Water Balance

KEY POINTS:

  • The kidneys play a key role in osmoregulation, which maintains the osmolarity of the body’s fluids.
  • Homeostatic osmolarity of blood is approximately 290 milliosomoles/liter.
  • Shifts in blood osmolarity trigger renal mechanisms that alter water reabsorption in urine to return to blood osmolarity to homeostasis.
  • Thus, urine osmolarity reflects these changes.

KEY DEFINITIONS: RELATE URINE OSMOLARITY TO BLOOD OSMOLARITY

  • Isosmotic urine has the same osmolarity as blood.
  • Hyperosmotic urine has higher osmolarity than blood.
  • Hypoosmotic urine has lower osmolarity than blood.

Water Deprivation:

Water deprivation triggers the production of hyperosmotic urine.

  • High solute concentration raises blood osmolarity.
  • Osmoreceptors in hypothalamus are activated.
    – In response, osmoreceptors trigger increased thirst
    – Osmoreceptors also trigger the pituitary gland to release ADH.
  • In the kidney, ADH increases the number of nephron principal cell aquaporins
    – More water is reabsorbed
  • Blood osmolarity returns to homeostasis.
  • Urine volume is reduced; osmolarity is increased.

Clinical Correlations:

  • One of the treatments for bedwetting is to give exogenous ADH (vasopressin) in order to reduce urine volume at night.
  • In the syndrome of inappropriate ADH (SIADH), circulating levels of ADH are abnormally elevated, which increases the amount of water reabsorption and produces hyperosmotic urine; ADH inhibitors can correct this.

Water excess:

Water excess triggers production of hyposmotic urine.

  • High body water content reduces blood osmolarity.
  • Hypothalamic osmoreceptors are not activated, so pituitary gland is not stimulated to release ADH.
  • In absence of ADH, fewer aquaporins in the nephron reabsorb water.
  • Excess water is released in the urine.
  • Blood osmolarity returns to homeostasis.
  • Urine volume is high, its osmolarity is low.

Clinical Correlations:

  • In diabetes insipidus, there is either pathologic failure of ADH release or failure of kidney detection of ADH; as a result, large volumes of dilute urine are produced. DI can be treated with exogenous ADH or other medications

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