• Ramin Sam, Peter Hart, Roxanna Haghighat, and Todd S Ing.
• Division of Nephrology, San Francisco General Hospital and the University of California, San Francisco, 1001 Potrero Ave, Building 100, Rm 342, San Francisco, CA 94110-1341, USA. samr@medsfgh.ucsf.edu
• Clin. Exp. Nephrol. 2012 Feb 1;16(1):136-46.

BackgroundA high incidence of hypernatremia is often observed in patients recovering from acute kidney injury (AKI) in intensive care units.MethodsAn unselected cohort of 20 adult patients recovering from AKI in the intensive care unit of a single institution during a 1-year period, were investigated. Serum and urine electrolytes, osmolality, urea nitrogen and creatinine were measured in an attempt to determine the cause of the hypernatremia.ResultsEighty-eight percent of patients who could not drink fluids were found to have hypernatremia (serum Na >145 mEq/L). Even though the hypernatremia was mild in most patients (146-160 mEq/L), the average rise in serum sodium concentration was 17.4 mEq/L. The average urine osmolality was 384 mmol/kg of which 47.6 and 32.8 mmol/kg were contributed by sodium and potassium, respectively. The patients had hypervolemia as evidenced by the presence of edema and an average weight gain of 21.5 kg at the onset of the hypernatremia. The rise in serum sodium level coincided with an increase in urine output.ConclusionThe hypernatremia is believed to be due to post-AKI diuresis in the face of inability to maximally concentrate the urine because of renal failure. The diuresis caused a disproportionate loss of water in excess of that of sodium in the absence of replenishment of the water loss. Additionally, the patients were hypervolemic due to the retention of large quantities of sodium and water as a result of infusion of substantial volumes of physiological saline prior to the development of hypernatremia.

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