Disorders in water balance cause changes in body fluid osmolality, affecting the amount of Na+ in the urine. This is due to decreased filtered Na+ levels, increased reabsorption in the proximal tubule and loop of Henle, and reduced delivery of Na+ to the ASDN. As a result, Na+ is virtually eliminated from the urine, leading to a decrease in urine volume. When there is a positive water balance (intake > excretion), body fluid osmolality decreases and hyponatremia occurs. Conversely, when there is a negative water balance (intake < excretion), body fluid osmolality increases and hypernatremia occurs.

The volume of the extracellular fluid (ECF) is determined by the amount of Na+ present in this compartment. To maintain a constant ECF volume (euvolemia), the excretion of NaCl must match its intake. The kidneys play a major role in regulating NaCl excretion from the body. Volume sensors located primarily in the vascular system monitor the volume and pressure. When ECF volume expands, neural and hormonal signals are sent to the kidneys to increase the excretion of NaCl and water, restoring euvolemia. Conversely, when ECF volume contracts, signals are sent to the kidneys to decrease NaCl and water excretion.

References:
- Berl T. Vasopressin antagonists. N Engl J Med. 2015;372:2207-2216.
- Bichet DG. Polyuria and diabetes insipidus. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.
- Brown D, Fenton RA. The cell biology of vasopressin action. In: Taal MW, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia: Saunders; 2012.
- Dantzler WH, et al. Urine-concentrating mechanism in the inner medulla: function of the thin limbs of the loops of Henle. Clin J Am Soc Nephrol. 2014;9:1781-1789.
- Danziger J, Zeidel M. Osmotic homeostasis. J Am Soc Nephrol. 2015;10:852-862.
- Knepper MA, et al. Molecular physiology of water balance. N Engl J Med. 2015;372:1349-1358.
- Nielsen S, et al. Aquaporin water channels in mammalian kidney. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.
- Robertson GL. Thirst and vasopressin. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.
- Sands JM, et al. Urine concentration and dilution. In: Taal MW, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia: Saunders; 2012.
- Sands JM, Layton HE. The urine concentrating mechanism and urea transporters. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.
Disorders of water balance alter body fluid osmolality. Because Na+ with its anions are the major determinant filtered amount of Na+ is decreased, (2) reabsorption in the proximal tubule and loop of Henle is enhanced (GFR is decreased, whereas proximal reabsorption is increased, and thus glomerulotubular balance does not occur under this condition), and (3) delivery of Na+ to the ASDN is reduced. This decreased delivery, together with enhanced Na+ and water reabsorption by the ASDN, virtually eliminates Na+ from the urine and reduces urine volume.
of ECF osmolality, disorders of water balance manifest as changes in ECF [Na+]. Positive water balance (intake > excretion) results in a decrease in body fluid osmolality and hyponatremia. Negative water balance (intake < excretion) results in an increase in body fluid osmolality and hypernatremia.
3. The volume of the ECF is determined by the amount of Na+ in this compartment. To maintain a constant ECFV (i.e., euvolemia) NaCl excretion must match NaCl intake. The kidneys are the major route for regulating excretion of NaCl from the body. Volume sensors located primarily in the vascular system monitor volume and pressure. When ECFV expansion occurs, neural and hormonal signals are sent to the kidneys to increase excretion of NaCl and water and thereby restore euvolemia. When ECFV contraction occurs, neural and hormonal signals are sent to the kidneys to decrease NaCl and water excretion and
Berl T. Vasopressin antagonists. N Engl J Med. 2015;372:2207-2216.
Bichet DG. Polyuria and diabetes insipidus. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.
Brown D, Fenton RA. The cell biology of vasopressin action. In: Taal MW, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia: Saunders; 2012.
Dantzler WH, et al. Urine-concentrating mechanism in the inner medulla: function of the thin limbs of the loops of Henle. Clin J Am Soc Nephrol. 2014;9:1781-1789.
Danziger J, Zeidel M. Osmotic homeostasis. J Am Soc Nephrol. 2015;10:852-862.
Knepper MA, et al. Molecular physiology of water balance. N Engl J Med. 2015;372:1349-1358.
Nielsen S, et al. Aquaporin water channels in mammalian kidney. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.
Robertson GL. Thirst and vasopressin. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.
Sands JM, et al. Urine concentration and dilution. In: Taal MW, et al., eds. Brenner and Rector’s The Kidney. 9th ed. Philadelphia: Saunders; 2012.
Sands JM, Layton HE. The urine concentrating mechanism and urea transporters. In: Alpern RJ, et al., eds. Seldin and Giebisch’s The Kidney: Physiology and Pathophysiology. 5th ed. Philadelphia: Academic Press; 2013.