathology, Hannover Medical School, Hannover, Germany.
Olena BabyakInstitute of Experimental Immunology, University Clinic and Rheinische Friedrich-Wilhelms Universität Bonn, Bonn, Germany.
Nicolas BraunsDepartment of Internal Medicine, Division of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Julia MilleckNephrology Section, First Medical Clinic, University Clinic and Rheinische Friedrich-Wilhelms Universität Bonn, Bonn, Germany.
Anne M BrelohDepartment of Internal Medicine, Division of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Susanne V FleigNephrology Section, First Medical Clinic, University Clinic and Rheinische Friedrich-Wilhelms Universität Bonn, Bonn, Germany; Department of Geriatrics, University Hospital RWTH Aachen, Aachen, Germany.
Katarzyna JobinInstitute of Experimental Immunology, University Clinic and Rheinische Friedrich-Wilhelms Universität Bonn, Bonn, Germany; Würzburg Institute of Systems Immunology, Max Planck Research Group at the Julius-Maximilians-Universität, Würzburg, Germany.
Lisa SchwarzDepartment of Urology, Pediatric Urology and Andrology, Justus Liebig University Giessen, Giessen, Germany.
Hermann HallerDepartment of Internal Medicine, Division of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Florian WagenlehnerDepartment of Urology, Pediatric Urology and Andrology, Justus Liebig University Giessen, Giessen, Germany.
Jan Hinrich BräsenNephropathology Unit, Institute for Pathology, Hannover Medical School, Hannover, Germany.
Christian KurtsInstitute of Experimental Immunology, University Clinic and Rheinische Friedrich-Wilhelms Universität Bonn, Bonn, Germany.
Sibylle von VietinghoffNephrology Section, First Medical Clinic, University Clinic and Rheinische Friedrich-Wilhelms Universität Bonn, Bonn, Germany; Department of Internal Medicine, Division of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany. Electronic address: Sibylle.von_Vietinghoff@ukbonn.de.
Medizinische Hochschule Hannover · DEUniversity of Bonn · DEUniversity of Giessen · DERWTH Aachen University · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urinary tract infections are common. Here, we delineate a role of extracellular DNA trap (ET) formation in kidney antibacterial defense and determine mechanisms of their formation in the hyperosmotic environment of the kidney medulla. ET of granulocytic and monocytic origin were present in the kidneys of patients with pyelonephritis along with systemically elevated citrullinated histone levels. Inhibition of the transcription coregulatory, peptidylarginine deaminase 4 (PAD4), required for ET formation, prevented kidney ET formation and promoted pyelonephritis in mice. ETs predominantly accumulated in the kidney medulla. The role of medullary sodium chloride and urea concentrations in ET formation was then investigated. Medullary-range sodium chloride, but not urea, dose-, time- and PAD4-dependently induced ET formation even in the absence of other stimuli. Moderately elevated sodium chloride promoted myeloid cell apoptosis. Sodium gluconate also promoted cell death, proposing a role for sodium ions in this process. Sodium chloride induced myeloid cell calcium influx. Calcium ion-free media or -chelation reduced sodium chloride-induced apoptosis and ET formation while bacterial lipopolysaccharide amplified it. Autologous serum improved bacterial killing in the presence of sodium chloride-induced ET. Depletion of the kidney sodium chloride gradient by loop diuretic therapy diminished kidney medullary ET formation and increased pyelonephritis severity. Thus, our data demonstrate that ETs may protect the kidney against ascending uropathogenic E. coli and delineate kidney medullary range sodium chloride concentrations as novel inducers of programmed myeloid cell death.

Indexed as

Extracellular TrapsPyelonephritisAnimalsCalciumDNAEscherichia coliKidneyMiceMonocytesNeutrophilsSodium ChlorideUreaCalciumDNASodium ChlorideUreaextracellular DNA trapsNaClpyelonephritis

Identifiers

PMID37098380
OpenAlexW4366778869

What OpenQuestion holds

Textmetadata
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.