Evidence map›Paper›PMID 42851467›Full record

ReviewClinical kidney journal2026

Targeting tissue immune memory in chronic-remitting autoimmune kidney diseases: current concepts and future therapies.

Malte Hellmig, Christian F Krebs

Abstract readReview
In one paragraph

Review in Clinical kidney journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Malte HellmigIII. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Christian F KrebsIII. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0003-2739-5578

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune-mediated kidney diseases have a substantial disease burden and frequent disease relapses significantly contribute to the high morbidity. Relapsing disease courses are associated with poor outcome and accelerated progression to end-stage renal disease. The pathomechanisms leading to relapse are diverse and only incompletely understood. Both adaptive and innate immune cells are implicated in the immune memory of these diseases. In addition to antigen-dependent mechanisms of T and B cells, persistent epigenetic and metabolic changes in adaptive and innate immune cells may sustain immunological memory and thereby provide a cellular and molecular basis for relapse. Treatment options, especially in frequently relapsing cases, are limited and memory immune cells often evade standard immunosuppressive therapies. As our understanding of immunological memory continues to improve, new treatment options emerge. Improved depletion of B cells, antigen-specific cell-based therapies and redirecting epigenetic alterations may target long-lasting immune memory. This could reduce relapse risk and improve long-term outcomes in patients with immune-mediated kidney diseases.

Indexed as

ANCAcrescentic glomerulonephritisimmune memorylupus nephritisT cell

Identifiers

PMID42851467
PMCPMC13645649

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.