ReviewSeminars in nephrology2009
Progression of glomerular and tubular disease in pediatrics.
Review in Seminars in nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Low Nephron Number and Kidney Disease.International journal of molecular sciences · 2026Review
- GloPath: An Entity-Centric Foundation Model for Glomerular Lesion Assessment and Clinicopathological Insights.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mas-related G protein-coupled receptor type D deficiency promotes tubulointerstitial injury and fibrosis associated with proteinuria in male mice.Physiological reports · 2026Article
- Cage-Farming Causes Histopathological Alterations in the Renal Tissues of the Rainbow TroutInternational journal of molecular sciences · 2025Article
- Magnetic resonance elastography-derived stiffness of the kidneys and its correlation with water perfusion.NMR in biomedicine · 2020Article
- Biomarkers of Acute and Chronic Kidney Disease.Annual review of physiology · 2019Review
- Genetic basis of nondiabetic end-stage renal disease.Seminars in nephrology · 2010Article
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 at 2 institutions in 1 country.
Funding
Abstract
Chronic kidney disease may be stimulated by many different etiologies, but its progression involves a common, yet complex, series of events that lead to the replacement of normal tissue with scar. These events include altered physiology within the kidney leading to abnormal hemodynamics, chronic hypoxia, inflammation, cellular dysfunction, and activation of fibrogenic biochemical pathways. The end result is the replacement of normal structures with extracellular matrix. Treatments presently are focused on delaying or preventing such progression, and are largely nonspecific. In pediatrics, such therapy is complicated further by pathophysiological issues that render children a unique population.
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.