ABSTRACT Aim In patients with chronic kidney disease (CKD), salt restriction has been shown to lower blood pressure and proteinuria and to provide kidney protective effects. However, the benefit of salt restriction in older adults with CKD remains unclear, particularly in advanced stages. Methods We conducted a single‐center retrospective cohort study of patients aged ≥ 75 years with CKD (estimated glomerular filtration rate [eGFR] < 60 mL/min/1.73 m2). Salt intake was estimated from spot urine using the Tanaka formula and categorized into quartiles. The primary outcome was a composite kidney endpoint of ≥ 30% eGFR decline or initiation of kidney replacement therapy. Cox proportional hazards models and competing risk analyses were performed, stratified by CKD stage. Results A total of 462 patients (median age, 79 years; 68.6% male) were included. Of these, 305 had CKD Stage 3 and 157 had Stages 4–5. During a median follow‐up of 2.79 years, 121 patients (26.2%) experienced the composite outcome. In Stage 3 CKD, higher salt intake was significantly associated with increased risk (adjusted HR 2.70; 95% CI 1.02–7.12; highest vs. lowest quartile), and findings were consistent across sensitivity analyses. In contrast, no significant association was observed in Stages 4–5. Conclusion Among older adults with CKD, excessive salt intake was associated with adverse kidney outcomes in CKD Stage 3 but not in Stages 4–5. These results suggest that salt restriction may be most beneficial in the early stages of CKD in this population.
We investigated the association between blood pressure (BP) and the risk of cardiovascular disease (CVD) in individuals with non-proteinuric chronic kidney disease (CKD) without diabetes. Using a large-scale nationwide administrative claims and health checkup database in Japan, we identified 287,238 non-diabetic adults with an estimated glomerular filtration rate <60 mL/min/1.73 m2 and negative/trace proteinuria. We examined the association between BP and CVD events by modeling BP both as a continuous variable and as a categorical variable according to the 2017 ACC/AHA guideline classification. The primary outcome was a composite of myocardial infarction, stroke, heart failure, and atrial fibrillation. Multivariable Cox regression analyses showed that higher systolic BP (SBP) was associated with increased CVD risk (hazard ratio [HR] 1.05 per 10 mmHg; 95% CI 1.04-1.05). Compared with normal BP, the HRs were 1.03 (95% CI 1.00-1.07) for elevated BP, 1.08 (1.05-1.11) for stage 1 hypertension, and 1.20 (1.17-1.24) for stage 2 hypertension. Restricted cubic spline analysis showed an increase in CVD risk at SBP levels above ~130 mmHg. However, among individuals receiving antihypertensive medication, a U-shaped association was observed, with an increased risk also evident at SBP levels below ~130 mmHg. In individuals with non-proteinuric CKD without diabetes, higher SBP was positively associated with increased cardiovascular risk. However, a U-shaped association observed among individuals receiving antihypertensive treatment suggests that the relationship between BP and cardiovascular risk may be complex in this population, highlighting the potential importance of individualized clinical assessment.
Yuta Suzuki, Masachika Nishikawa, Hidehiro Kaneko et al.· Hypertension Research· 0 citations
Purpose
To evaluate the therapeutic potential of nicotinamide mononucleotide (NMN) for modulating the neurovascular inflammatory microenvironment and blunting tissue remodeling in neovascular age-related macular degeneration (nAMD).
Methods
A laser-induced choroidal neovascularization (CNV) model was established in C57BL/6J mice, and CNV lesion size was quantified on RPE/choroid flat mounts. Immunostaining evaluated myeloid cell accumulation and fibrosis-associated remodeling. Quantitative RT-PCR and Western blotting assessed inflammatory/angiogenic gene expression and signaling activation in the retina and RPE/choroid. In vitro, lipopolysaccharide (LPS)-stimulated bEnd.3 and primary mouse RPE cells and TGF-β-stimulated THP-1-derived macrophage cells were used to model inflammatory and profibrotic responses.
Results
NMN treatment significantly reduced CNV size in the laser-induced CNV model. This was accompanied by decreased myeloid cell accumulation within CNV lesions. NMN attenuated inflammatory and angiogenesis-related gene expression in the RPE/choroid and neural retina and reduced downstream signaling activation. In vitro, NMN suppressed LPS-induced inflammatory and proangiogenic responses in primary RPE cells and bEnd.3 endothelial cells and inhibited NF-κB activation. NMN further attenuated tissue remodeling, as shown by reduced collagen I-positive area under prolonged and delayed dosing regimens, together with decreased F4/80-positive area and α-smooth muscle actin-positive area within CNV lesions. In TGF-β-induced THP-1-derived macrophage cells, NMN suppressed profibrotic responses.
Conclusions
Our findings indicate that NMN reduces inflammatory signaling and alleviates the inflammatory microenvironment in CNV, accompanied by decreased angiogenesis-related gene expression and fibrosis-related remodeling. By attenuating inflammatory activation and tissue remodeling processes, NMN warrants further evaluation as an adjunctive approach to limit CNV progression and late-stage tissue remodeling in nAMD.
Jue Wang, Hideto Osada, Steve Chen et al.· Investigative Ophthalmology...· 0 citations
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