Abstract Periodontitis has been linked to chronic kidney disease (CKD) through systemic inflammation. However, evidence in early CKD remains limited. We analyzed 6 179 participants from a population-based cohort (median age 62 years; 51% women). Periodontitis was classified according to the 2017 American Academy of Periodontology / European Federation of Periodontology criteria. Kidney function was assessed by the combined creatinine- and cystatin C–based estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (uACR). Associations of periodontitis stages and mean clinical attachment loss (CAL) with eGFR and uACR were examined using multivariable linear regression adjusted for age, sex, diabetes, and smoking. Mediation analyses tested indirect effects of high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6). Prevalence of severe periodontitis increased from 14% in individuals with normal kidney function (eGFR ≥60 mL/min per 1.73 m²) to 36% in those with moderately reduced eGFR (<60 mL/min per 1.73 m²) and from 21% in individuals without albuminuria (<10 mg/g) to 32% in those with moderately increased albuminuria (29–300 mg/g). After adjustment, Stage IV periodontitis was independently associated with lower eGFR (β−1.08 mL/min per 1.73 m²; 95% CI−2.04 to −0.12) and higher Blom-transformed uACR (β 0.09; 95% CI 0.01–0.16) compared with Stage I/II. hsCRP partially mediated these associations, accounting for 35% of the association with eGFR and 10% with uACR. These findings suggest that both inflammatory and non-inflammatory pathways may link periodontitis to early CKD. Periodontitis was associated with reduced eGFR and higher uACR in early CKD. While overlapping risk factors contribute, an independent association remained, only partly explained by systemic inflammation.
Schmidt-Lauber et al. (Sun,) studied this question.