ReviewPediatric nephrology (Berlin, Germany)2012
Tubulointerstitial injury and the progression of chronic kidney disease.
Review in Pediatric nephrology (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 2 of them syntheses that pooled 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.
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
123 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Is serum hemoglobin level an independent prognostic factor for IgA nephropathy?: a systematic review and meta-analysis of observational cohort studies.Renal failure · 2023Pooled it
- Adverse Effects of fine particulate matter on human kidney functioning: a systematic review.Environmental health : a global access science source · 2022Pooled it
- Proteomics of highly post-translationally modified proteins in kidney tubulointerstitium.bioRxiv : the preprint server for biology · 2026Article
- SOCS2 Downregulation Is Associated with a Ferro-Aging-Related Transcriptomic Signature in Proximal Tubular Cells in Chronic Kidney Disease.Biomedicines · 2026Article
- Pulmonary fibroblast subsets demonstrate differentially enriched signaling pathways during fibrosis resolution and repair.JCI insight · 2026Article
- Therapeutic and mechanistic insights on mitochondrial transplantation in kidney disease.Nature reviews. Nephrology · 2026Review
- A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein.Cell death discovery · 2026Article
- Urine-derived stem cells in kidney disease: progress, challenges, and future directions.Stem cell research & therapy · 2026Review
- Chronic exposure to low levels of glyphosate and metals induces kidney dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Lead-Induced Nephrotoxicity and Its Therapeutic Interventions: An Updated Review.Biological trace element research · 2026Review
- Association of troponin-defined myocardial injury with adverse long-term survival among patients with chronic kidney disease.PloS one · 2026Observational
- Sedentary behavior as an emerging risk factor for chronic kidney disease: a narrative review.Clinical and experimental nephrology · 2026Review
- Correlations Between Trimethylamine-N-Oxide, Megalin, Lysine and Markers of Tubular Damage in Chronic Kidney Disease.Toxins · 2025Article
- Plasma complement proteins as biomarkers and therapeutic targets in chronic kidney disease: a Mendelian randomization analysis.Renal failure · 2025Article
- Biomarkers of Kidney Failure and All-Cause Mortality in CKD.Journal of the American Society of Nephrology : JASN · 2025Article
- Potential Association Between Darbepoetin Alfa Administration and Reduced Proteinuria in Real-World Clinical Practice: A Post Hoc Analysis of the BRIGHTEN Study.Nephrology (Carlton, Vic.) · 2025Observational
- Clinicopathological findings of tubulointerstitial nephritis: a cross-sectional analysis of the Japan Renal Biopsy Registry (J-RBR).Clinical and experimental nephrology · 2025Article
- Hypertensive Nephrosclerosis: Pathological Changes and Overlap with Diabetic Nephropathy.Cureus · 2025Review
- Patterns of Glomerular Injury: Histopathological Classification and Clinical Correlation.Cureus · 2025Review
- Carcinogenesis Associated with Toxin Nephropathy: Proposed Mediation by Phosphate Toxicity.Cells · 2025Review
63 more citing papers are in PubMed but not listed here.
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
Abstract
In chronic kidney disease (CKD), once injury from any number of disease processes reaches a threshold, there follows an apparently irreversible course toward decline in kidney function. The tubulointerstitium may play a key role in this common progression pathway. Direct injury, high metabolic demands, or stimuli from various other forms of renal dysfunction activate tubular cells. These, in turn, interact with interstitial tissue elements and inflammatory cells, causing further pathologic changes in the renal parenchyma. The tissue response to these changes thus generates a feed-forward loop of kidney injury and progressive loss of function. This article reviews the mechanisms of this negative cycle mediating CKD.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.