In October: Reviews on lupus nephritis; autoimmune disease metabolism; the potassium switch; and epigenetics in kidney development, plus Commentaries on kidney protection in T1DM; gaps in care for young adults; nephrology in Taiwan; and palliative care go.nature.com/4Al56fw

Recommendations for the management of frailty in chronic kidney disease: a consensus report dlvr.it/TVf9hr

Cardiovascular–kidney–metabolic syndrome as a mitochondrial systems disorder dlvr.it/TVd51y

An integrated single-cell atlas of hypertension dlvr.it/TVczs0

Ferroptosis in kidney disease dlvr.it/TVXtNx

Megalin: from structure to function dlvr.it/TVXV45

The role of senescence in kidney ageing, injury and fibrosis dlvr.it/TVcYgN

Enhanced urea uptake promotes bleeding in advanced CKD dlvr.it/TVbgZR

Epidemiology, mechanisms and clinical implications of heat-related kidney disease dlvr.it/TVVtSL

Primary cilia: master conductors of cellular communication in development and disease dlvr.it/TVZqBY

Uprooting inequity: cultivating a flourishing and socially accountable nephrologist workforce for Indigenous peoples dlvr.it/TVVDXl

Our new Review is out in @NatRevNeph : "Nucleic acid sensing pathways in kidney disease development. rdcu.be/E4LcDJnuvDba When RNA and DNA end up in the wrong compartment, or contain the wrong modifications the cell no longer recognizes them as self. Damaged mitochondria spill mtDNA and mtRNA into the cytosol, genotoxic stress releases nuclear DNA fragments, and epigenetic dysregulation reawakens endogenous retroelements. Sensors such as cGAS–STING, AIM2, RIG-I and MDA5, and the endosomal Toll-like receptors read these misplaced nucleic acids as if they were an infection. The interferon and inflammasome programs that follow drive regulated cell death, sterile inflammation and fibrotic remodelling, in the glomerulus and in the tubule alike, across acute kidney injury, diabetic kidney disease and lupus nephritis. This has been a long-standing interest of our laboratory, and the Review builds directly on that work: Mitochondrial damage and cytosolic mtDNA activate STING and drive renal inflammation and fibrosis — Cell Metabolism 2019: doi.org/10.1016/j.cmet.2019.… NLRP3 and STING are central to APOL1-associated podocytopathy — Journal of Clinical Investigation 2021: doi.org/10.1172/JCI136329 Increased endogenous retrovirus expression triggers fibroinflammation in kidney disease — Nature Communications 2023: doi.org/10.1038/s41467-023-3… NAD+ precursor supplementation prevents mtRNA/RIG-I-dependent inflammation during kidney injury — Nature Metabolism 2023: doi.org/10.1038/s42255-023-0… Endoplasmic reticulum stress and the STING pathway converge in kidney fibrosis — Kidney International 2025: doi.org/10.1016/j.kint.2024.… The therapeutic landscape is genuinely encouraging. STING and TLR inhibitors, and strategies that restore nucleic acid clearance, protect the kidney in preclinical models. The challenge ahead is precision: these pathways also defend us, so the targeting will need to be cell-type specific and stage specific. Warm congratulations to Magaiver Andrade-Silva, Cherry Kang and Yena Jang. doi.org/10.1038/s41581-026-0…

City design for kidney health dlvr.it/TVT5l3

Mechanisms of regeneration and maladaptive repair in acute kidney injury dlvr.it/TVQS2L

Kidney research at an inflection point: why the next decade must be different dlvr.it/TVMfL7