Chronic kidney disease (CKD) is a progressive, irreversible condition that imposes a substantial burden of morbidity and mortality. While inadequate glycemic and blood pressure control remain its central drivers, dietary patterns are increasingly recognized as modifiable determinants of disease trajectory. Ultra-processed foods (UPFs), now pervasive in contemporary diets, have attracted particular attention due to their distinct physicochemical properties and biological effects. These products are industrial formulations that undergo multiple processing steps and are typically characterized by low nutritional quality, high energy density, and extensive use of additives. Epidemiological data suggest an association between higher UPF intake and adverse renal outcomes, yet the underlying mechanisms remain insufficiently defined. We posit inflammaging, a chronic, low-grade inflammatory state linked to biological aging, as a conceptual framework through which UPF-related renal injury may be interpreted. Within this context, gut dysbiosis and excess dietary phosphate emerge as potential mediators. Although no causal relationship has been established until now, there is mounting evidence interconnecting UPF’s consumption, hidden dietary phosphorus, chronic low-grade inflammation, accelerated aging and gut dysbiosis with CKD progression. We highlight critical research gaps and emphasize the need for policy and population-level strategies to reduce UPF consumption and slow CKD progression.
Kounatidis et al. (Wed,) studied this question.