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Diabetes insipidus hund

Bei dem zentralen Diabetes insipidus (Syn. Diabetes insipidus neurohormonalis) ist die Ursache ein Fehlen oder eine unzureichende Produktion des "antidiuretischen Hormons" ADH (Syn.: Vasopressin) im Hypothalamus, ein fehlender Transport des ADH vom Hypothalamus über den Hypophysenstiel in die Hypophysenhinterlappen oder ein Fehlen der Speicherung oder ausbleibende Sekretion des ADH im Hypophysenhinterlappen. Das ADH wirkt auf die Nierentubuli antidiuretisch - es wirkt also der Harnausscheidung entgegen - und führt zur Bildung eines konzentrierteren Urins. Für den ADH-Mangel können ein Schädel-Hirn-Trauma mit Abriss des Hypophysenstiels, eine Zyste, eine Operation, eine Entzündung, eine infiltrative Erkrankung, eine Blutung, ein Infarkt oder ein Tumor im Hypothalamus oder der Hypophyse verantwortlich sein. Aber auch ein familiärer Diabetes insipidus mit einem congenitalen, autosomal-dominant vererbten Erbfehler ist möglich als Ursache. Bei einem Drittel aller Diabetes insipidus-Fälle ist die Ursache nicht bekannt und es wird eine Autoimmunerkrankung mit Autoantikörper gegen die vasopressinproduzierenden Zellen vermutet.

Bei beiden Formen scheidet die Niere vermehrt Wasser aus. Wenn Wasser nicht genügend durch Trinken ersetzt wird, kommt es zu einer Konzentrierung von Natrium im Blut (Hypernatriämie), einer sogenannten hypertonen Dehydration.

Das auffälligste Symptom für den Hundebesitzer ist ein, oft plötzlich einsetzender, unstillbarer Durst (Polydipsie) verbunden mit einer stark erhöhten Ausscheidung von Urin (Polyurie).

Die Hunde scheinen ihren Durst kaum stillen zu können und reagieren bei Wasserentzug schnell mit Anzeichen einer Dehydration. Anzeichen einer Dehydration sind, je nach Schweregrad

- der Speichel wird zunehmend zähflüssiger

- angehobene Hautfalte verstreicht nur langsam, bis hin zum völligem „stehen bleiben“ der Falte

- schwacher Puls im fortgeschrittenen Stadium

- Bewusstseinsstörungen bis hin zum Koma

- Der Harn verändert sich in eine unkonzentrierte Flüssigkeit und erscheint „dünner“ als normal, weniger gefärbt und geruchloser.

Wie alles begann und Leben mit der Krankheit:

Eines Tages wurde Nigel krank. Er war apathisch und fühlte sich nur wohl, wenn er stundenlang in der prallen Sonne liegen konnte. Stellte ich ihm einen Sonnenschirm an seinen Liegeplatz, dann schob er sich Zentimeter für Zentimeter wieder in die Sonne. Es dauerte lange, bis er endlich wieder richtig auf den Pfoten war. Kurz darauf begann er Tag für Tag seinen ganzen Napf (1 ½ Liter) leer zu trinken. Hat mich zwar gewundert, aber nicht beunruhigt. Nach wenigen Tagen musste ich innerhalb kürzester Zeit nachfüllen und Nigel trank wieder alles leer. Schließlich begann er zu betteln, weil er noch mehr haben wollte. Gleichzeitig wollte er das viele Wasser umgehend wieder los werden.

Ich brachte ihn zum Tierarzt, denn das Ganze sah irgendwie nach Diabetes mellitus aus. Der Zuckertest fiel negativ aus und ich zog mit langem Gesicht wieder ab. Als Nigel dann pro Tag mehr als fünf, mitunter sogar über zehn Liter trank packte mich die Panik. Vor allem, weil ich keine Nacht mehr durchschlafen konnte. Ständig weckte er mich, weil die Blase drückte. Etwa alle zwanzig Minuten kam er winselnd an mein Bett. Ich war körperlich und nervlich völlig am Ende. Also drängte ich auf eine große Diagnose, die dann das ganze Ausmaß der Katastrophe zu Tage brachte. Der niederschmetternde Befund lautete: Diabetes insipidus.

