ReviewNature reviews. Nephrology2025
Crosstalk between glomeruli and tubules.
Review in Nature reviews. Nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effect of statin therapy on renal and lipid outcomes in CKM syndrome stage 2: a meta-analysis of randomized controlled trials.BMC nephrology · 2025Pooled it
- Tubulointerstitial inflammation in glomerular diseases: mechanistic pathways, prognostic value, and translational therapeutic targets.Renal failure · 2026Review
- Fractional Excretion of Total Protein and Long-Term Kidney Outcomes in Patients With Biopsy-Proven Diabetic Nephropathy: The N-BDN Study.Diabetes, obesity & metabolism · 2026Observational
- Article
- Association between thrombomodulin and the prevalence of renal calculus: a cross-sectional study from Wuhan central hospital.World journal of urology · 2026Article
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- Renoprotective effects of tubular glucagon receptor activation mediated by V-ATPase.Science advances · 2026Article
- A TGF-β1/LEF1/β-catenin/JLP network motif regulates autophagy and tubule injury in renal fibrosis.JCI insight · 2026Article
- Glomerulo-Tubular Crosstalk in Diabetic Kidney Disease: From Pathophysiology to Novel Therapeutics.Electrolyte & blood pressure : E & BP · 2026Review
- GloPath: An Entity-Centric Foundation Model for Glomerular Lesion Assessment and Clinicopathological Insights.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Next-generation therapeutics for diabetic kidney disease.Nature reviews. Nephrology · 2026Review
- Proximal Tubule Reabsorption and CKD Progression in the General Population.Kidney international reports · 2026Article
- Tubular Epithelia-Specific Deletion of MCP-1 Does Not Afford Protection Against Adriamycin-Induced Kidney Injury.International journal of molecular sciences · 2026Article
- Urokinase Promotes Redundantly Intratubular C3a-Formation But Not ENaC-Driven Hypertension in DOCA/Salt Kidney Injury.Hypertension (Dallas, Tex. : 1979) · 2026Article
- The Chronic Elevated Consumption ofInternational journal of molecular sciences · 2026Article
- Astragaloside IV: A multipotent phytochemical for treating fibrotic diseases (Review).International journal of molecular medicine · 2026Review
- Chinese Herb-Induced Type II Crescentic Glomerulonephritis: A Case Report of Four Patients.Kidney medicine · 2026Article
- Article
- Knowledge Mapping of Macrophages in Renal Fibrosis: A Bibliometric Analysis from 2014 to 2025.Journal of inflammation research · 2026Review
- Lipid metabolism drives podocyte injury in diabetic kidney disease.Frontiers in immunology · 2026Review
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
Models of kidney injury have classically concentrated on glomeruli as the primary site of injury leading to glomerulosclerosis or on tubules as the primary site of injury leading to tubulointerstitial fibrosis. However, current evidence on the mechanisms of progression of chronic kidney disease indicates that a complex interplay between glomeruli and tubules underlies progressive kidney injury. Primary glomerular injury can clearly lead to subsequent tubule injury. For example, damage to the glomerular filtration barrier can expose tubular cells to serum proteins, including complement and cytokines, that would not be present in physiological conditions and can promote the development of tubulointerstitial fibrosis and progressive decline in kidney function. In addition, although less well-studied, increasing evidence suggests that tubule injury, whether primary or secondary, can also promote glomerular damage. This feedback from the tubule to the glomerulus might be mediated by changes in the reabsorptive capacity of the tubule, which can affect the glomerular filtration rate, or by mediators released by injured proximal tubular cells that can induce damage in both podocytes and parietal epithelial cells. Examining the crosstalk between the various compartments of the kidney is important for understanding the mechanisms underlying kidney pathology and identifying potential therapeutic interventions.
Indexed as
Identifiers
39643696What 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.