ReviewClinical kidney journal2023
Gluconeogenesis in the kidney: in health and in chronic kidney disease.
Review in Clinical kidney journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Advancements in early biomarkers of acute kidney injury: from traditional indicators to a paradigm shift in lactate metabolism.Annals of medicine · 2026Review
- Renal glucose metabolic enzyme expression during AKI-to-CKD transition.International urology and nephrology · 2026Article
- Insulin resistance and hyperinsulinaemia in kidney disease: mechanisms and metabolic effects.Nature reviews. Nephrology · 2026Review
- Proximal Tubule-Specific Genetic Deficiency of PPARα Worsens Systemic Lipid and Glucose Metabolism During Fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Tissue-Specific Diversity of Nuclear-Encoded Mitochondrial Genes Related to Lipid and Carbohydrate Metabolism in Buffalo.Molecular biotechnology · 2026Article
- Hepatocyte nuclear factor 1 in renal lipid metabolism: molecular mechanisms and therapeutic potentials.Cell biology and toxicology · 2025Review
- The SLC-ome of membrane transport: From molecular discovery to physiology and clinical applications.Physiological reviews · 2025Review
- Lactate and lactylation in the kidneys: Current advances and prospects (Review).International journal of molecular medicine · 2025Review
- Assessing Creatine-Related Gene Expression in Kidney Disease: Can Available Data Give Insights into an Old Discussion?Nutrients · 2025Review
- The emerging role of exosomal LncRNAs in chronic fatigue syndrome: from intercellular communication to disease biomarkers.Frontiers in molecular biosciences · 2025Review
- The gut-kidney axis is regulated by astragaloside IV to inhibit cyclosporine A-induced nephrotoxicity.Frontiers in pharmacology · 2025Article
- G6PC1 expression as a prognostic biomarker associated with metabolic reprogramming and tumor microenvironment in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Handling the sugar rush: the role of the renal proximal tubule.American journal of physiology. Renal physiology · 2024Review
- Tanshinone I improves renal fibrosis by promoting gluconeogenesis through upregulation of peroxisome proliferator-activated receptor-γ coactivator 1α.Renal failure · 2024Article
- Metabolic reprogramming and renal fibrosis: what role might Chinese medicine play?Chinese medicine · 2024Review
- Review
- Megalin Knockout Reduces SGLT2 Expression and Sensitizes to Western Diet-induced Kidney Injury.Function (Oxford, England) · 2024Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) is a global health issue with increasing prevalence. Despite large improvements in current therapies, slowing CKD progression remains a challenge. A better understanding of renal pathophysiology is needed to offer new therapeutic targets. The role of metabolism alterations and mitochondrial dysfunction in tubular cells is increasingly recognized in CKD progression. In proximal tubular cells, CKD progression is associated with a switch from fatty acid oxidation to glycolysis. Glucose synthesis through gluconeogenesis is one of the principal physiological functions of the kidney. Loss of tubular gluconeogenesis in a stage-dependent manner is a key feature of CKD and contributes to systemic and possibly local metabolic complications. The local consequences observed may be related to an accumulation of precursors, such as glycogen, but also to the various physiological functions of the gluconeogenesis enzymes. The basic features of metabolism in proximal tubular cells and their modifications during CKD will be reviewed. The metabolic modifications and their influence on kidney disease will be described, as well as the local and systemic consequences. Finally, therapeutic interventions will be discussed.
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What Socratic 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 Socratic graph.