J Uribarri1, S Prabhakar, T Kahn. 1. Renal Division, Mount Sinai School of Medicine, New York, USA. jaime.uribarri@mssm.edu
Abstract
BACKGROUND: Low serum sodium is uncommon in peritoneal dialysis (PD), which is surprising in view of the important role of normal kidney function to regulate water and sodium balance. METHODS: We report 2 cases of persistent hyponatremia with balance studies in Case 1. We performed measurements of dialysate sodium and volume output over 24 hours in a group of chronic PD patients. RESULTS: The low serum sodium concentration did not vary too much with overall fluid removal via dialysis in patient 1, mainly because large quantities of sodium were removed in the dialysate. In the 24-hour studies, a significant relationship was found between net daily PD sodium removal and net daily dialysate volume removed (r = 0.65). There was no relationship between net daily PD sodium removal and serum sodium concentration. There was a linear direct correlation between serum and dialysate sodium concentration (r = 0.8) as shown by others previously. CONCLUSIONS: These results suggest that the main determinant of PD sodium loss is net dialysate ultrafiltration volume. Water loss via dialysis is necessarily associated with sodium loss. In order to maintain a normal serum sodium concentration salt intake must be proportional to the water loss induced by dialysis. The stimuli that allow dialysis patients to maintain this delicate balance between water and salt intake are of considerable interest but remain undetermined.
BACKGROUND: Low serum sodium is uncommon in peritoneal dialysis (PD), which is surprising in view of the important role of normal kidney function to regulate water and sodium balance. METHODS: We report 2 cases of persistent hyponatremia with balance studies in Case 1. We performed measurements of dialysate sodium and volume output over 24 hours in a group of chronic PDpatients. RESULTS: The low serum sodium concentration did not vary too much with overall fluid removal via dialysis in patient 1, mainly because large quantities of sodium were removed in the dialysate. In the 24-hour studies, a significant relationship was found between net daily PDsodium removal and net daily dialysate volume removed (r = 0.65). There was no relationship between net daily PDsodium removal and serum sodium concentration. There was a linear direct correlation between serum and dialysate sodium concentration (r = 0.8) as shown by others previously. CONCLUSIONS: These results suggest that the main determinant of PDsodium loss is net dialysate ultrafiltration volume. Water loss via dialysis is necessarily associated with sodium loss. In order to maintain a normal serum sodium concentration salt intake must be proportional to the water loss induced by dialysis. The stimuli that allow dialysis patients to maintain this delicate balance between water and salt intake are of considerable interest but remain undetermined.