by Alicia M Prater PhD

Created on: February 24, 2012   Last Updated: April 27, 2012

The kidneys are responsible for controlling fluid balance in the body. During dehydration, which is a lack of water in the body, the kidneys act to retain more water in the blood and maintain the balance. This change in function is directed by  vasopressin, also known as antidiuretic hormone, a hormone secreted from the pituitary gland. This hormone is secreted during dehydration and other conditions in which the water-solute balance in the blood is not maintained, and then binds to receptors on the kidney cells, promoting reabsorption of water into the bloodstream and decreasing urine output. In chronic dehydration, this hormone is expressed at consistently high levels, leading to changes in the structure and function of the kidneys.

Changes in kidney function

The morphology, or structure, of the kidney is adjusted in the presence of dehydration to allow for more concentrated urine, which then results in more water in the bloodstream. This involves an alteration in the kidney’s function, including increased permeability of the collecting ducts to water, increased sodium transport in the distal tubules, and increased permeability of the tubule to urea. This greatly increases the work load on the kidney, increasing the glomerular filtration rate and renal plasma flow, which over the long term can be a risk factor for some diseases.

Changes in kidney morphology

To achieve these altered functions in response to vasopressin, the structures of the kidney undergo changes. For acute adjustments in fluid balance, aquaporin 2 is the main protein involved in the permeability of the collecting duct to water. This protein is located in the luminal membrane, but in chronic dehydration other aquaporins (specifically aquaporin 3 and 4) are expressed and present in the basal lateral membrane. The expression of urea transporters in the collecting duct and loop of Henle is also up-regulated during chronic dehydration. Another alteration is activation of the sodium transporter known as the amiloride-sensitive epithelial sodium channel in the connecting tubule and collecting duct. This is seen in conjunction with increased expression of certain sodium channel subunits according to a 2003 review in the European Journal of Clinical Nutrition.

Risk factor for disease

Chronic dehydration is thought to be a risk factor for chronic renal failure; diabetic nephropathy, a renal complication in diabetes mellitus; and hypertension, a sodium-sensitive condition. A study in 2006 found that patients with long-term intravenous nutrition (called parenteral nutrition) or chronic intestinal failure have impaired renal function due to chronic dehydration. Consistent mild dehydration is also a risk factor for kidney stones, urinary tract cancer, colon cancer, and mitral valve prolapse when it is accompanied by poor fluid intake according to the National Health and Medical Research Council of Australia.

To summarize, during chronic dehydration the kidneys reabsorb more water into the blood stream in response to consistently high levels of vasopressin. To facilitate the change in kidney function, the proteins involved in water, sodium, and urea transport and absorption in the kidney are up-regulated or expressed in different locations as necessary to maintain fluid balance. This alteration in kidney function is a risk factor for various diseases.

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