The basis for hyponatremia is a negative balance for sodium (Na+) plus potassium (K+) and/or a positive balance for water. In patients with normal renal function, vasopressin is needed to prevent the excretion of electrolyte-free water. Vasopressin is not important when there is little residual renal function. If hyponatremia is accompanied by a quantitatively appropriate gain in weight, this implies that a gain of electrolyte-free water was the basis for hyponatremia. In the absence of this weight gain, a loss of salts is to be suspected. If the extracellular fluid (ECF) volume is obviously low, hyponatremia is due to a deficit of NaCl, unless there is a deficit of K+. With a KCl deficit and a contracted ECF volume, there should also be a large shift of Na+ into cells, so metabolic alkalosis would not be an expected finding. In contrast, those patients with no change in weight who have a normal or expanded ECF volume are subdivided into those with a gain of solutes restricted to the ECF compartment (glucose, mannitol), or those with a deficit of solutes of intracellular fluid origin, which implies that a catabolic state (malnutrition) may be present.

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 ≤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).