Evidence map›Paper›PMID 37762322›Full record

ReviewInternational journal of molecular sciences2023

Pathway from Acute Kidney Injury to Chronic Kidney Disease: Molecules Involved in Renal Fibrosis.

Andrei Niculae, Mihai-Emil Gherghina, Ileana Peride, Mirela Tiglis, Ana-Maria Nechita, Ionel Alexandru Checherita

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
13.3field-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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  15. A macrophage-endothelial cell axis in kidney diseases.International urology and nephrology · 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

6 authors at 2 institutions in 1 country.

Andrei NiculaeDepartment of Nephrology, Clinical Department No. 3, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.ORCID 0000-0003-2866-8806
Mihai-Emil GherghinaDepartment of Nephrology, Ilfov County Emergency Clinical Hospital, 022104 Bucharest, Romania.
Ileana PerideDepartment of Nephrology, Clinical Department No. 3, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.ORCID 0000-0002-4912-6590
Mirela TiglisDepartment of Anesthesia and Intensive Care, Emergency Clinical Hospital of Bucharest, 014461 Bucharest, Romania.ORCID 0000-0003-3542-3217
Ana-Maria NechitaDepartment of Nephrology, "St. John" Emergency Clinical Hospital, 042122 Bucharest, Romania.
Ionel Alexandru ChecheritaResearch Department, Emergency Clinical Hospital of Bucharest, 014461 Bucharest, Romania.ORCID 0000-0002-9741-5530
Clinical Emergency Hospital Bucharest · ROCarol Davila University of Medicine and Pharmacy · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is one of the main conditions responsible for chronic kidney disease (CKD), including end-stage renal disease (ESRD) as a long-term complication. Besides short-term complications, such as electrolyte and acid-base disorders, fluid overload, bleeding complications or immune dysfunctions, AKI can develop chronic injuries and subsequent CKD through renal fibrosis pathways. Kidney fibrosis is a pathological process defined by excessive extracellular matrix (ECM) deposition, evidenced in chronic kidney injuries with maladaptive architecture restoration. So far, cited maladaptive kidney processes responsible for AKI to CKD transition were epithelial, endothelial, pericyte, macrophage and fibroblast transition to myofibroblasts. These are responsible for smooth muscle actin (SMA) synthesis and abnormal renal architecture. Recently, AKI progress to CKD or ESRD gained a lot of interest, with impressive progression in discovering the mechanisms involved in renal fibrosis, including cellular and molecular pathways. Risk factors mentioned in AKI progression to CKD are frequency and severity of kidney injury, chronic diseases such as uncontrolled hypertension, diabetes mellitus, obesity and unmodifiable risk factors (i.e., genetics, older age or gender). To provide a better understanding of AKI transition to CKD, we have selected relevant and updated information regarding the risk factors responsible for AKIs unfavorable long-term evolution and mechanisms incriminated in the progression to a chronic state, along with possible therapeutic approaches in preventing or delaying CKD from AKI.

Indexed as

Acute Kidney InjuryKidney Failure, ChronicRenal Insufficiency, ChronicFibrosisHumansKidneyacute kidney injurychronic kidney diseasepro-fibrotic factorsrenal fibrosis pathwaystreatment

Identifiers

PMID37762322
PMCPMC10531003
OpenAlexW4386713468

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.