ReviewAdvances in chronic kidney disease2017
The Tubulointerstitial Pathophysiology of Progressive Kidney Disease.
Review in Advances in chronic kidney disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.
What it found
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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
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- The association between hypertriglyceridemic-waist phenotype and chronic kidney disease: a cohort study and meta-analysis.Scientific reports · 2022Pooled it
- Dickkopf-3 (DKK3) in Urine Identifies Patients with Short-Term Risk of eGFR Loss.Journal of the American Society of Nephrology : JASN · 2018Trial
- Epigenetically silencing gluconeogenic enzyme PCK1 by EZH2 promotes renal tubulointerstitial fibrosis.Molecular biomedicine · 2026Article
- An Acidic Tubulointerstitial Microenvironment Delays Cell-Cycle Progression in Proximal Tubule Cells and Fibroblasts and Synergizes With Lactate to Drive Phenotypic Alterations.Acta physiologica (Oxford, England) · 2026Article
- Cell based therapy in chronic kidney disease: emerging evidence for a fifth pillar in guideline directed medical therapy.Clinical and experimental nephrology · 2026Review
- Low-intensity extracorporeal shock wave therapy ameliorates fibrosis and renal function in a preclinical model of chronic kidney disease.Anatomy & cell biology · 2026Article
- Transcriptomic Exploration of Tetrahydrocurcumin Effects in Chronic Kidney Disease.Biomedicines · 2026Article
- Preferential renal tubular injury and increased renal sympathetic activity occur during the early stages of DOCA-salt hypertension in male rats.Physiological reports · 2026Article
- Prognostic significance of interstitial fibrosis and tubular atrophy in biopsy-proven diabetic kidney disease: a single-center retrospective cohort study.Frontiers in endocrinology · 2026Article
- Therapeutic Advances in Diabetic Kidney Disease: 30 Years of Evidence and the Rise of the "Fantastic Four" in Nephrology.Cardiorenal medicine · 2026Review
- Emerging roles of cannabinoid pathways in renal injury and repair.Frontiers in pharmacology · 2026Review
- Shen Shuai II Recipe alleviates renal fibrosis in chronic kidney disease by improving of hypoxia and inhibition of TLR4/MyD88/NF-κB/NLRP3 pathway.Renal failure · 2025Article
- Cage-Farming Causes Histopathological Alterations in the Renal Tissues of the Rainbow TroutInternational journal of molecular sciences · 2025Article
- Kidney transcriptomics signature of prospective rapid diabetic kidney disease progression.BMC nephrology · 2025Article
- Diffusion Tensor Imaging (DTI) as a Non-Invasive Tool for Assessing Pediatric Kidney Transplants: A Feasibility Study.Pediatric transplantation · 2025Article
- Neutrophil percentage-to-albumin ratio is associated with all cause and cardiovascular disease mortality in chronic kidney disease based on NHANES 2001-2018.Scientific reports · 2025Article
- Urinary Dickkopf-related protein 3 as a novel biomarker for kidney function decline in children with Alport syndrome.Pediatric nephrology (Berlin, Germany) · 2025Article
- Advances in Nano-Immunomodulatory Systems for the Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Acidosis-induced p38-kinase activation triggers an IL-6-mediated crosstalk of renal proximal tubule cells with fibroblasts leading to their inflammatory response.Cell communication and signaling : CCS · 2025Article
- Tubular FoxP2 and Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025Article
32 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
1 author at 1 institution in 1 country.
Funding
Abstract
Accumulating evidence suggests that the central locus for the progression of CKD is the renal proximal tubule. As injured tubular epithelial cells dedifferentiate in attempted repair, they stimulate inflammation and recruit myofibroblasts. At the same time, tissue loss stimulates remnant nephron hypertrophy. Increased tubular transport workload eventually exceeds the energy-generating capacity of the hypertrophied nephrons, leading to anerobic metabolism, acidosis, hypoxia, endoplasmic reticulum stress, and the induction of additional inflammatory and fibrogenic responses. The result is a vicious cycle of injury, misdirected repair, maladaptive responses, and more nephron loss. Therapy that might be advantageous at one phase of this progression pathway could be deleterious during other phases. Thus, interrupting this downward spiral requires narrowly targeted approaches that promote healing and adequate function without generating further entry into the progression cycle.
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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.