ReviewNature reviews. Nephrology2026
Next-generation therapeutics for diabetic kidney disease.
Review in Nature reviews. Nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The Role ofGenes · 2026Pooled it
- Efficacy and safety of traditional Chinese medicine decoctions in breast cancer treatment: a network meta-analysis.Frontiers in oncology · 2026Pooled it
- Evaluating Kidney Responses to Angiotensin-Converting Enzyme Inhibition at the Single-Cell Level.Journal of the American Society of Nephrology : JASN · 2026Article
- Multimodal Magnetic Resonance Imaging in Diabetic Kidney Disease: From Pathophysiological Insights to Clinical Applications.Diagnostics (Basel, Switzerland) · 2026Review
- LncRNA MALAT1 drives diabetic kidney injury via Nrf2 suppression in glomerular endothelium.Scientific reports · 2026Article
- Recent Advances in Kidney Disease Diagnosis and Treatment: Bridging Molecular Insights and Clinical Practice.Diagnostics (Basel, Switzerland) · 2026Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus is the leading cause of chronic kidney disease and kidney failure worldwide, and diabetic kidney disease (DKD) is associated with excess cardiovascular and all-cause mortality. The pathophysiology of DKD is complex and multifactorial, characterized by physiologically redundant haemodynamic, metabolic and inflammatory pathways that promote maladaptive renal remodelling and accelerate disease progression. Current management of DKD centres around four key pillars of guideline-directed medical therapy (GDMT): renin-angiotensin-aldosterone system inhibitors, sodium-glucose cotransporter-2 inhibitors, non-steroidal mineralocorticoid receptor antagonists and glucagon-like peptide-1 receptor agonists. These therapies are increasingly used in combination for cardiorenal protection in DKD. However, substantial residual cardiorenal risk persists even among patients receiving optimal GDMT. Next-generation therapies for DKD that are currently in development include various incretin-based therapies, endothelin receptor antagonists, aldosterone synthase inhibitors, soluble guanylate cyclase agonists and anti-inflammatory agents. These therapies are expected to complement current GDMT and further improve kidney and cardiovascular outcomes in patients with DKD.
Indexed as
Identifiers
41526484What 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.