Background High peritoneal transport is associated with high mortality and technical failure in peritoneal dialysis (PD). Baseline peritoneal solute transport rate (PSTR) as measured by the peritoneal equilibration test (PET) within 6 months after PD initiation varies between patients. Sodium is reported to be stored in the skin or muscle of dialysis patients. This study investigated whether excessive salt intake in uremic mice caused peritoneal alterations without exposure to PD fluid. Methods Sham-operated (Sham) and subtotal nephrectomized (Nx) mice were randomly given tap water or 1% sodium chloride (NaCl)-containing water for 8 weeks. PET was then performed to evaluate peritoneal function. Human mesothelial cell line Met-5A was used for in vitro studies. Results We observed higher PSTR in Nx mice with 1% NaCl-containing drinking water (Nx + salt) compared with those with tap water (Nx + water), along with enhanced angiogenesis and inflammation in the peritoneum. Blockade of interleukin (IL)-6 signaling rescued peritoneal transport function in Nx + salt mice. In cultured Met-5A, additional NaCl in the medium upregulated IL-6 as well as vascular endothelial growth factor-A, associated with increased expression and nuclear translocation of tonicity-responsive enhancer binding protein (TonEBP). Knockdown of TonEBP lowered the induction caused by high tonicity. Peritoneal TonEBP expression was higher in Nx + salt mice, while removal of high-salt diet lowered TonEBP level and improved peritoneal transport function. Conclusions Excessive dietary salt intake caused peritoneal membrane functional and structural changes under uremic status. TonEBP regulated hypertonicity-related inflammatory changes and might play a crucial role in high baseline peritoneal transport.

D/Ps of some molecules did not correlate with D/P creatinine. Factors other than molecular weight, such as charge and protein binding rate, are involved in peritoneal transport rates. Metabolomic analysis appears useful to analyze small molecular uremic toxins, which could accumulate in PD patients, and the status of peritoneal membrane transport for each molecule.

Background: Preservation of residual renal function (RRF) is an important factor in achieving adequate peritoneal dialysis (PD) therapy for patients with end-stage renal disease (ESRD). We investigated whether dietary salt restriction was effective during conservative therapy as a factor to prevent decreased RRF after starting PD therapy. Methods:We retrospectively observed 30 patients introduced to PD in a single center. To investigate the relationship between effects of a salt diet and decreased RRF in PD patients for the first year after starting PD, we divided patients into two groups according to salt intake before starting PD therapy: Group 1, <6 g/day; and Group 2, ≥6 g/day. Sodium intake was calculated using samples from 24-hour urinary collection and/or 24-hour peritoneal dialysate collection.Results: Before starting PD, residual renal Kt/V (rKt/V) and CCre (rCCre) were significantly lower in Group 1 than in Group 2 (p<0.001 and p<0.005, respectively). Normalized protein-equivalent of nitrogen appearance was also significantly lower in Group 1 than in Group 2 (p<0.001), suggesting that Group 1 might also maintain good control of protein. Moreover, compared with Group 2, decline rates in rKt/V and rCCre during the first year were significantly lower in Group 1 (p<0.005 and p<0.001, respectively). Conclusion:Our results suggested that restricting salt intake was not only important to preserve RRF during the conservative therapy period in ESRD patients, but also might be important to prevent early decreases in RRF among PD patients.Hiramatsu T (2020) Dietary salt restriction during conservative therapy may prevent declines in residual renal function for the first year after starting peritoneal dialysis in patients with end-stage renal diseases