BACKGROUND: Hyponatremia has a number of different causes; some may have serious untoward implications for patients undergoing chronic ambulatory peritoneal dialysis (CAPD). OBJECTIVE: To determine the pathophysiology of hyponatremia in patients on CAPD. METHODS: A retrospective analysis was carried out on 210 patients on CAPD. We selected patients with 2-4 consecutive periods when the plasma sodium concentration was < or =130 mmol/L and again when it was > 133 mmol/L. Exclusion criteria included hyperglycemia, orthostatic hypotension, edema, and inadequate records. RESULTS: An electrolyte-free water gain appeared to be the main cause of hyponatremia in only 1 of 5 patients because this was the only patient with a significant increase in body weight. In 1 patient, there was weight loss in the hyponatremic period, suggesting tissue catabolism was present. In 3 patients, there was neither weight gain nor evidence for a contracted extracellular fluid volume in the hyponatremic period, suggesting that intracellular potassium and phosphate loss could be the major mechanism for their hyponatremia. CONCLUSION: When hyponatremia is due to a catabolic state, its management should aim to restore intracellular fluid composition (i.e., to correct malnutrition).
BACKGROUND:Hyponatremia has a number of different causes; some may have serious untoward implications for patients undergoing chronic ambulatory peritoneal dialysis (CAPD). OBJECTIVE: To determine the pathophysiology of hyponatremia in patients on CAPD. METHODS: A retrospective analysis was carried out on 210 patients on CAPD. We selected patients with 2-4 consecutive periods when the plasma sodium concentration was < or =130 mmol/L and again when it was > 133 mmol/L. Exclusion criteria included hyperglycemia, orthostatic hypotension, edema, and inadequate records. RESULTS: An electrolyte-free water gain appeared to be the main cause of hyponatremia in only 1 of 5 patients because this was the only patient with a significant increase in body weight. In 1 patient, there was weight loss in the hyponatremic period, suggesting tissue catabolism was present. In 3 patients, there was neither weight gain nor evidence for a contracted extracellular fluid volume in the hyponatremic period, suggesting that intracellular potassium and phosphate loss could be the major mechanism for their hyponatremia. CONCLUSION: When hyponatremia is due to a catabolic state, its management should aim to restore intracellular fluid composition (i.e., to correct malnutrition).