Diabetes Insipidus

What is diabetes insipidus, what causes it, what its symptom?  What is the difference between diabetes mellitus and diabetes insipidus? How is Diabetes insipidus treated? How can it be prevented, what are the risk factors? All these questions and more shall be answered in this article.

Diabetes insipidus is an uncommon condition in which the kidney are unable to prevent the excretion of water. It is characterised by extreme thirst even when fluids are drunk (polydipsia), and the passing out of large amounts of greatly diluted urine (polyuria) even when fluid intake is curtailed.

Diabetes insipidus should however not be confused with diabetes mellitus. Though sharing the word diabetes, they are completely different conditions. The term diabetes is derived from the Latin word diabetes meaning siphon and is a way to describe the other common similarity experienced by sufferers of both- the production and passing out of large amounts of urine (polyuria). 

Similarly owing to the large discharge of urine, sufferers of both, tend to experience severe thirst although this is not always the case in Diabetes insipidus. The clear difference between them though is that while diabetes mellitus results from a deficiency in insulin or the body’s resistance to insulin leading to abnormally high blood sugar, diabetes insipidus is occasioned by deficiency in ADH the hormone that helps to regulate blood water level or the improper response of the kidney to ADH occasioned by a defect or damage to the kidney itself. The occurrence rate for diabetes insipidus in the general population is 3 in every 100,000.

There are different types of DI. The most common one is called Central DI (CDI) which is caused by a deficiency of Anti diuretic hormone (ADH), the hormone also known as arginine vasopressin (AVP). The second type due to the kidney or nephrons not working properly is called Nephrogenic diabetes insipidus (NDI) and develops when the kidneys or nephrons don’t respond to ADH the way they are supposed to.

So how exactly are the kidneys supposed to respond to ADH? Well the kidneys filter our blood many times during the day, helping to regulate the volume of water in our body by enabling us  reabsorb most of the water and thus concentrating our urine when needed or removing excess fluid from the blood stream and storing it in the bladder as urine before we urinate. This process is in part governed by ADH which when our bodies begin to become dehydrated stimulates the kidney tubules to release water back into the blood stream rather than excrete so much of it as urine. The problem arises when there is a defect in the kidney tubules. This defect may be caused by various factors; genetic, drug usage (for example lithium and demeclocycline) or a chronic kidney disorder. As a result the kidneys no longer work properly and large amounts of water are excreted into the urine instead.

On the other hand, Central diabetes insipidus is usually caused by damage to the pituitary gland or hypothalamus both found in the brain. This is key because it is in this gland, the hypothalamus that ADH is produced whereas the produced ADH is then stored in the pituitary gland for onward release into the blood stream. Damage to these two glands may be due to head injury, genetic problems, infection, surgery, tumour or loss of blood supply to the gland.

Other forms of Di are, Gestational Diabetes Insipidus which occurs during pregnancy and post-partum period and Dipsogenic or primary polydipsia which results from excessive intake of fluid due to either mental illness or damage to the bodies thirst mechanism.

Several tests are available to test for this condition, amongst which are Desmopressin (DDAVP) challenge, Urinalysis, Magnetic Resonance Imaging of the head, Urine output test, Urine concentration test and blood sodium osmolality. 

Urinalysis, urine output test and urine concentration and blood osmolality test, tests which involve the measurement of blood glucose bicarbonate and calcium levels can be used to distinguish DI from other causes of excess urination.  To distinguish the main forms of DI however desmopressin stimulation is usually used. It can be taken as a spray, tablet or injection. Where desmopressin leads to a reduction in urine output and increases urine osmolality, the DI is due to deficiency in hypothalamic production of ADH and thus DI type is likely Central Diabetes Insipidus. Where urine output or osmolality does not change, then DI is due to kidney or nephron defect and thus DI is nephrogenic.

Once known, how then does one go about treating this condition? Well the line of action is to treat the underlying cause. Thus while Central diabetes Insipidus may be managed with vasopressin (desmopressin), medication induced nephrogenic DI may be stopped by the stoppage of such medications. In addition to this, Nephrogenic DI is also treated with diuretics and anti-inflammatory medicines, whereas hereditary nephrogenic DI and lithium induced nephrogenic DI are treated by drinking fluids sufficient to balance out urine output in addition to medication that reduce urine output.

Generally speaking the prognosis for DI is good so far as the underlying cause of the condition is treated. Where this is done, death or serious problems can be avoided. If a sufferer retains normal thirst control and drinks enough fluids, his body fluid and salt balance will remain within the normal threshold. However where sufficient fluid is not consumed, then dehydration and electrolyte imbalance may result. Conversely dangerous electrolyte imbalance may occur if in the treatment of DI with vasopressin the body’s thirst control is still not normal and the subject continues to drink more fluids than his body needs.