Schatzie is a three year old spayed female Schnauzer with a two to three month long history of polyuria/polydipsia.  Her coat quality has recently decreased, and she is now hyponatremic.  She receives supplemental salt, and occasionally vomits after administration of the salt, and has occasional diarrhea.

The first most serious problem is that Schatzie has hyponatremia, a problem that is likely causing the other problems on the list.  A decreased level of sodium in the plasma can cause swelling in the brain, because with less solutes in the blood, water will move to a place with a higher solute concentration. It could be causing the osmolality of the plasma to be low as well. (Abbot and Friedman, 2012).

Schatzie’s second most serious problem is swelling in the ventricles of the brain.  This problem is likely caused by the hyponatremia. It is a serious problem because it can lead to herniation of the brain stem and then death (Adrogue and Madias, 2012). Although this problem can lead to serious consequences, it is still caused by the hyponatremia, and is therefore second on the list.

The third most serious problem is that Schatzie has a low plasma osmolality.  As mentioned earlier, low sodium could be a cause of low electrolytes.  The body needs electrolytes to function properly, and cells can lyse due to insufficient electrolytes (Burg et al., 2007). 

Schatzie has a large list of problems that could be linked together in a couple of ways, although many of these problems may be incidental or even due to normal physiology.  One possible differential linking these symptoms is diabetes insipidus.  Diabetes insipidus is characterized by polyuria and polydipsia, one of Schatzie’s owners’ primary complaints.  Patients with central diabetes insipidus experience polyuria and polydipsia due to a lack of antidiuretic hormone production by the anterior pituitary gland.  A lack of the substance that causes them to retain water causes the dogs to urinate, and as a result, they drink more in an unconscious attempt to maintain a normal osmotic balance.  Schatzie is not able to maintain a normal osmotic balance, as shown by the low plasma osmolality.  Loss of salt through this process would explain Schatzie’s hyponatremia. 

The same symptoms could also be caused by nephrogenic diabetes insipidus, a disease where the kidneys cannot respond to ADH.  ADH is made in the supraoptic nucleus in the supraoptic region of the hypothalamus.  It is secreted from the posterior pituitary so that the body can retain solutes and water in order to maintain homeostasis.  Schatzie would continue to urinate excessively, and drink an excessive amount as a result.  In order to differentiate between the two diseases, an MRI was probably taken to see if there was a tumor on the pituitary gland that could be causing primary diabetes insipidus to occur.  No such tumor was found, and it would be useful to undertake an ADH response test to see if Schatzie can respond to ADH.

The low sodium does explain the swelling in the brain.  Sodium cannot cross the blood-brain barrier, but water can.  Normally, water is removed when it goes crosses the barrier into the blood due to the hypertonicity of the blood. When there is a hydrostatic gradient, water will flow from an area of low osmolality to high osmolality.  When there is low sodium, water does not leave the brain (Abbot and Friedman, 2012). The decreased osmolality of the blood means that there is an osmolality in the brain that is relatively increased from normal, and edema in the brain ensues.  While diabetes insipidus normally involves an increase of sodium in the blood, it is possible for an animal (or a human) to drink so much due to increased thirst that they actually become hyponatremic (Fasanello and Vu, 2012).

This disease does not explain why Schatzie’s urine specific gravity is normal, and in fact is contradicted by the normal value.  With a normal specific gravity, it would appear that Schatzie isn’t even polydipsic.  If Schatzie were drinking a lot, her urine would be dilute, yet it is not.

The disease also does not explain Schatzie’s enlarged ventricles in her brain.  However, the opposite problem, Syndrome of Inappropriate Antidiuretic, could most all of her symptoms other than polyuria and polydipsia, and is much more likely in this case.  With SIADH, the pituitary releases ADH in an increased amount, so Schatzie would retain water. ADH is normally secreted from the supraoptic nucleus in the supraoptic region of the hypothalamus, and from there goes to the posterior pituitary, where it is released into the bloodstream. In normal physiology, it is produced in response to low blood pressure. The body would retain water due to increased sodium retention, as water will remain within hyposmolar area as opposed to flowing into a hyperosmolar area. The pituitary could overproduce SIADH due to a tumor, perhaps, and this reason could be why Schatzi had an MRI performed on her. The MRI was probably also performed to check to see if she has swelling in her brain, due to the aforementioned affects of osmolality on edema.

If she retains water, the ratio of sodium to water decreases, resulting in hyponatremia and hyposmolality, as shown in Figure 1.  Schatzie has decreased hypochloremia and bicarbonate for the same reason, as these are all the major electrolytes in the blood.  Schatzie would have a normal urine specific gravity because her body still has a high enough amount sodium to concentrate the urine properly (the syndrome of inappropriate antidiuresis).  The osmolality of the urine would be similarly unaffected, although the normal values are variable (Ayoub et al., 2013).

As mentioned earlier, these dogs can have swelling in the brain due to the low sodium to water ratio (Shiel et al. 2009).  An MRI was probably taken for this reason, to see how severe the problem is.  This swelling is dangerous if not corrected, and Schatzie need immediate medical attention. The swelling will worsen as the body retains more water, and Schatzie will begin to experience edema in other places (Adrogue and Madias, 2012).

Treatment could include continuing to add sodium, restricting water, or adding a vasopressin antagonist (Fleeman et al., 2000).  Sodium does not seem to be working, and restricting water may bring in the difficulty of a lack of owner compliance.  If the owner thinks the dog is thirsty, he or she may choose to give the dog water anyway.  The vasopressin antagonists have shown to be a good alternative to the other options (Fleeman et al., 2000).

Schatzie is probably not actually polydipsic.  Her owners may think she is drinking more, but she may not be. A fluid deprivation test may be useful in clearing up this confusion. Schatzi is also probably is urinating less, if anything, because she makes too much ADH, causing her to retain water.  There were also several incidental findings, or problems that were not important in this case.  Her slightly enlarged heart is probably an incidental finding, as is the decreased coat quality.  

Figure 1. SIADH

It is extremely difficult to figure out the connection between the heart, brain, and kidneys.  We haven’t learned much yet about the integration of these body systems, and it took a lot of research to figure out these connections. 

I found it difficult to sort through which problems were incidental and which were pertinent to Schatzie’s problem.  Some of the symptoms listed did say that they were incidental, such as some brain abnormalities, while others required more thought.  For example, an elevated urine pH of 8.5 was at first concerning, but then after more thought, I realized that it could be normal based on when Schatzie last ate a meal. The raw diet was also misleading, but as what Schatzie ate wasn't listed, I did not pursue this as a possible cause of disease.

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Burg, M, Ferraris, J, and Dmitrieva, N. (2007): Cellular response to hyper osmotic stresses. Physiological Reviews. 87: 1441. PubMed ID 17928589.

Fasanello, R and Vu, T. (2012): Paradoxical hyponatremia and polyurodipsia in a patient with lithium-induced nephrogenic diabetes insipidus. Journal of the American Osteopathic Association. 112:588. PubMed ID 22984230.

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