ReviewPediatric nephrology (Berlin, Germany)2014
Remnant nephron physiology and the progression of chronic kidney disease.
Review in Pediatric nephrology (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 3 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
68 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- The NLRP3 inflammasome in chronic kidney disease progression: systematic review of preclinical models reveals a critical gap in pyroptosis research and therapeutic translation.Molecular biology reports · 2026Pooled it
- Urinary nephrin-a potential marker of early glomerular injury: a systematic review and meta-analysis.Journal of nephrology · 2024Pooled it
- An evidence-based systematic review of the off-label uses of lisinopril.British journal of clinical pharmacology · 2018Pooled it
- Low Nephron Number and Kidney Disease.International journal of molecular sciences · 2026Review
- Constitutive YAP activation in distal nephron segments disrupts epithelial identity and nephron patterning.JCI insight · 2026Article
- Nanoparticle Clearance and New Horizons in Engineered Drug Delivery.Pharmaceutics · 2026Review
- The urinary albumin-to-creatinine ratio can direct personalized prevention and treatment for cardiovascular and chronic kidney disease.Journal of internal medicine · 2026Review
- Constitutive Yap activation in distal nephron segments disrupts epithelial identity and nephron patterning.bioRxiv : the preprint server for biology · 2025Article
- Defining Disease Modification in IgA Nephropathy: Toward a Paradigm Shift in Management.Kidney international reports · 2025Review
- Hyperplastic growth, not hydrostatic distension, in endolymphatic hydrops in humans challenges the classic view of Meniere's disease.Scientific reports · 2025Article
- Uncommon Factors Leading to Nephrotic Syndrome.Biomedicines · 2025Review
- State of the art: Renal recovery after AKI - from basic science to clinical practice.Intensive care medicine · 2025Review
- Finerenone: Potential Clinical Application Across the Spectrum of Cardiovascular Disease and Chronic Kidney Disease.Journal of clinical medicine · 2025Review
- Unraveling the Mechanisms of Magnesium Supplementation in Alleviating Chronic Kidney Disease Complications and Progression: Balancing Risks and Benefits.Biological trace element research · 2025Review
- Methylseq, single-nuclei RNAseq, and discovery proteomics identify pathways associated with nephron-deficit CKD in the HSRA rat model.American journal of physiology. Renal physiology · 2025Article
- Decline in eGFR and mortality among type II diabetic patients: a 3-year prospective cohort study from Palestine.BMC nephrology · 2025Article
- Biomaterial-assisted organoid technology for disease modeling and drug screening.Materials today. Bio · 2025Review
- Article
- Machine learning models predict the progression of long-term renal insufficiency in patients with renal cancer after radical nephrectomy.BMC nephrology · 2024Article
- EPRS1-mediated fibroblast activation and mitochondrial dysfunction promote kidney fibrosis.Experimental & molecular medicine · 2024Article
8 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.
Funding
Abstract
In chronic kidney disease, ongoing failure of individual nephrons leads to the progressive loss of renal function. This process results in part from a cellular and molecular response to injury that represents an attempt to maintain homeostasis but instead initiates a program that damages the nephron. As nephrons are lost, compensation by the remaining nephrons exacerbates glomerular pathophysiology. The delivery of excessive amounts of biologically active molecules to the distal nephron and tubulointerstitium generates inflammation and cellular dedifferentiation. Energy requirements of hyperfunctioning nephrons exceed the metabolic substrate available to the renal tubule, and inadequacy of the local vascular supply promotes hypoxia/ischemia and consequent acidosis and reactive oxygen species generation. In this way, mechanisms activated to maintain biological balance ultimately lead to demise of the nephron.
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.