DI Chap. 67

Question 1

Primary diabetes insipidus is most commonly acquired and central in origin. Common causes:

Secondary diabetes insipidus is usually renal in origin. Common causes include:

manifestation of DI that requires emergency intervention is severe hypernatremia and dehydration caused by:

Answer 1

trauma and intracranial masses.

hypercalcemia, gram-negative sepsis, and severe hypokalemia

urinary free water losses without appropriate intake

Question 2

DI is either (3):

Answer 2

lack of the hormone vasopressin (ADH)
lack of renal receptors to vasopressin
inability of those receptors to respond to vasopressin

Question 3

Explain DI in the context of Urine Concentration Mechanism and hyposthenuric:

Answer 3

normally functioning kidney, as the solute within the tubule travels through thick ascending LOH

• sodium (and subsequently chloride) is extracted by an energy-requiring ion pump from the solute in an area that is impermeable to water
• this unusual feat renders the remaining solute hyposthenuric
• of lower osmolality than serum
• final urine concentration then depends on ADH
• when presence or function of vasopressin is lacking (diabetes insipidus), the final urine concentration can remain hyposthenuric
• or can be isosthenuric or even mildly hypersthenuric with partial disease

Question 4

posterior pit:

what reg ADH release (4):

Answer 4

secrete oxytocin and vasopressin

osmolatily
barorecp ECV
ATII
thirst

1% in plasma osmolality
drop in blood volume of approximately 10%

Question 5

importance of concentrated medullary interstitium

Answer 5

Theoretically the maximum urine concentration of a given animal would be equal to the maximum solute concentration of the medullary interstitium.

Question 6

CDI ddx:

why MUST you rule of HAC:

Answer 6

neoplastic, traumatic, inflammatory, congenital, and idiopathic conditions

Glucocorticoid administration is thought to decrease vasopressin release in dogs and therefore can be included in the causes of canine acquired CDI

GC suppress ADH release
Alcohol suppress ADH release

Question 7

NDI primary vs secondary

mst common secondary causes (7):

Answer 7

primary NDI is uncommon and often congenital (young male dogs likely -linked very rare)

secondary NDI is extremely common

gram-negative sepsis - interf. with binding
hypercalcemia - interf. with binding
hypokalemia -interf. with binding
portal systemic shunts
liver insufficiency - no urea production (med. washout)
hypoadrenocorticism (more common in dogs)
hyperthyroidism (more common in cats)

Question 8

explain medullary washout as cause of secondary NDI:

Addison’s and medullary washout:

Liver insufficiency

Lack of Na for concentrated medulla:

Answer 8

medullary washout, is absent, the urine will not become concentrated; it will be isosthenuric or even hyposthenuric

polyuric and polydipsic animals (lask aldosterone)
insufficient sodium in dogs with hypoadrenocorticism (medullary wash out)

functional secondary NDI, despite absolutely normal renal function and normal vasopressin concentrations.

insufficient urea

functional secondary NDI

Question 9

Dignosis:

Answer 9

high on ddx: severe PU/PD & hyposthenuric

The first step exclude other common causes PU/PD

Question 10

CHEM R/O secondary NDI:

why MUST you rule of HAC:

Answer 10

hypercalcemia
severe hypokalemia
low serum urea
low sodium w Addison’s

Glucocorticoid decrease ADH release = acquired CDI

Question 11

CKD and USG

Answer 11

CKD as a cause of PU/PD unlikely if hyposthenuric

Question 12

common scenario we are faced with is an older dog with severe polyuria, polydipsia, and hyposthenuric urine and no abnormal findings on physical examination, complete blood count, serum biochemistry profile, urinalysis (except the hyposthenuria), urine culture, and abdominal radiographs or ultrasonography. At this point in our diagnostic workup, the most likely remaining ddx (4):

Answer 12

hyperadrenocorticism CDI or NDI

primary or psychogenic polydipsia

Question 13

next step exclude hyperadrenocorticism:

Answer 13

HAC less likely based on a urine cortisol/creatinine ratio within RI
or LDDS test with results within the reference range
ACTH stim less advisable option for this purpose because in many dogs with hyperadrenocorticism the results of an adrenocorticotropic hormone stimulation test lie within the normal reference range

It is absolutely essential to make every effort to exclude hyperadrenocorticism in these cases. If this step is missed and a water deprivation test or desmopressin acetate trial is used to confirm CDI, a misdiagnosis may occur.

Question 14

Next step exclude psychogenic polydipsia:

serum osmolality test may be used to attempt to diagnose psychogenic polydipsia. What finding would you expect?:

Answer 14

primary disturbance PD (vs. PU)

polydipsia should always be slightly overhydrated (with a low serum sodium concentration and low serum osmolality)

dogs with other causes of polyuria and polydipsia including diabetes insipidus should be slightly dehydrated (with a relatively high serum sodium concentration and serum osmolality).

< 280 mOsm/L most consistent w psychogenic polydipsia

> 280 mOsm/L is hard to interpret because even if the dog did have psychogenic polydipsia, if it did not drink excessively that day

Question 15

A modified water deprivation test results:

Answer 15

CDI and NDI will not be able to concentrate

appropriate rise in USG suggestive of psychogenic polydipsia

Question 16

Causes of misdiagnoses

Answer 16

Medullary washout
Partial CDI, or a relative lack of vasopressin
hyperadrenocorticism may appear to have CDI or partial CDI per a water deprivation test, leading to a misdiagnosis

(MoA) Glucocorticoid decrease ADH release = acquired CDI

Question 17

risk of water dep. test:

test should be stopped at ___% :

Answer 17

hyperNa
despite aggressive fluid therapy, normal sodium concentrations may be difficult to restore. Desmopressin therapy is warranted in this case to slow the free water loss associated with the marked polyuria and to allow normalization of serum sodium concentrations

5% dehydration

Question 18

Desmopressin trial:
decribe:
interpret:

Answer 18

safer

1. days 5, 6, and 7 of therapy urine collected AM
2. samples brought to veterinarian for USG
3. owners are encouraged to measure water intake during the trial if possible

given mild water deprivation and desmopressin
dog’s urine concentration will steadily increase over trial
medullary washout will be eliminated slowly if present
dog with CDI should have a marked increase in USG
no increase in urine concentration by the end of the trial would be consistent with NDI or psychogenic polydipsia

Question 19

treatment:
desmopressin:
which DI:
route:

Answer 19

desmopressin
CDI
oral
human nasal preparation as eyedrops 
IV in hosp.

other therapies can also be used in those with CDI as well as those with NDI include therapies aimed at
1. lowering total body sodium - thiazide diuretics & salt-restricted diets
minimal success in those with NDI

Question 20

to tx. vs. not to treat:

Answer 20

Another option for owners of pets suffering from CDI or NDI is not to treat. Theoretically, as long as these animals are allowed free access to water, are allowed to urinate outside, and are kept in conditions that help prevent dehydration through additional fluid loss (shade, no strenuous exercise in warm conditions), they will remain hydrated and may exhibit no clinical signs. This is especially important because of the high cost of desmopressin therapy for dogs with CDI and the lack of effective therapy for dogs with NDI.

Question 21

DI in hosp:

When is desmopressin therapy (injectable or eyedrops) should be considered:

Answer 21

first challenge is recognition by the clinician
then aggressive fluids, therapy for acute or chronic hypernatremia, and possibly desmopressin

when dehydration and hypernatremia persist despite appropriate fluid therapy, urine volumes are high, and

Question 22

Px.

Answer 22

primary NDI is guarded because NO of therapy for this condition