Res(e)t and Relaxation: Intractable Hypernatremia

Introduction: Sodium and water homeostasis is regulated by vasopressin (AVP) release from the anterior pituitary and its antidiuretic action on the kidney. Osmoreceptors detect changes in plasma tonicity. The osmotic threshold (or osmostat) for AVP release is ˜285 mOsmol/kg H20. Case Description: A 3-y boy with global developmental delay, cerebral palsy and G-tube dependence presented with pneumonia. The plasma sodium (PNa) improved from 154mmol/L to 151mmol/L with increased water intake. On follow up, PNa was 157mmol/L: he was admitted for further investigations. There was persistent sialorrhea and diaphoresis, but no medication changes, excess water losses or increased salt intake. He had stable vitals, 100g drop in weight and unremarkable examination. With no intervention, repeat bloodwork showed PNa 150mmol/L, plasma osmolality (POsm) 309 mOsm/kg H20, urine osmolality (UOsm) 1019 mOsm/kg and FeNa 0.5%. All other serum electrolytes and renal indices were unremarkable. Active increase in free water intake above his usual total fluid intake resulted in a PNa nadir of 146mmol/L, with urine osmolality of 187 mOsm/kg. These data show evidence of free water loss while still hypernatremic. After returning to his TFI, PNa settled around 151 mmol/L, with UOsm 600 mOsm/kg, and has remained stably high ever since. Discussion: We describe a case of hypertonic hypernatremia and concomitant highly concentrated urine, indicating excellent urinary concentrating ability and adequate ADH production, effectively ruling out diabetes insipidus. Once PNa dropped below 150mmol/L (but never less than 146), enhanced free water excretion was invariably observed. We hypothesized that these findings are in keeping with an osmostat that is reset at a higher POsm to trigger ADH release: a rarer form of reset osmostat (RO), which is more commonly associated with hyponatremia (type C SIADH). We estimate that the threshold is ˜150mmol/L instead of the usual 145. The etiology remains unclear with no hypothalamic lesion and no evidence of anterior pituitary dysfunction, and perhaps long term hypodipsia contributed. An overview of published literature on reset osmostat hypernatremia will be discussed. RO should be considered when dealing with a patient with an unusually difficult-to-control dysnatremia, when there is evidence of normal kidney function, and intact urine diluting and concentrating ability.

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