Pathogenesis and kidney prognosis of renal amyloidosis.

Alvin Hu, Raad B Chowdhury, Giada Bianchi

Abstract readReview

In one paragraph

Review in Cellular and molecular life sciences : CMLS, 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

3 authors.

Alvin HuDivision of Renal Medicine, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0002-3820-2316

Raad B ChowdhuryDivision of Renal Medicine, Brigham and Women's Hospital, Boston, MA, USA.ORCID http://orcid.org/0000-0002-9347-6299

Giada BianchiHarvard Medical School, Boston, MA, USA. GBIANCHI1@BWH.HARVARD.EDU.ORCID http://orcid.org/0000-0003-3673-0104

Funding

National Institute of Health/National Cancer Institute K08CA245100

6 · The paper itself

Abstract

Light chain (AL), serum amyloid A (AA), transthyretin (ATTR), leukocyte cell derived chemotaxin 2 (ALECT2), and fibrinogen Aa (AFib) amyloidosis are some of the most common types of protein-deposition disorders involving the kidney. Each amyloidogenic protein differs in its origin and little is known about the exact mechanisms that govern renal tropism and tissue injury for each amyloid subtype. While amyloidogenic precursor protein is different in each subtype of amyloidosis, its aggregation into fibrils depositing in target organs and leading to disruption of tissue architecture and progressive organ failure is a common denominator. Each amyloidogenic protein is characterized by a unique pattern of deposition in the renal parenchyma with variability in expected clinical outcomes. In this review, we focus on describing the distinct pathophysiologic mechanisms at the level of the kidneys of AL, AA, ATTR, ALECT2, and AFib amyloidosis.

Indexed as

AmyloidosisKidneyKidney DiseasesAmyloidAnimalsFibrinogenHumansIntercellular Signaling Peptides and ProteinsPrealbuminPrognosisSerum Amyloid A ProteinAmyloidFibrinogenIntercellular Signaling Peptides and ProteinsLECT2 protein, humanPrealbuminSerum Amyloid A ProteinAAALALECT2AmyloidosisATTREnd stage renal diseaseRenal

Identifiers

PMID41975145

DOI10.1007/s00018-025-06030-y

PMCPMC13187075

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LicenceCC BY-NC-ND

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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.