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Hypernatremia during Correction of Hypercalcemia

Accessible online at: www.karger.com/journals/nef Dear Sir, Hypernatremia has been occasionally reported in patients with hypercalcemia due to a renal concentrating defect which becomes apparent when the calcium concentration exceeds 11 mg/dl [1–3]. Hypercalcemic diabetes insipidus has recently been shown to result from inhibition of arginine vasopressin stimulated water flux by activation of collecting duct calcium-sensing receptors [4]. However, hypernatremia during the correction of hypercalcemia has not been reported yet. An 85-year-old woman who developed progressive increase in serum sodium levels during hospitalization was referred to us for consultation. The patient, who was on thiazides for hypertension and on calcium and vitamin D preparations for osteoporosis, was admitted to the clinic with high fever, nausea, constipation, and symptoms of a urinary tract infection. On admission, laboratory investigation showed: urea 192 mg/dl, creatinine 2.2 mg/dl, calcium 16.7 mg/dl, phosphate 3.9 mg/dl, potassium 2.6 mmol/l, sodium 143 mmol/l, chloride 100 mmol/l, and urine osmolality 540 mosm/kg. Urine culture grew Escherichia coli. A second-generation cephalosporin was administered intravenously, while careful hydration was instituted with 2.5 liters of sodium chloride 0.9% daily with a KCl solution (27 mEq K+ in each liter of saline solution) to restore intravascular volume as well as potassium and calcium balance. Due to protracted nausea, she was not able to drink water. However, despite the progressive improvement of renal function as well as potassium and calcium levels (serum creatinine reached 1.7 and 1.4 mg/dl, serum potassium 3.25 and 3.4 mmol/l, and serum calcium 13.8 and 13.1 mg/dl, respectively, during the 2 following days), a gradual increase in serum sodium levels was detected (serum sodium levels increased to 150 and 157 mmol/l during the 2 following days). A half-normal sodium chloride solution was then introduced. Two days later, the patient’s serum laboratory data revealed: creatinine 1.1 mg/dl, urea 116 mg/dl, calcium 9.9 mg/dl, potassium 3.83 mmol/l, sodium 146 mmol/l, and chloride 112 mmol/l. In our case severe hypercalcemia was due to a combination of factors such as administration of calcium, vitamin D, and thiazides and severe intravascular volume depletion leading to prerenal azotemia. Drug cessation and hydration with saline solutions resulted in a complete normalization of serum calcium levels. Hypernatremia resulted from the ongoing hypercalcemia-induced as well as fever-induced hypotonic losses coupled with the inability to drink water and the administration of a relatively hypertonic solution, since the addition of potassium chloride can significantly increase the osmolality of administered fluids (1 liter of sodium chloride 0.9% plus 54 mmol of KCl has an osmolality of 360 mosm/kg). Thus, the administered potassium chloride must be taken into account when calculating the amount of solutes given, especially during the correction of electrolyte abnormalities [5]. We conclude that during the correction of hypercalcemia the administration of normal saline along with potassium chloride to replenish intravascular volume and to restore potassium balance can lead to hypernatremia, particularly in cases with a poor water intake.