<b><i>Introduction:</i></b> The mortality of peritoneal dialysis (PD) patients remains high. The neutrophil to lymphocyte ratio (NLR), as an indicator of systemic inflammation, has been considered to be a predictor of cardiovascular and all-cause mortality in hemodialysis patients. The present study aims to investigate the relationship between NLR and long-term outcome in PD patients. <b><i>Materials and Methods:</i></b> The study included patients who initiated PD for at least 3 months between January 1, 2013, and December 31, 2015. All the patients were followed up until death, cessation of PD, or to the end of the study (June 31, 2018). NLR was calculated as the ratio of neutrophils to lymphocytes. <b><i>Results:</i></b> A total of 140 patients were included in this study. The median NLR reported was 2.87. Patients with lower NLR showed a higher survival rate than patients with higher NLR (log rank 6.886, <i>p</i> = 0.009). Furthermore, patients with higher NLR had a significantly higher cardiovascular mortality (log rank 5.221, <i>p</i> = 0.022). Multivariate Cox proportional hazards model showed that older age (HR 1.054, 95% CI 1.017–1.092, <i>p</i> = 0.004), higher Ca × P (HR 1.689, 95% CI 1.131–2.523, <i>p</i> = 0.010), and higher NLR (HR 2.603, 95% CI 1.037–6.535, <i>p</i> = 0.042) were independent predictors of increased all-cause mortality. NLR was also independently associated with cardiovascular mortality (HR 2.886, 95% CI 1.005–8.283, <i>p</i> = 0.039). Higher NLR (HR 2.667, 95% CI 1.333–5.337, <i>p</i> = 0.006), older age (HR 1.028, 95% CI 1.005–1.052, <i>p</i> = 0.016), and history of cardiovascular disease (HR 1.426, 95% CI 1.195–3.927, <i>p</i> = 0.031) were significantly independently associated with poor peritonitis-free survival in this study. <b><i>Conclusions:</i></b> NLR could be a strong predictor of long-term outcome in PD patients.

Cone Dystrophy with Supernormal Rod Response (CDSRR) is a rare autosomal recessive disorder leading to severe visual impairment in humans, but little is known about its unique pathophysiology. We have previously shown that CDSRR is caused by mutations in the KCNV2 (Potassium Voltage-Gated Channel Modifier Subfamily V Member 2) gene encoding the Kv8.2 subunit, a modulatory subunit of voltage-gated potassium (Kv) channels. In a recent study, we validated a novel mouse model of Kv8.2 deficiency at a late stage of the disease and showed that it replicates the human electroretinogram (ERG) phenotype. In this current study, we focused our investigation on young adult retinas to look for early markers of disease and evaluate their effect on retinal morphology, electrophysiology and immune response in both the Kv8.2 knockout (KO) mouse and in the Kv2.1 KO mouse, the obligate partner of Kv8.2 in functional retinal Kv channels. By evaluating the severity of retinal dystrophy in these KO models, we demonstrated that retinas of Kv KO mice have significantly higher apoptotic cells, a thinner outer nuclear cell layer and increased activated microglia cells in the subretinal space. Our results indicate that in the murine retina, the loss of Kv8.2 subunits contributes to early cellular and physiological changes leading to retinal dysfunction. These results could have potential implications in the early management of CDSRR despite its relatively nonprogressive nature in humans.