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250   Diabetes Insipidus




            Diabetes Insipidus                                                                     Client Education
                                                                                                         Sheet
  VetBooks.ir

                                                may also result in reduced ADH secretion.
            BASIC INFORMATION
                                                                                     q  2h  (q  4h  during  the  night)  for  24
                                                Animals without a discernible underlying   ○   The owner should collect urine samples
           Definition                           cause are classified as having idiopathic CDI.  hours. If Uosm in one of these samples
           Inadequate urine-concentrating ability due to   •  In  NDI,  the  kidneys  are  unable  to  con-  is  >  1000 mOsm/kg  (USG  >  1.030),
           insufficient antidiuretic hormone (ADH; i.e.,   centrate urine despite adequate circulating   primary PD is diagnosed. If all samples
           vasopressin) secretion (central diabetes insipi-  levels of ADH. Frequently, the cause of   have Uosm < 1000 mOsm/kg (USG <
           dus  [CDI])  or  action  (nephrogenic  diabetes   inadequate ADH action remains unknown   1.030), a vasopressin analog (desmopressin
           insipidus [NDI])                     (i.e., idiopathic NDI). NDI may also be a   acetate [DDAVP]) is administered for 5
                                                consequence of other disorders (i.e., second-  days: one drop of an intranasal solution
           Epidemiology                         ary NDI).                            (100 mcg/mL)  is  administered  by  the
           SPECIES, AGE, SEX                    ○   Escherichia coli endotoxins (e.g., pyometra,   owner in the conjunctival sac q 8h. During
           •  Affects dogs and cats               pyelonephritis)  and hypercalcemia may   the last day of DDAVP administration,
           •  No breed, sex, or age predisposition  interfere with the renal action of ADH.  the owner should collect another series of
                                                ○   In dogs, glucocorticoids (endogenous   urine samples as before. If Uosm remains
           Clinical Presentation                  hypercortisolism or therapeutic  admin-  < 1000 mOsm/kg in these samples, CDI is
           DISEASE FORMS/SUBTYPES                 istration) and mineralocorticoids (hyper-  very unlikely, and the patient has primary
           •  CDI: hypothalamic/pituitary gland disorder  aldosteronism) interfere with the renal   PD or NDI instead.
           •  NDI: disorder at the renal level    action of ADH.                 •  Water deprivation test
                                              •  Congenital  NDI  and  congenital  CDI  are   ○   Used for differentiating NDI from
           HISTORY, CHIEF COMPLAINT             rare.                                primary  PD  (i.e.,  after  CDI  has  been
           •  The major manifestations are polyuria (PU)                             excluded)
            and polydipsia (PD). The PU may result in    DIAGNOSIS                 ○   Should not be performed if azotemia or
            hypovolemia.                                                             dehydration is present
           •  Stupor, disorientation, ataxia, and seizures   Diagnostic Overview   ○   The patient must be monitored throughout
            possible when a large neoplasm in the area   The diagnostic approach to diabetes insipidus   the test.
            of the pituitary is the underlying cause or   is directed at ruling out metabolic, endocrine,   ○   Procedure
            when insufficient drinking has resulted in   or other causes of PU/PD by using a CBC,   ■   Fast  the  patient  for  12  hours  before
            (life-threatening) hypertonic encephalopathy.  routine biochemistry profile (including plasma   the test.
                                              osmolality), urinalysis, urine culture, and test(s)   ■   At the start of water deprivation, empty
           PHYSICAL EXAM FINDINGS             for adrenal gland disorders. After other dif-  the patient’s bladder, and determine
           •  Usually normal                  ferential diagnoses are excluded, differentiation   the patient’s body weight, plasma
           •  Dehydration may be noted if the animal has   of CDI from NDI or primary PD requires serial   osmolality,  and  USG  or  preferably
            not had free access to water.     measurements of urine osmolality (Uosm), a   Uosm.
           •  Neurologic  abnormalities  (e.g.,  stupor,   trial therapy with exogenous ADH, and eventu-  ■   Withhold water and monitor clinical
            disorientation,  ataxia) possible with   ally, a water deprivation test.   demeanor, body weight (after emptying
            severe hypernatremia or with CDI due to                                    bladder), and USG (or Uosm) q 2h.
            hypothalamic/pituitary mass lesion  Differential Diagnosis                 After a urine sample has been collected,
                                              Other causes of PU/PD (pp. 812, 1271, and   the bladder must be emptied.
           Etiology and Pathophysiology       1442)                                  ■   The test is stopped when 5% of body
           •  Normal daily water consumption < 100 mL/                                 weight has been lost, USG increases to
            kg/d for dogs and < 250 mL/d for cats  Initial Database                    > 1.030 or Uosm to > 1000 mOsm/kg,
           •  ADH is released by the neurohypophysis (i.e.,   •  CBC: usually normal; mild hemoconcentra-  USG or Uosm do not increase for >
            posterior pituitary) in response to increased   tion may be seen if the animal is dehydrated  6 hours, or the pet becomes clinically
            plasma osmolality and, to a lesser degree, to   •  Serum  biochemical  profile:  usually  no   dehydrated or depressed.
            reduced blood volume.               abnormalities except for slight hypernatremia   ■   Slowly reintroduce water when the test
           •  ADH  binds  to  vasopressin-2  receptors   and elevated plasma osmolality in cases of   is completed.
            in the renal distal tubules and collecting   inadequate replenishment of excreted water  ○   Interpretation
            ducts. Activation of these receptors results   •  Urinalysis: usually hyposthenuria to isosthe-  ■   USG or Uosm in patients with primary
            in insertion of water channels (aquaporins)   nuria (urine specific gravity [USG] < 1.013,   PD should slowly increase to > 1.030
            in the luminal membrane of the tubular   often < 1.008) but may be higher in cases   or > 1000 mOsm/kg, respectively.
            cells, leading to increased water absorp-  of partial CDI or NDI         ■   Patients with NDI will show little or
            tion from the lumen of the ducts into   •  Other tests to rule out causes of secondary   no increase in USG or Uosm.
            the  renal  interstitium.  The  end  result  is   NDI include urine culture, Leptospira serol-  ○   Possible  complications  of  the  test:
            concentrated urine.  Water resorption also   ogy, abdominal ultrasonography, and testing   hypernatremia/hypertonic dehydration
            depends on the osmotic gradient of the renal    for hyperadrenocorticism (p. 485).  (irritability, weakness, ataxia, stupor,
            interstitium.                                                            coma)
           •  CDI  results  from  a  lack  of  hypothalamic   Advanced or Confirmatory Testing  •  CT or MRI (p. 1132) of the hypothalamic/
            production or release of ADH secondary   •  Random plasma osmolality: a large overlap   pituitary area can be used to determine
            to immune-mediated destruction of ADH-  exists among CDI, NDI, and primary PD.   whether a cranial mass is the cause of CDI.
            producing neurons, cerebral trauma (head   Plasma osmolality < 280 mOsm/kg suggests   •  Endogenous creatinine or iohexol clearance
            injury), intracranial neoplasia (often a pitu-  primary PD.            testing or nuclear scintigraphy to estimate
            itary tumor), or other hypothalamic/pituitary   •  Serial measurements of urine osmolality and   glomerular filtration rate may be used to
            lesions. In dogs, hyperadrenocorticism   trial therapy with exogenous ADH  rule out renal insufficiency.

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