1. Apply for Social Security Disability or Supplemental Social Security

2. Call your state department of health and human services/hygiene and ask if there is a diabetes division. If so, ask them for help.

3. Apply for medical assistance through your state.

4. Consider finding health insurance that is reasonably cost effective.

1. Call you state insurance commission for help.

2. See if your state has a law that requires insurance companies to pay for a 90-day supply of maintenance medication. (Maryland, for example, does.)

3. See if your state has a law that requires insurance companies to pay for “diabetic” supplies. (Maryland does and it requires payment for “insulin dependent diabetes and non-insulin dependent diabetes.” NOTE: no mention of “mellitus” or “insipidus” in Maryland’s law.)

The 24-hour urine volume is high (greater than 40 m./kg/BW) and the osmolality is low (less than 300 mosmoles/kg). Serum electrolytes are usually normal.

If they do produce values similar to DI, it can only mean that the refeeding syndrome results in some type of DI. The most likely cause is iatrogenic (due to administration of excess fluid) but NDI and even CDI is also possible.

The water deprivation test should be prolonged no longer than is necessary to raise the serum sodium concentration slightly above the normal range. If this does not occur within a few hours (for example, if you begin to concentrate your urine), the test can be shorted by giving an intravenous infusion of a concentrated salt solution (3% saline). This test should not be done overnight. For more information about the water deprivation test, refer to DiF’s web site at www.diabetesinsipidus.org/water_deprivation_protocol.htm.

The posterior pituitary bright spot is absent in most if not all patients with CDI, irrespective of the cause. However, it is not completely specific for CDI because the bright spot is also absent in 10% to 30% of normal healthy adults and in about the same fraction of patients with other types of DI (nephrogenic, dipsogenic, psychogenic). Therefore, it supports but does not completely prove the diagnosis of CDI.

In young infants, the treatment of CDI can be very difficult because they must drink more water than adults and the dDAVP treatment prevents them from excreting the excess water. Therefore, they are much more likely to develop water intoxication (hypothermia) when given doses of dDAVP sufficient to completely prevent DI. I would recommend that you try 3 things: 1 . Provide a formula with the smallest amount of solute free water possible; and 2. reduce the dose of dDAVP until urine output roughly equals the daily intake of formula; and 3. Allow the child to drink enough pure water (not juice or milk) to replace her insensible losses (10 to 30 ml/kg body weight depending on temperature, activity).

There are some children who take dDAVP for CDI. It is not known to cause blood clots in them or in adults. If given at doses much higher than are commonly used to treat DI, dDAVP can stimulate release of a clotting factor, but this increase does not itself cause clotting without some injury or other stimulus. Coumadin is not the only drug that inhibits clotting, but it is one of the easiest to use and may be the best for the type of clotting abnormality in the patient. This should be discussed with the doctors involved.

* What is the best way to distinguish between partial CDI and dipsogenic DI or another form of primary polydipsia?

One of the biggest problems in the differential diagnosis of DI is distinguishing partial CDI from dipsogenic DI or other forms of primary polydipsia. There are two ways to make this distinction. One way is to measure plasma AVP during a suitable osmotic stimulus such as fluid deprivation with or without hypertonic saline infusion. The decision on whether or not to use hypertonic saline depends on how the patient responds to fluid deprivation. If the latter results in concentration of the urine before plasma osmolality and sodium concentration reach the level necessary to unambiguously differentiate a normal from a subnormal rise in plasma AVP (Posm 295 to 300, Pna 143 to 146 ) then hypertonic saline should be given until the desired endpoint is reach at which time the measurement of plasma AVP is repeated. The other way to make this distinction is give a closely monitored therapeutic trial of dDAVP at doses sufficient to completely normal urine osmolality and volume for 24 to 48 hours. If this treatment also normalizes thirst and fluid intake without inducing hyponatremia, the patient probably (>95%) has partial CDI. If, however, this treatment results in hyponatremia within 24 to 48 hours, the patient probably has dipsogenic DI or some other form of primary polydipsia. Further information concerning these procedures can be found in (1) Robertson GL, Endocrinology and Metabolism Clinics of North America 24(3): 549-572, 1995. (2)Robertson, GL Annual Review of Medicine, 39: 425542, 1988.

Diagnosis of DI is very clear and simple when there is a complete absence of secretion or action of AVP, but this is the least common...it’s hard to diagnose a partial case. I have another doubt. In your revision of DI you say that “when the fluid deprivation test results in urinary concentration (...) there are three remaining diagnostic possibilities (partial neurohypophyseal, partial nephrogenic, or dipsogenic DI), and the change in urine osmolality produced by administering AVP or dDAVP is of no value in differentiating between them.”

