Nephrology

Remote ischemic preconditioning halves CA-AKI after high-risk PCI

In this double-blind RCT of 420 high-risk PCI patients, remote ischemic preconditioning reduced CA-AKI from 15.0% to 8.1% (RR 0.54, 95% CI 0.31–0.94). The intervention was simple limb-cuff inflation–deflation before PCI, with no RIPC-related adverse events reported. Creatinine change at 48 hours and NGAL-defined subclinical AKI did not significantly differ between groups. Dialysis-requiring AKI, in-hospital mortality, and 30-day MACE were similar, indicating benefit confined to CA-AKI incidence reduction. 1

PLA2R epitope–guided rituximab improves 12‑month remission in membranous nephropathy

This multicenter RCT randomized 64 PLA2R1-positive membranous nephropathy patients to standard GEMRITUX versus personalized rituximab guided by PLA2R epitope spreading. In the personalized arm, spreaders received immediate high-dose rituximab, while non-spreaders used delayed low-dose GEMRITUX-style dosing if still nephrotic at six months. At month 12, partial or complete remission was higher with personalized treatment (67% vs 35%, p=0.01), with better eGFR preservation (p=0.0498). Spontaneous remission and adverse event rates were similar, suggesting biomarker-guided dosing improved efficacy without over-treatment. 2

Each additional controlled risk factor lowers CKD onset and progression in hypertension

This cohort of 77,356 hypertensive adults followed for 13.4 years related CKD outcomes to the number of controlled baseline risk factors. Control of systolic blood pressure, LDL cholesterol, fasting glucose, and BMI each conferred an 18% lower incident CKD risk (HR 0.82, 95% CI 0.81–0.84). Controlling all four versus ≤1 factor reduced incident CKD risk by 42% (HR 0.58, 95% CI 0.52–0.63) and narrowed the gap versus normotensives. In 9,543 hypertensive and 6,799 non-hypertensive participants, each additional controlled factor also cut CKD progression risk by 18% (HR 0.82, 95% CI 0.78–0.86). 3

PIEZO2 identified as a key mechanosensor regulating renin and hyperfiltration

This Cell study shows the force-gated cation channel PIEZO2 is expressed in renin-producing juxtaglomerular granular cells. Conditional PIEZO2 loss in cells of renin lineage elevated renin and dysregulated the renin–angiotensin–aldosterone system. PIEZO2-deficient renin-lineage cells displayed abnormal calcium dynamics in vivo, directly linking mechanotransduction to renin control. PIEZO2 loss drove renin-dependent, MAS-receptor–dependent glomerular hyperfiltration during acute and chronic blood volume challenges. 4