Nigel bekommt seitdem jeden Abend 2 Tropfen Minirin in die Augen. Damit trinkt er etwas weniger, schläft dann ungefähr zwei Stunden am Stück. Ich habe mich inzwischen daran gewöhnt, 2 x oder öfter pro Nacht aufstehen zu müssen. Denn trotz allem trinkt er noch immer mindestens vier Liter. Und regt er sich über irgendetwas auf, dann kann es durchaus noch ein Napf mehr sein.

Inzwischen leben wir vier volle Jahre mit der Krankheit. Das heißt: er mit der Krankheit, ich mit den Folgen. Eine noch höhere Medikamentendosis ist in sofern nicht sinnvoll, da Nigel dann benommen wirkt und teilnahmslos in der Ecke liegt. Solange er keine Schmerzen, guten Appetit und Freude am Leben hat nehme ich gern allen Stress auf mich. Zugleich geht die Behandlung richtig ins Geld. 2,5 ml Minirin kosten durchschnittlich 50 Euro, reichen aber nicht mal einen Monat, dann kommen noch die Tierarzt- und Rezeptkosten. Ich weiß oft nicht wie es weitergehen soll, nur, dass ich für Nigel mein letztes Hemd weggeben würde.

Schmerzen hat Nigel definitiv nicht. Ich gehe mit ihm regelmäßig alle 6 Wochen zum Arzt, schon weil wir dann ein neues Rezept für die nächsten 1 1/2 Monate brauchen. Er fühlt sich oft schlapp, was bei seinen Diagnosen durchaus normal ist. Wir gehen also nur noch kurze Runden. Sollte sich sein Zustand so verschlimmern, dass er Schmerzen bekäme oder er das Fressen verweigern würde, dann wäre ich die Letzte, die ihn leiden ließe. Ich hoffe inständig, dass mir das erspart bleibt und dass ich ihn irgendwann am Morgen leblos finde, weil er friedlich in der Nacht für immer eingeschlafen ist.

Niemand kann mir wirklich erklären, wie die Nieren und das Herz diesen Marathon durchhalten.

Da fliegt die Menschheit zum Mond, verpulvert Milliarden in sinnlosen Kriegen und ist einfach nicht in der Lage ein wirksames Medikament zu entwickeln, welches Diabetes insipidus dauerhaft in den Griff bekommt.

Nigel ist ein Phänomen. ich wundere mich immer wieder, wie selbstverständlich er schon seit so vielen Jahren mit all seinen Handicaps lebt.

Nun steuern wir gemeinsam seinen 14 Geburtstag im Juli an. Immerhin werden andere Hunde selbst bei bester Gesundheit nicht so alt.

Nephrogenic Diabetes Insipidus

What is nephrogenic diabetes insipidus?

Diabetes insipidus is caused by problems related to a hormone called antidiuretic hormone or ADH. ADH is produced in a part of the brain called the hypothalamus. It's stored in the pituitary gland. Release of ADH is triggered by fluid loss or dehydration. When it's released, it causes the kidneys to retain water. This results in a decrease and concentration of urine.

In nephrogenic diabetes insipidus, enough ADH is produced. But the kidneys are partially or completely blind to it. Typically, the kidneys' ADH sensors are missing or defective. As a result, ADH flows by without effect. The kidneys don't absorb enough water. Instead, they excrete abundant dilute urine as if no ADH were present.

What are the symptoms of nephrogenic diabetes insipidus?

The lack of ability by the kidneys to conserve water leads to the symptoms of nephrogenic diabetes insipidus. They include:

Excessive thirst
Excessive urine production (polyuria).

