ReviewRenal failure2025
Assessment, molecular mechanisms and therapeutic targets for renal functional reserve.
Review in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Temporal Recurrent Neural Networks for Predicting Acute Kidney Injury Recovery by Time of Discharge.AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science · 2026Article
- Association Between the Modified Furosemide Response Index and Prognosis in Patients with Chronic Kidney Disease: A Retrospective Cohort Study Based on the MIMIC-IV Database.International journal of nephrology and renovascular disease · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) represents a significant global health challenge. Despite the availability of treatments, there remains a considerable residual risk of disease progression with current therapeutic approaches. Glomerular filtration rate (GFR) can increase due to various physiological and pathological stress responses, and the difference between the maximum GFR and the baseline GFR is termed renal functional reserve (RFR). A decline in RFR has been observed to occur well before CKD is clinically diagnosed. In addition, prolonged pathological stimulation of RFR may promote the development of other metabolic, hemodynamic, inflammatory, and fibrotic processes, which can ultimately drive CKD progression. This review consolidates the current evidence on the molecular mechanisms that underlie the initiation and decline of RFR, a phase that remains largely unaddressed as a primary treatment target but is gaining recognition for its critical role in CKD pathophysiology. Additionally, various methods for the safe and effective assessment of RFR are discussed. Recent clinical trial highlight promising new drug therapies and dietary strategies for the management of subclinical stages of CKD.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.