In my experience in well over 200 patients with various types of DI, the indirect test (comparison of urine osmolalities after fluid deprivation and AVP (or dDAVP), gives the same diagnostic results as measurements of AVP or a therapeutic trial of dDAVP only in patients with severe DI (urine not concentrated during fluid deprivation). In those who concentrate their urine during fluid deprivation, the subsequent response to dDAVP does not correlate at all with the diagnosis obtained by AVP assay or by the patients response to treatment with dDAVP. Therefore, I do not think it is helpful in anyway and do not even give the AVP or dDAVP anymore if the patient concentrates his or her urine during the fluid deprivation. In this situation, we give give an infusion of hypertonic saline to raise the plasma osmolality and sodium to ~300 and 145, respectively, and obtain another sample for AVP assay. If an assay is not available to you, a good alternative way to make the diagnosis is to conduct a closely monitored, 24 to 48 hour trial of dDAVP therapy (20 mcg in q8h, 200 mcg po q8h or 2mcg s.c. q12 h). If this treatment completely abolishes polyuria and polydipsia without inducing hyponatremia, it is 95% certain that the patient has CDI. If the dDAVP has no effect even when given parenterally, the patient has NDI. If, however, the treatment abolishes the polyuria but has a lesser or delayed effect on thirst and/or water intake and produces significant hyponatremia, the odds are very high (>85%)that the patient has some form of primary polydipsia either alone or in combination with CDI (about 5% of patients with CDI also have damage to their thirst mechanism which causes hyperdipsia).

By negative tests I assume you mean her 24-hour urine volume is normal and that the polyuria occurs only when she is swimming. This could be due to retention of excess salt/water in legs when standing on land followed by urinary excretion when gravitational/hydrostatic pressures reversed by water immersion and horizontal position during swim. If this is true she may also excrete more salt and water when she goes to bed at night. Does she have nocturia? If so, I would check circadian urines to see if she has nocturnal polyuria.

As far as I know, spironolactone should not effect your patient’s response to dDAVP. It may increase her urinary excretion of sodium and decrease excretion of potassium but both effects should be relatively small, transient, and of no appreciable consequence for her urine output. As a related issue, have you explored the possibility of polycyctic ovarian disease or one of the types of congenital adrenal hyperplasia that also results in overproduction of androgens?

There are at least two laboratories that currently sequence the AVP-neurophysin II gene in patients with suspected familial CDI of the autosomal dominant type. One is the laboratory of Dr. Soren Rittig, Skyby University Hospital, Aarhus, Denmark. The other is at Northwestern University Medical School in Chicago, Illinois, USA. Other laboratories in Boston, Massachusetts (Dr. Joe Majzoub) and Cinncinati, Ohio (Dr. Davis Repaske) have also sequenced this gene, however I do not know if they do it on a regular basis.

I cannot explain this patient’s DI. It can result from hypoxia severe enough to produce generalized “brain death” but that apparently is not present in this patient. Neither hypothermia or sever acidosis are known to cause DI but they conceivably could do so.

The posterior pituitary bright spot is absent in most if not all patients with CDI, irrespective of the cause. However, it is not completely specific for CDI because the bright spot is also absent in 10% to 30% of normal healthy adults and in about the same fraction of patients with other types of DI (nephrogenic, dipsogenic, psychogenic). Therefore, it supports but does not completely prove the diagnosis of CDI.

The first thing to do is to determine whether Max has DI or diabetes mellitus. If he has DI, the next thing is to find out which type it is. If it really is NDI, there is no completely effective treatment, but the best probably would be a thiazide diuretic and a diet as low in salt and protein as possible. If, however, he has CDI, it can be controlled completely with dDAVP, which, in a dog, you would probably need to give by injection. [Editor’s note: We have heard that the nasal spray dDAVP solution is sometimes given as an eye drop in dogs.]

The dDAVP itself should not cause vomiting. However, it may do so by producing water intoxication if fluid intake is excessive. This possibility can be checked by measuring serum sodium. If it is low, the dDAVP should be reduced or stopped altogether until the reason for the excessive intake can be determined and eliminated. If the excessive intake cannot be eliminated, treatment with dDAVP may not be possible and other approaches will be necessary.

You indicated that your dog has NDI. Normally, NDI is not normally treated with DDAVP. My first thought is to revisit the diagnosis. I assume she is a spayed female and that diabetes mellitus, bladder infections, and both liver and pancreatic inflammations have been ruled out. Also, what diet is the dog on? If she is having serious kidney issues, diet can make a difference in her health including the excess water drinking. Has the dog’s vasopressin been measured? In humans this is done by blood test. The test is somewhat expensive and you may wish to discuss the cost with your veterinarian. If a normal amount of vasopressin is present in the blood, this normally would not suggest CDI. In humans, DI is diagnosed and the type of DI is determined with a water deprivation test. There is a protocol for conducting this test in humans on DiF’s web site at the following address www.diabetesinsipidus.org/water_deprivation_protocol.htm. If the dog does have NDI, you may discuss with your veterinarian treating it in the way that NDI is treated in humans. In humans, NDI is not easy to live with and not easy to treat. When it is treated, it is my understanding that the goal is to depress the sodium level in the body by a combination of a low sodium diet and thiazide diuretics. Otherwise, depending on the cost that you wish to spend on testing, you may simply wish to use dDAVP if it helps and stop it if it is not helping.

There is no reason a dog with DI could not develop bladder enlargements and infections, the same as humans.

It is doubtful that the medication you refer to would cause DI.

It is unlikely that dDAVP caused liver enlargement in your dog. It is more probable that whatever caused the DI also caused the liver enlargement. I do not know what kinds of disease

dogs are prone to but if it were a human I would be concerned about metastatic tumors or an infiltrative disease such as sarcoidosis or amyloid.