In some people, these symptoms can become extreme and cause dehydration. Excessive fluid losses can also cause electrolyte imbalances. Symptoms of electrolyte imbalances include:

For someone without nephrogenic diabetes insipidus, the extreme thirst it creates can be hard to understand. Some people need to drink a large glass of liquid every 15 minutes, all day, every day. And since the kidneys aren't holding that water in, that means a lot of bathroom breaks.

But why "insipidus"? People with diabetes insipidus aren't insipid, but their urine is. Insipid can mean dull or lacking flavor. Believe it or not, doctors long ago would taste urine to detect illness. Unlike diabetes mellitus, which results in sweet tasting urine, diabetes insipidus creates watery, flavor-free urine.

What are the causes of nephrogenic diabetes insipidus?

In infants, nephrogenic diabetes insipidus is most commonly caused by an inherited genetic mutation present at birth. As a result, the receptor for ADH doesn't function properly.

In adults who develop nephrogenic diabetes insipidus, genetics aren't the cause. Instead, medicines or electrolyte abnormalities cause the condition. Causes of nephrogenic diabetes insipidus in adults include:

Lithium, a drug most commonly taken for bipolar disorder; up to 20% of people taking lithium will develop nephrogenic diabetes insipidus.
Other medicines, including demeclocycline (Declomycin), ofloxacin (Floxin), orlistat (alli, Xenical), and others
High levels of calcium in the blood (hypercalcemia)
Low levels of potassium in the blood (hypokalemia)
Kidney disease, especially polycystic kidney disease

The other form of diabetes insipidus is known as central diabetes insipidus. In central diabetes insipidus, the kidneys function normally, but not enough ADH is produced in the brain. Central diabetes insipidus has similar symptoms to nephrogenic diabetes insipidus. However, central diabetes insipidus can be treated by replacing ADH with a medication called desmopressin.

How is nephrogenic diabetes insipidus treated?

Nephrogenic diabetes insipidus can be difficult to treat. Since the kidneys can't respond to ADH, giving more ADH doesn't help. There's no good way to get the kidneys to respond to the ADH that's there. In fact, treatment options are limited.

If a drug like lithium is responsible, switching medicines might improve nephrogenic diabetes insipidus.

Most adults with nephrogenic diabetes insipidus are able to keep up with fluid losses by drinking water. For some people, though, the symptoms of near-constant thirst and urination can become intolerable. Some treatments can reduce the symptoms of nephrogenic diabetes insipidus, at least somewhat:

Diet. A low-salt, low-protein diet reduces urine output.
Nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen (Motrin), indomethacin (Indocin), and naproxen (Naprosyn) also can reduce urination.
Diuretics. It might seem paradoxical, but "water pills" like hydrochlorothiazide and amiloride can ease excessive urination from nephrogenic diabetes insipidus.

All adults and children with nephrogenic diabetes insipidus should take frequent bathroom breaks. This helps to avoid over-distending the bladder, which can cause long-term problems, though rarely.

The most important treatment for nephrogenic diabetes insipidus is to ensure constant access to lots of water. Not keeping up with fluid losses can lead to dehydration or electrolyte imbalances, which can sometimes be severe. Seek medical help if symptoms don't improve after rehydrating, eating fresh fruit, and taking a multivitamin.

Fujiwara, T. Journal of the American Society of Nephrology, 2005; vol 16: pp 2836-2846.

Boton, R. American Journal of Kidney Disease, 1987; vol 10: pp 329-345.

Rose, B. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th edition, McGraw Hill, 2001.

Garofeanu, C. American Journal of Kidney Disease, 2005; vol 45: pp 626-637.

MedlinePlus: "Diabetes Insipidus."

Libber, S. Journal of Pediatrics, 1986; vol 108: pp 305-311.

Monnens, L. Clinical Science, 1984; vol 66: pp 709-715.

Streitz J, Jr. Journal of Urology, 1988; vol 139: pp 784-785.

