Patients with diabetes insipidus produce urine which is too dilute. This can lead to a form of dehydration known as hypernatraemia where there is a reduction in body water relative to sodium, making the body fluids more concentrated (hyperosmolar).(i)
Hypernatraemia can occur in the following ways:
• loss of water without a corresponding loss of sodium (hypovolaemic hypernatraemia)
• increase in salt intake without an increase in water intake. (hypervolaemic hypernatraemia).
Both these situations result in cellular dehydration, hyperosmolar body fluids and increased extracellular sodium concentration.(ii)
Hyperosmolality can also result from an excess of other osmolytes (osmotically active substances), for example glucose in diabetes or urea in renal failure. Thus, if insulin production is inadequate (as in diabetes mellitus), the excess circulating glucose can lead to hyperosmolality. Hyperosmolality causes cells to shrink as water leaves them by osmosis, in order to compensate for the fluid deficit in extracellular compartments.(i) Cellular volume changes have been implicated in several complications of diabetes, including diabetic ketoacidosis, peripheral neuropathy, retinopathy and cataract formation.(iii) In addition, dehydration has also been shown to accelerate the developmiint of diabetic ketoacidosis during insulin deficiency in Type 1 diabetes, and to promote the development of hyperglycaemia.(iv) (See also Obesity)
Last updated: November 2004
(i) The kidney at a glance. Eds C O’Callaghan and BM Brenner. London: Blackwell Science 2000
(ii) Principles of Human Nutrition. Ed M Eastwood. Chapter 8: Water, electrolytes, minerals and trace elements. London: Chapman & Hall 1997
(iii) McManus ML, Churchwell KB. Clinical significance of cellular osmoregulation. In: Strange K (ed) Cellular and Molecular Physiology of Cell Volume Regulation. Boca Raton FL: CRC Press 1994:63-77, as quoted in Stookey JD. Another look at fuel + O2 -> CO2 + H2O. Developing a water-oriented perspective. Medical Hypotheses 1999;52:285-290
(iv) Burge MR, Garcia N, Qualis CR, Schade DS. Differential effects of fasting and dehydration in the pathogenesis of diabetic ketoacidosis. Metabolism 2001;50:171-177
