ArticleKidney international2018
A molecular morphometric approach to diabetic kidney disease can link structure to function and outcome.
Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 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
46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.
- Genome-wide meta-analysis and omics integration identifies novel genes associated with diabetic kidney disease.Diabetologia · 2022Pooled it
- Urinary Proteomics Identifies Cathepsin D as a Biomarker of Rapid eGFR Decline in Type 1 Diabetes.Diabetes care · 2022Pooled it
- Plasma proteome signatures of ASK1 inhibition by selonsertib associate with efficacy in the MOSAIC randomized trial for diabetic kidney disease.BMC nephrology · 2025Trial
- Review
- Urinary microenvironment-degradable nanocapsules for traceable therapy of diabetic nephropathy.Materials today. Bio · 2026Article
- Systematic proteomics analysis of lysine acetylation reveals critical features of renal proteins in kidney calculi formation.PloS one · 2026Article
- 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
- Kidney transcriptomics signature of prospective rapid diabetic kidney disease progression.BMC nephrology · 2025Article
- Role of inflammasomes in diabetes mellitus: mechanisms, complications, and therapeutic potential.Molecular biology reports · 2025Review
- The CLCA1/TMEM16A/Cl- current axis associates with H2S deficiency in diabetic kidney injury.JCI insight · 2025Article
- Inulin andFrontiers in endocrinology · 2025Article
- Profiling of insulin-resistant kidney models and human biopsies reveals common and cell-type-specific mechanisms underpinning Diabetic Kidney Disease.Nature communications · 2024Article
- Combination therapy for kidney disease in people with diabetes mellitus.Nature reviews. Nephrology · 2024Review
- VDR restores the expression of PINK1 and BNIP3 in TECs of streptozotocin-induced diabetic mice.Life science alliance · 2024Article
- Association between red cell distribution width/serum albumin ratio and diabetic kidney disease.Journal of diabetes · 2024Article
- Molecular mechanisms and therapeutic potential of natural flavonoids in diabetic nephropathy: Modulation of intracellular developmental signaling pathways.Current research in pharmacology and drug discovery · 2024Review
- DNA methylation markers for kidney function and progression of diabetic kidney disease.Nature communications · 2023Article
- Diagnostic criteria and etiopathogenesis of type 2 diabetes and its complications: Lessons from the Pima Indians.Presse medicale (Paris, France : 1983) · 2023Review
- Transcriptomics-proteomics Integration reveals alternative polyadenylation driving inflammation-related protein translation in patients with diabetic nephropathy.Journal of translational medicine · 2023Article
- Single-cell transcriptomics reveals a mechanosensitive injury signaling pathway in early diabetic nephropathy.Genome medicine · 2023Article
Corrections and comments
- Commented on by
Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Diabetic kidney disease is the leading cause of kidney failure. However, studies of molecular mechanisms of early kidney damage are lacking. Here we examined for possible linkage between transcriptional regulation and quantitative structural damage in early diabetic kidney disease in Pima Indians with type 2 diabetes. Tissue obtained from protocol kidney biopsies underwent genome-wide compartment-specific gene expression profiling and quantitative morphometric analysis. The ultrastructural lesion most strongly associated with transcriptional regulation was cortical interstitial fractional volume (VvInt), an index of tubule-interstitial damage. Transcriptional co-expression network analysis identified 1843 transcripts that correlated significantly with VvInt. These transcripts were enriched for pathways associated with mitochondrial dysfunction, inflammation, migratory mechanisms, and tubular metabolic functions. Pathway network analysis identified IL-1β as a key upstream regulator of the inflammatory response and five transcription factors cooperating with p53 to regulate metabolic functions. VvInt-associated transcripts showed significant correlation with the urine albumin to creatinine ratio and measured glomerular filtration rate 10 years after biopsy, establishing a link between the early molecular events and long-term disease progression. Thus, molecular mechanisms active early in diabetic kidney disease were revealed by correlating intrarenal transcripts with quantitative morphometry and long-term outcomes. This provides a starting point for identification of urgently needed therapeutic targets and non-invasive biomarkers of early diabetic kidney disease.
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.