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Diabetes insipidus

Diabetes insipidus er en sygdom, hvor hunden ikke kan koncentrere sin urin, og derfor mister store mængder væske gennem urinudskillelsen. Man skelner mellem to former:

En hjerneform, hvor der er nedsat produktion af et hormon (antidiuretisk hormon, ADH) i hjernen. Hormonet er nødvendigt, for at nyrerne kan koncentrere urinen.
En nyreform, hvor ADH-hormonet ikke virker, som det skal i nyrerne.

Hvad er symptomerne på diabetes insipidus?

Øget tissetrang og drikkelyst
Udskillelse af meget tynd vandig urin
Hunden kan ikke holde på vandet

Hvordan kan din dyrlæge stille diagnosen diabetes insipidus?

Nyreformen kan ses som en følgesygdom til en række hormonsygdomme og infektionssygdomme, som kan påvirke nyrerne, f.eks. cushings syndrom, addisons syndrom, pyometra og leverlidelser.

Normal vandindtagelse hos hunde overstiger normalt ikke 1 liter pr. 10 kg hund.

af dyrlæger Henrik Strange og Kirsten Boeck Cushings syndrom er betegnelsen for et sygdomskompleks, der opstår, når organismen igennem længere tid udsættes for en øget mængde binyrebarkhormon. Disse …

Af dyrlæge Helle Johansen. Hvad er addisons syndrom? Addisons syndrom er en lidelse i binyrernes yderste lag, binyrebarken, der medfører nedsat eller ophørt produktion af livsvigtige hormoner som ko…

Af specialdyrlæger i Onkologi Peter Maasbøl Skov og Steen Engermann samt dyrlæge Mogens Brix Christensen. Hvad er kræft hos hunde og katte? Ordet kræft kommer af det latinske ord cancer. Det er en f…

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Diabetes Insipidus

By Deborah S. Greco, DVM, PhD, DACVIM, Senior Research Scientist, Nestle Purina PetCare

The Pituitary Gland

Overview of the Pituitary Gland

Cushing Disease (Hyperadrenocorticism)

Nonfunctional Pituitary Tumors

Hirsutism Associated with Adenomas of the Pars Intermedia

Adult-onset Panhypopituitarism

Juvenile-onset Panhypopituitarism

Central diabetes insipidus is caused by reduced secretion of antidiuretic hormone (ADH). When target cells in the kidney lack the biochemical machinery necessary to respond to the secretion of normal or increased circulating levels of ADH, nephrogenic diabetes insipidus results. It occurs infrequently in dogs, cats, and laboratory rats, and rarely in other animals.

The hypophyseal form develops as a result of compression and destruction of the pars nervosa, infundibular stalk, or supraoptic nucleus in the hypothalamus. The lesions responsible for the disruption of ADH synthesis or secretion in hypophyseal diabetes insipidus include large pituitary neoplasms (endocrinologically active or inactive), a dorsally expanding cyst or inflammatory granuloma, and traumatic injury to the skull with hemorrhage and glial proliferation in the neurohypophyseal system.

Clinical Findings:

Affected animals excrete large volumes of hypotonic urine and drink equally large amounts of water. Urine osmolality is decreased below normal plasma osmolality (

300 mOsm/kg) in both hypophyseal and nephrogenic forms, even if the animal is deprived of water. The increase of urine osmolality above that of plasma in response to exogenous ADH in the hypophyseal form, but not in the nephrogenic form, is useful in the clinical differentiation of the two forms of the disease.

The posterior lobe, infundibular stalk, and hypothalamus are compressed or disrupted by neoplastic cells. This interrupts the nonmyelinated axons that transport ADH from its site of production (hypothalamus) to its site of release (pars nervosa).

