ReviewJournal of translational medicine2011
Etiopathology of chronic tubular, glomerular and renovascular nephropathies: clinical implications.
Review in Journal of translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis 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
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Pooled it
- Searching for Potential Markers of Glomerulopathy in Urine by HS-SPME-GC×GC TOFMS.Molecules (Basel, Switzerland) · 2021Trial
- Population pharmacokinetic and pharmacodynamic analysis of BIIB023, an anti-TNF-like weak inducer of apoptosis (anti-TWEAK) monoclonal antibody.British journal of clinical pharmacology · 2016Trial
- Network Pharmacology and Molecular Docking-Based Investigation of Empagliflozin's Therapeutic Potential in Chronic Kidney Disease.Life (Basel, Switzerland) · 2026Article
- Exploration of SOCS3 and HSPA1A in PANoptosis during acute myocardial infarction and chronic kidney disease.Frontiers in cellular and infection microbiology · 2026Article
- Protective Role of Coffee in Thioacetamide-induced Nephrotoxicity: A Study in Rats.Current pharmaceutical biotechnology · 2026Article
- Metabolomics reveals alterations in gut-derived uremic toxins and tryptophan metabolism in feline chronic kidney disease.The veterinary quarterly · 2025Article
- Article
- Serial Combination of Toxic and Ischemic Renal Damages Causes Subsequent Chronic, Irreversible, and Progressive Renal Disease in Rats.International journal of molecular sciences · 2025Article
- Hypertensive Nephrosclerosis: Pathological Changes and Overlap with Diabetic Nephropathy.Cureus · 2025Review
- Evaluating the impact of Arteriovenous Fistula (AVF) creation on kidney function.Journal of nephrology · 2025Observational
- High Prevalence of Lesions of Systemic Hypertension in Bile-Extracted Asiatic Black Bears (Animals : an open access journal from MDPI · 2025Article
- DOME: Directional medical embedding vectors from Electronic Health Records.Journal of biomedical informatics · 2025Article
- Article
- Localized histopathological effects of high-salt intake on the aorta and kidney in rats.Frontiers in physiology · 2025Article
- Article
- Review
- Stroke-Induced Renal Dysfunction: Underlying Mechanisms and Challenges of the Brain-Kidney Axis.CNS neuroscience & therapeutics · 2024Review
- Early Diagnosis and Treatment of Kidney Injury: A Focus on Urine Protein.International journal of molecular sciences · 2024Review
- The impact of hypoxia preconditioning on mesenchymal stem cells performance in hypertensive kidney disease.Stem cell research & therapy · 2024Article
18 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
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) comprises a group of pathologies in which the renal excretory function is chronically compromised. Most, but not all, forms of CKD are progressive and irreversible, pathological syndromes that start silently (i.e. no functional alterations are evident), continue through renal dysfunction and ends up in renal failure. At this point, kidney transplant or dialysis (renal replacement therapy, RRT) becomes necessary to prevent death derived from the inability of the kidneys to cleanse the blood and achieve hydroelectrolytic balance. Worldwide, nearly 1.5 million people need RRT, and the incidence of CKD has increased significantly over the last decades. Diabetes and hypertension are among the leading causes of end stage renal disease, although autoimmunity, renal atherosclerosis, certain infections, drugs and toxins, obstruction of the urinary tract, genetic alterations, and other insults may initiate the disease by damaging the glomerular, tubular, vascular or interstitial compartments of the kidneys. In all cases, CKD eventually compromises all these structures and gives rise to a similar phenotype regardless of etiology. This review describes with an integrative approach the pathophysiological process of tubulointerstitial, glomerular and renovascular diseases, and makes emphasis on the key cellular and molecular events involved. It further analyses the key mechanisms leading to a merging phenotype and pathophysiological scenario as etiologically distinct diseases progress. Finally clinical implications and future experimental and therapeutic perspectives are discussed.
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.