Urea for hyponatremia? Kidney International Richard H. Sterns, Stephen M. Silver, John K. Hix  Kidney International  Volume 87, Issue 2, Pages 268-270 (February 2015) DOI: 10.1038/ki.2014.320 Copyright © 2015 International Society of Nephrology Terms and Conditions

Figure 1 Expected osmotic effects of rapid administration of 30g (500mosmol) of urea to a 50-kg woman with 25liters of total body water, serum sodium 120mmol/l, and urine osmolarity 500mosmol/l. (a) Initial distribution. Administered urea rapidly enters muscle cells, distributing in total body water, which results in a 20-mosmol increase in plasma osmolality, with no expansion of extracellular fluid (ECF) volume. Because urea is slow to cross the blood–brain barrier, with a reflection coefficient of 0.5, a 10-mosmol osmotic gradient from plasma to brain is created, which draws water out of the brain. Over time, the urea gradient across the blood–brain barrier diminishes for two reasons: (1) slow diffusion of urea into the brain; and (2) loss of urea from the plasma caused by urea excretion in the urine. (b) Effect of urea excretion. Beginning immediately, administered urea is excreted in the urine, so that with normal renal function, all is excreted within approximately 12h, resulting in the loss of 1 liter of electrolyte-free water. As urea is excreted, the decrease in plasma urea causes a fall in plasma osmolality, but the loss of water increases the plasma sodium concentration by 5mequiv./l, which prevents water from reentering the brain. Kidney International 2015 87, 268-270DOI: (10.1038/ki.2014.320) Copyright © 2015 International Society of Nephrology Terms and Conditions