ArticleKidney international2022
Molecular programs associated with glomerular hyperfiltration in early diabetic kidney disease.
Article in Kidney international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Endothelial dysfunction in human diabetic vascular complications: translating single-cell transcriptomics into therapeutic opportunities.Molecular medicine (Cambridge, Mass.) · 2026Review
- A MEF2C transcription factor network regulates proliferation of glomerular endothelial cells in diabetic kidney disease.Kidney international · 2026Article
- Endothelial Ffar4 protects against diabetic kidney disease by potentiating endogenous retinoic acid metabolism.Cellular & molecular biology letters · 2026Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- Diabetes and its complications: molecular mechanisms, prevention and treatment.Signal transduction and targeted therapy · 2026Review
- Genome-Wide Association Study of Quantitative Kidney Function in 52,531 Individuals with Diabetes Identifies Five Diabetes-Specific Loci.Journal of the American Society of Nephrology : JASN · 2025Article
- Unraveling diabetic kidney disease: insights from single-cell RNA sequencing.International urology and nephrology · 2025Review
- Elucidating the function of clusterin in the progression of diabetic kidney disease.Frontiers in pharmacology · 2025Review
- The advance of single cell transcriptome to study kidney immune cells in diabetic kidney disease.BMC nephrology · 2024Review
- Krüppel-like factor 2 is an endoprotective transcription factor in diabetic kidney disease.American journal of physiology. Cell physiology · 2024Review
- Combination therapy for kidney disease in people with diabetes mellitus.Nature reviews. Nephrology · 2024Review
- The key mediator of diabetic kidney disease: Potassium channel dysfunction.Genes & diseases · 2024Review
- Trajectories of eGFR and risk of albuminuria in youth with type 2 diabetes: results from the TODAY cohort study.Pediatric nephrology (Berlin, Germany) · 2023Article
- Enhanced Levels of Glycosphingolipid GM3 Delay the Progression of Diabetic Nephropathy.International journal of molecular sciences · 2023Article
- Diagnostic criteria and etiopathogenesis of type 2 diabetes and its complications: Lessons from the Pima Indians.Presse medicale (Paris, France : 1983) · 2023Review
- Single-cell transcriptomics reveals a mechanosensitive injury signaling pathway in early diabetic nephropathy.Genome medicine · 2023Article
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18 authors at 5 institutions in 3 countries.
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Abstract
Hyperfiltration is a state of high glomerular filtration rate (GFR) observed in early diabetes that damages glomeruli, resulting in an iterative process of increasing filtration load on fewer and fewer remaining functional glomeruli. To delineate underlying cellular mechanisms of damage associated with hyperfiltration, transcriptional profiles of kidney biopsies from Pima Indians with type 2 diabetes with or without early-stage diabetic kidney disease were grouped into two hyperfiltration categories based on annual iothalamate GFR measurements. Twenty-six participants with a peak GFR measurement within two years of biopsy were categorized as the hyperfiltration group, and 26 in whom biopsy preceded peak GFR by over two years were considered pre-hyperfiltration. The hyperfiltration group had higher hemoglobin A1c, higher urine albumin-to-creatinine ratio, increased glomerular basement membrane width and lower podocyte density compared to the pre-hyperfiltration group. A glomerular 1240-gene transcriptional signature identified in the hyperfiltration group was enriched for endothelial stress response signaling genes, including endothelin-1, tec-kinase and transforming growth factor-β1 pathways, with the majority of the transcripts mapped to endothelial and inflammatory cell clusters in kidney single cell transcriptional data. Thus, our analysis reveals molecular pathomechanisms associated with hyperfiltration in early diabetic kidney disease involving putative ligand-receptor pairs with downstream intracellular targets linked to cellular crosstalk between endothelial and mesangial cells.
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