ReviewFrontiers in pharmacology2026
Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteinuria is a well-established risk factor for chronic kidney disease progression, and its reduction is associated with improved kidney outcomes. During proteinuric chronic kidney diseases, the abnormal passage of plasma-derived proteins through the damaged glomerular filtration barrier can lead to the activation of various pathophysiological processes in the tubular compartment. These mainly comprise complement activation and excessive proximal tubule reuptake of filtered proteins, such as albumin and associated lipids, which trigger cytotoxic effects through the dysregulation of multiple signaling pathways. Collectively, these signaling events can induce proximal tubular cell apoptosis or the acquisition of injury phenotypes, characterized by the paracrine release of bioactive substances that promote infiltration of immune cells and fibroblast-to-myofibroblast differentiation, eventually contributing to the development of tubulointerstitial fibrosis and progressive loss of kidney function. In this review, we provided an up-to-date overview of the complex mechanisms behind the toxic effects of ultrafiltered proteins on the tubulointerstitium under proteinuric conditions. The mechanistic insights that have been gained recently could be valuable for the future development of new classes of drugs to be used in combination with, or as an alternative to, the currently approved anti-proteinuric treatments in patients who are poorly responsive or unable to tolerate them, respectively.
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.