When we think of diabetes, it is probably
about diabetes mellitus, which is all about the elevated glucose level in blood
plasma. We all know this already. So how about diabetes insipidus?
Few centuries ago, physicians tasted urine from
patients to diagnose disease; if it is sweet, they suspect diabetes mellitus,
and if it is flavorless, it is diabetes insipidus.
Diabetes insipidus results in excessive
thirst and urination, and the etiology of this condition is by complications
related to vasopressin, also known as antidiuretic hormone (ADH), which is
produced by hypothalamus, and stored in posterior pituitary gland. This hormone
is released when there is a decrease in blood pressure, and its release causes
kidneys to reabsorb water to maintain homeostatic balance in blood pressure.
Ultimately, this leads into highly concentrated urine production.
Simply, the symptoms of diabetes insipidus are
characterized by polydipsia, drinking a lot of water, and polyuria, excreting a
lot of water in urine; these obviously lead into dehydration, sometimes at
severe degree. The excessive dehydration may also cause imbalances in
electrolyte. This disease is caused by either vasopressin-insufficiency or vasopressin-insensitivity,
which is quite similar to the cause of the pathogenic conditions observed in
diabetes mellitus. In both cases, the kidneys cannot reabsorb water, and the
water is excreted as urine.
The most important aspect in treating diabetes
insipidus is to drink a lot of water because it replaces the constant loss of
water by urination. If the disease is caused by vasopressin-deficiency, then
the low level of vasopressin can be handled by taking vasopressin supplementary
medication, orally or nasally. If diabetes insipidus is caused by
vasopressin-insensitivity, then it gets a bit complicated to deal with it.
Surprisingly, the vasopressin-insensitivity condition is treated with a
diuretic; taking diuretic hydrochlorothiazide decreases reabsorption of water
and sodium in distal convulated tubule, which eventually causes dieresis. Therefore,
the overall plasma volume gets decreased, and thereby, decreasing in glomerular
filtration rate (GFR) and enhancing the absorption of water and sodium in
proximal convulated tubule. Ultimately, this results in conservation of plasma
fluid volume.
References:
Loffing J. 2004. Paradoxical antidiuretic
effect of thiazides in diabetes insipidus: another piece in the puzzle.” J. Am.
Soc. Nephrol. 15 (11): 2948-50.
I'm really glad you posted about diabetes insipidus. I did my biochemistry project on diabetes mellitus, but didn't get to research diabetes insipidus. I think that it's important for future health care providers to be able to distinguish the two. It is my understanding that diabetes insipidus does not have to do with an insulin deficiency, whereas diabetes mellitus does. I was reading an article about how yogurt consumption can decrease risk for diabetes mellitus (type 2) that I found interesting. Here's the link if you'd like to read about it: http://www.medicalnewstoday.com/articles/285964.php
ReplyDeleteThank you for your comment, Megan! As I mentioned in my article, diabetes insipidus deals with vasopressin secretion and its sensitivity, while, diabetes mellitus involves insulin. Although, these conditions are manipulated by two different hormones, the pattern of the pathogenesis in both conditions is quite similar to one another somehow. I guess this is why both of these conditions are titled as 'diabetes....'
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