with diabetes insipidus diabetes means
an increased passing of urine and
insipidus means tasteless
so diabetes insipidus is a condition
characterized by the production of large
quantities of dilute and tasteless urine
the tasteless urine of diabetes
insipidus distinguishes it from diabetes
mellitus which describes sweet-tasting
urine and to answer your question yes
urine was really tasted at one point in
time to make that distinction
now in the brain there's a region called
the hypothalamus
inside the hypothalamus are
osmoreceptors which can sense the
osmolality of the blood or basically how
concentrated it is
osmolality is the concentration of
dissolved particles in the blood plasma
or the liquid portion of blood
there are a number of dissolved
particles in the blood plasma but the
major ones are glucose sodium and blood
urea nitrogen
and the normal osmolality is between 285
and 295 ml osmols per kilogram
during periods of dehydration there's an
increase in concentration of these
particles in the blood and so osmolality
increases
the osmoreceptors and the hypothalamus
detect that increased osmolality and
that triggers the sensation of thirst
which tells us to drink more water
the water then gets absorbed and dilutes
the blood
bringing the osmolality back to normal
in addition to osmoreceptors the
hypothalamus has a cluster of neurons
that are found in a specific spot called
the supraoptic nucleus
these neurons produce a hormone called
antidiuretic hormone or adh
adh is also called vasopressin because
it causes smooth muscle around the blood
vessels to contract which increases
blood resistance and raises the blood
pressure
when the osmoreceptors detect high
osmolality they signal the superoptic
nucleus to send adh down the supraoptico
hypophyseal tract
which runs through the infundibulum or
pituitary stock and into the posterior
pituitary gland
where it's then released into the blood
adh travels to the kidneys specifically
to the distal convoluted tubule and the
collecting ducts of the nephrons and
binds to a receptor called vasopressin
receptor 2 or avpr2
when avpr2 is bound proteins called
aquaporins which usually sit in vesicles
inside the cells of the distal
convoluted tubule and collecting ducts
start to embed themselves in the apical
surface of the cells which is the side
that faces the lumen of the tubule
these aquaporins ultimately allow water
and only water to travel out of the
lumen of the tubule and into the cells
lining the nephron
and ultimately back into the blood
just like drinking more water this
dilutes the blood and returns plasma
osmolality to a normal level
this reabsorption process though also
decides how much water leaves the body
as urine and how concentrated that urine
is
which is one of the things that keeps a
normal urine osmolality between 300 and
900 ml osmols per kilogram
diabetes insipidus is when the kidneys
reabsorb too little water from the lumen
of the tubule
and this causes the body to produce
unusually large quantities of urine
which is called polyuria
since there's less water in the blood
plasma osmolality increases and that
triggers thirst and causes an individual
to drink a lot which is called
polydipsia
there are four types of diabetes
insipidus each with its own underlying
cause
the first type is central diabetes
insipidus which is when there's a
problem in the hypothalamus or pituitary
gland preventing adh production or
release
as a result there's insufficient adh in
the blood and that means that there's
less vasoconstriction
and that there aren't enough aquaporins
in the kidneys
central diabetes insipidus is often
caused by damage to the hypothalamus
osmoreceptors the supraoptic nucleus or
the supraoptical hypophyseal tract but
in other cases the exact cause is hard
to identify
the second type is nephrogenic diabetes
insipidus
which is when there's a problem with the
kidneys themselves which makes them
unresponsive to adh
that can happen due to a genetic defect
which can lead to abnormal vasopressin
receptors or aquaporin proteins that are
unresponsive to adh
in addition there are medications like
lithium that can decrease the production
of aquaporin proteins in the collecting
duct
finally there are kidney disorders like
polycystic kidney disease that can cause
diabetes insipidus
the third type is gestational diabetes
insipidus which happens when the
placenta of a pregnant woman releases an
enzyme called vasopressonase
that breaks down vasopressin or adh
as a result adh might still be produced
and released as normal but it doesn't
get to exert its full effect on the
blood vessels or kidneys
in women with gestational diabetes
insipidus vasopressinase is produced
starting in week 8 of pregnancy and
peaks in the third trimester
as a result the symptoms typically
worsen during the course of the
pregnancy right up until birth when the
placenta is removed but can continue for
up to two months after birth due to
residual vasopressinase
the fourth type is dipsogenic diabetes
insipidus or psychogenic polydipsia
which is caused by drinking way too much
water
dipsogenic diabetes insipidus is often
psychological in nature like in
individuals with schizophrenia who might
compulsively drink water
in contrast to the other three types of
diabetes insipidus dipsogenic diabetes
insipidus leads to a decrease in blood
osmolality
the hypothalamus decreases the release
of adh as a normal physiological
response and the kidneys try to excrete
water which leads to polyuria or excess
urination
the symptoms of diabetes insipidus are
polyuria and polydipsia
a person with diabetes insipidus
typically makes over three liters of
dilute urine each day
diabetes insipidus can quickly lead to
dehydration and low blood pressure
the increase in plasma osmolality can
result in fatigue nausea poor
concentration or confusion
the diagnosis of diabetes insipidus
might start with a blood osmolality test
which would show an increased blood
osmolality of above 295 milliosmoles per
kilogram in central gestational and
nephrogenic diabetes insipidus
if blood osmolality is in the usual
range but an individual is still
experiencing both polyuria and
polydipsia then it might be due to
dipsygenic diabetes insipidus which
would be confirmed by finding out if the
person is drinking massive amounts of
water
in addition a water deprivation test can
be done this is where an individual
doesn't drink water for a few hours then
hourly measurements of urine volume and
osmolality are done
in a person with diabetes insipidus
urine osmolality will usually stay below
300 ml osmols per kilogram
despite having no fluid intake
after taking an adh analog like
desmopressin which is the medication
that works like adh
the urine osmolality might return to a
normal level between 300 and 900 ml
osmols per kilogram
suggesting that the cause is a low level
of adh
this would be evidence for both central
and gestational diabetes insipidus which
can be distinguished by looking at
whether the person's pregnant or not
if the adh analog causes urine
osmolality to increase only slightly
then the kidneys aren't responding to
the adh meaning that it's nephrogenic
diabetes insipidus
treating central and gestational
diabetes insipidus relies on
desmopressin to make up for the lack of
adh in the blood
for nephrogenic diabetes insipidus drugs
like thiazide diuretics can be given to
increase urine excretion of sodium since
sodium contributes to blood osmolality
getting rid of sodium reduces blood
osmolality and stops the hypothalamus
from stimulating thirst
in the case of dipsogenic diabetes
insipidus behavioral therapy can help
reduce fluid consumption
all right as a quick recap
diabetes insipidus is caused by
excessive water loss through urine
central diabetes insipidus is due to adh
not being produced or released
and nephrogenic diabetes insipidus is
the result of the kidneys not being able
to respond to adh
gestational diabetes insipidus is caused
by vasopressinase which breaks down adh
and is produced in the placenta of some
pregnant women
and dipsogenic diabetes insipidus is
caused by excessive water intake
commonly due to psychological conditions
helping current and future clinicians
focus
learn retain and thrive learn more