Association between salt intake and long-term mortality in hemodialysis patients: A retrospective cohort study.

BACKGROUND: The association between salt intake and clinical outcomes in hemodialysis patients has been controversial. This study aimed to clarify the association between salt intake and mortality in hemodialysis patients. METHOD: The present study included patients who underwent hemodialysis from June 1st 2016 to May 31st 2020. Corrected salt intake by ideal body weight was the main predictor of outcomes. Ideal body weight was calculated assuming that the ideal body mass index is 22 kg/m2 for the Japanese population. The multivariate Cox proportional hazards model was used to determine the association between corrected salt intake and mortality, adjusting for potential confounders. The outcomes considered were all-cause mortality and cumulative incidence of cardiovascular events at year 4. RESULT: A total of 492 adult patients were enrolled in the study. The mean daily salt intake and corrected salt intake at baseline were 9.5 g/day and 0.17 g/kg/day, respectively. The low corrected salt intake group (< 0.13 g/kg/day) demonstrated the highest 4-year all-cause mortality. No association was observed between corrected salt intake and the cumulative incidence of cardiovascular events. In multivariate Cox proportional hazards analysis, only the group with corrected salt intake of 0.16-0.20 g/kg/day was associated with a decreased hazard risk for all-cause death compared with the low corrected salt intake group. CONCLUSION: The present study found that a low salt intake was associated with high all-cause mortality in hemodialysis patients. Reduced long-term survival may be attributed to malnutrition resulting from excessive salt restriction.

Quantification of autonomic nervous activity by heart rate variability and approximate entropy in high ultrafiltration rate during hemodialysis.

BACKGROUND: Few studies have focused on the imbalance of the autonomic nervous system in ultrafiltration rate (UFR) subjects without blood pressure variation during maintenance hemodialysis (HD), although the role of autonomic nervous system activation during HD has been proposed to be an important factor for the maintenance of blood pressure. METHODS: Variations over time in autonomic nervous activity due to differences in UFR were evaluated by measuring heart rate variability (HRV) and approximate entropy (ApEn) in 35 HD patients without blood pressure variations during HD session. The subjects were divided into 3 groups, those with UFR <10 ml/h/kg; ≥10 ml/h/kg but ≤15 ml/h/kg; and >15 ml/h/kg, and Holter ECG was recorded continuously during HD session using frequency analysis of RR intervals. High frequency (HF) and low frequency (LF) spectral components are found to be representative of the parasympathetic nervous system and sympathovagal balance, respectively, with the ratio of LF to HF of HRV providing a measure of sympathetic nervous system. RESULTS: In subjects with UFR >15 ml/h/kg, HF components were significantly lower, and LF/HF and ApEn values were significantly higher, in the latter half of an HD session than before starting HD. CONCLUSION: Removing water from these subjects would promote sustained sympathetic nervous overactivity. These findings indicate that the UFR during HD needs to be set at ≤15 ml/h/kg.

Immunohistochemical detection of ENaCbeta in the terminal Schwann cells associated with the periodontal Ruffini endings of the rat incisor.

Epithelial sodium channels (ENaCs) are a subfamily of ion channels within the degenerin/ENaC (DEG/ENaC) superfamily. Previous studies have shown the immunolocalization of ENaC in the neural elements of the cutaneous mechanoreceptors as well as dorsal root and trigeminal ganglion neurons, indicating the involvement of this molecule in mechanotransduction. The present study examined the expression of ENaCbeta, a major component of ENaC protein, in the mechanoreceptive Ruffini endings in the periodontal ligament of the rat incisors by immunohistochemistry. The expression of ENaCbeta in the trigeminal ganglion--which innervates the periodontal Ruffini endings--was also investigated at the mRNA and protein levels. Furthermore, double staining and a nerve injury experiment were applied to clarify its detailed localization in the periodontal Ruffini endings. ENaCbeta immunoreaction in the trigeminal ganglion was recognizable in the comparatively large neurons which have been considered to mediate mechanotransduction. Immunohistochemistry for ENaCbeta demonstrated dendritic ramifications of the Ruffini endings as well as the rounded cells in the periodontal ligament. Double staining with ENaCbeta and either PGP9.5 or S-100 protein showed immunoreaction for ENaCbeta in both the axonal and glial elements in the periodontal ligament. Some ENaCbeta positive cells with rounded profiles were reactive to non-specific cholinesterase activity. Furthermore, a transection of the inferior alveolar nerve failed to eliminate the rounded cells with ENaCbeta reaction, indicating that they were the terminal Schwann cells associated with the periodontal Ruffini endings. These findings suggest that ENaCbeta is a key mechanotransducing channel in the periodontal Ruffini endings. Probably, the terminal Schwann cells together with the axon terminals regulate mechanotransduction in the periodontal endings.