Evidence map›Paper›PMID 38339031›Full record

ReviewInternational journal of molecular sciences2024

From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease.

Tzu-Hsuan Yeh, Kuan-Chieh Tu, Hsien-Yi Wang, Jui-Yi Chen

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
20.0field-weighted citation impact, top 1% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

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  14. [A high temporal resolution dynamic TNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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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

4 authors at 2 institutions in 1 country.

Tzu-Hsuan YehDivision of Nephrology, Department of Internal Medicine, Chi Mei Medical Center, Tainan 71004, Taiwan.
Kuan-Chieh TuDivision of Cardiology, Department of Internal Medicine, Chi Mei Medical Center, Tainan 71004, Taiwan.
Hsien-Yi WangDivision of Nephrology, Department of Internal Medicine, Chi Mei Medical Center, Tainan 71004, Taiwan.
Jui-Yi ChenDivision of Nephrology, Department of Internal Medicine, Chi Mei Medical Center, Tainan 71004, Taiwan.
Chi Mei Medical Center · TWChia Nan University of Pharmacy and Science · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This article provides a thorough overview of the biomarkers, pathophysiology, and molecular pathways involved in the transition from acute kidney injury (AKI) and acute kidney disease (AKD) to chronic kidney disease (CKD). It categorizes the biomarkers of AKI into stress, damage, and functional markers, highlighting their importance in early detection, prognosis, and clinical applications. This review also highlights the links between renal injury and the pathophysiological mechanisms underlying AKI and AKD, including renal hypoperfusion, sepsis, nephrotoxicity, and immune responses. In addition, various molecules play pivotal roles in inflammation and hypoxia, triggering maladaptive repair, mitochondrial dysfunction, immune system reactions, and the cellular senescence of renal cells. Key signaling pathways, such as Wnt/β-catenin, TGF-β/SMAD, and Hippo/YAP/TAZ, promote fibrosis and impact renal function. The renin-angiotensin-aldosterone system (RAAS) triggers a cascade leading to renal fibrosis, with aldosterone exacerbating the oxidative stress and cellular changes that promote fibrosis. The clinical evidence suggests that RAS inhibitors may protect against CKD progression, especially post-AKI, though more extensive trials are needed to confirm their full impact.

Indexed as

Acute Kidney InjuryRenal Insufficiency, ChronicAcute DiseaseBiomarkersDisease ProgressionFibrosisHumansKidneyBiomarkersacute kidney diseaseacute kidney injurybiomarkerchronic kidney disease

Identifiers

PMID38339031
PMCPMC10855633
OpenAlexW4391434521

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.