This is based on chronic polyuria that does not respond to dehydration and is not due to primary renal disease. To evaluate the ability to concentrate urine, a water deprivation test should be done if the animal is not dehydrated and does not have renal disease. The bladder is emptied, and water and food are withheld (usually 3–8 hr) to provide a maximum stimulus for ADH secretion. The animal should be monitored carefully to prevent a loss of >5% body wt and severe dehydration. Urine and plasma osmolality should be determined; however, because these tests are not readily available to most practitioners, urine specific gravity is frequently used instead. At the end of the test, urine specific gravity is >1.025 in those animals with only a partial ADH deficiency or with antagonism to ADH action caused by hypercortisolism. There is little change in specific gravity in those animals with a complete lack of ADH activity, whether due to a primary loss of ADH or to unresponsiveness of the kidneys.

An ADH response test should follow to differentiate among conditions that may result in large volumes of urine that is chronically low in specific gravity but otherwise normal. These include nephrogenic diabetes insipidus (an inability of the kidneys to respond to ADH), psychogenic diabetes insipidus (a polydipsia in response to some psychological disturbance but a normal response to ADH), and hypercortisolism (which results in a partial deficiency of ADH activity due to the antagonistic effect of cortisol on ADH activity in the kidneys). This test also can be used to evaluate animals in which a water deprivation test could not be performed. Urine specific gravity is determined at the start of the test, desmopressin acetate is administered (2–4 drops in the conjunctival sac), the bladder is emptied at 2 hr, and urine specific gravity is measured at set intervals (4, 8, 12, 18, and 24 hr) after ADH administration. Specific gravity peaks at >1.026 in animals with a primary ADH deficiency, is significantly increased above the level induced with water deprivation in those with a partial deficiency in ADH activity, and shows little change in those with nephrogenic diabetes insipidus.

If osmolality is measured, the ratio of urine to plasma osmolality after water deprivation is >3 in healthy animals, 1.8–3 in those with moderate ADH deficiency, and 2 in animals with primary ADH deficiency, between 1.1 and 2 in those with inhibitors to ADH action, and 50%) during the first treatment day strongly suggests an ADH deficiency and a diagnosis of central diabetes insipidus or partial nephrogenic diabetes insipidus.

Diabetes insipidus also needs to be distinguished from other diseases with polyuria. The most common are diabetes mellitus with glycosuria and high urine specific gravity, and chronic nephritis with a urine specific gravity that is usually low and shows evidence of renal failure (protein, casts, etc).

Polyuria may be controlled using desmopressin acetate, a synthetic analogue of ADH. The initial dose is 2 drops applied to the nasal mucosae or conjunctivae; this is gradually increased until the minimal effective dose is determined. Maximal effect usually occurs in 2–6 hr and lasts for 10–12 hr. Water should not be restricted. Treatment should be continued once or twice daily for the life of the animal.

The Pituitary Gland

Overview of the Pituitary Gland

Cushing Disease (Hyperadrenocorticism)

Nonfunctional Pituitary Tumors

Hirsutism Associated with Adenomas of the Pars Intermedia

Adult-onset Panhypopituitarism

Juvenile-onset Panhypopituitarism

Was This Page Helpful?

Also of Interest

Test your knowledge

Which of the following serum biochemical abnormalities is most likely to occur in a dog with primary hypothyroidism?

MSD and the MSD Veterinary Manual

Merck & Co., Inc., Kenilworth, NJ, USA (known as MSD outside of the US and Canada) is a global healthcare leader working to help the world be well. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Veterinary Manual was first published in 1955 as a service to the community. The legacy of this great resource continues as the Merck Veterinary Manual in the US and Canada and the MSD Veterinary Manual outside of North America.

© 2018 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, NJ, USA

Diabetes insipidus hund

Diabetes insipidus (DI) is a disorder of water balance. The animal is unable to concentrate urine, so the urine volume is very high and the urine is dilute. "Insipid" means tasteless -- referring to the dilute urine. This disease is rare in both dogs and cats. The condition is usually permanent, and the prognosis is good. Without treatment, dehydration leads to stupor, coma, and death. This is a completely different disease from Diabetes Mellitus (DM), a disorder of sugar metabolism involving the hormone insulin. We include the information here because people are often looking for resources and we had some owners of pets with DM who also have experience with DI.

Types of diabetes insipidus

Central Diabetes Insipidus - caused when the pituitary gland does not secrete enough antidiuretic hormone (ADH) [also called vasopressin]. This type of DI may be the caused by a congenital defect, trauma, a tumor on the pituitary gland, or unknown causes.

Nephrogenic Diabetes Insipidus - caused when the kidneys do not respond to the ADH that is produced by the pituitary gland. This type of DI may be caused by a congenital defect, drugs, or caused by other metabolic disorders

Diagnosis

Diagnosis includes ruling out other diseases such as hyperadrenocorticism (Cushing's disease), diabetes mellitus, hyperthyroidism (in cats), renal failure, liver disease, pyometra (infection of the uterus), and other disorders.

Images of the pituitary gland may be taken to determine if there is a tumor.

A water deprivation test or an ADH trial with DDAVP may be done. These tests determine if the animal is able to produce more concentrated urine as water is withheld or following the injection of DDAVP (the drug used to treat DI).

Treatment

Central DI is treated with desmopressin , a drug that mimics the actions of ADH. It is available under the trade name DDAVP and as a generic. DDAVP is available in several formulations: as a nasal spray pump; as a liquid for use with rhinal tube; as an injectable liquid; and in tablets. Most pet owners use the nasal spray or rhinal liquid formulations and use them as eye drops, nose drops, or inject it subcutaneously.

Nephrogenic DI is commonly treated with thiazide diuretics. These drugs help to concentrate the urine. An oral drug called chlorothiazide acts on the kidneys to help concentrate the urine. Other treatments may include chloropropamide, which increases the effects of ADH on the kidney. But chloropropamide is not always successful. Nonsteroidal anti-inflammatory drugs may be used in dogs.

No therapy may be chosen, and the pets can survive as long as plenty of water is always available . You CAN NOT limit their water intake . When Sonny's DI first started, he would lay in front of his water bowl and just drink and drink and drink. Of course he also had to go outside very frequently, and his urine was like water - literally.

Ziggy, Puff, and Simone are three kitties with DI. Ziggy also has diabetes mellitus (yes, both diseases can occur together . remember they are totally separate diseases).

I did lose a few drops (expensive and precious, I might add) the first few times I used it. The drops come out of the bottle very easily, so I make sure I have Ferris' eye ready to receive the drop before I even turn the bottle over.

I have tried other eye drop bottles but found the Clear Eyes one to be sleekly designed and thus I can get every drop of Desmopressin out of it.

References

The 5 Minute Veterinary Consult: Canine and Feline Larry Tilly and Francis W.K. Smith, Jr. 1997.

Veterinary Drug Handbook. Second Edition. Donald C. Plumb. 1995.

Pocket Companion to the Fourth Edition of Textbook of Veterinary Internal Medicine Stephen J. Ettinger.

The Cornell Book of Cats : A Comprehensive and Authoritative Medical Reference for Every Cat and Kitten. Mordecai Siegal (Editor), et al.1997.

Updated June 2002

Copyright. All rights reserved.

This site is for information purposes only. Please consult your veterinarian.

Diabetes Insipidus

By Deborah S. Greco, DVM, PhD, DACVIM, Senior Research Scientist, Nestle Purina PetCare

The Pituitary Gland

Overview of the Pituitary Gland

Cushing Disease (Hyperadrenocorticism)

Nonfunctional Pituitary Tumors

Hirsutism Associated with Adenomas of the Pars Intermedia

Adult-onset Panhypopituitarism

Juvenile-onset Panhypopituitarism

Central diabetes insipidus is caused by reduced secretion of antidiuretic hormone (ADH). When target cells in the kidney lack the biochemical machinery necessary to respond to the secretion of normal or increased circulating levels of ADH, nephrogenic diabetes insipidus results. It occurs infrequently in dogs, cats, and laboratory rats, and rarely in other animals.

The hypophyseal form develops as a result of compression and destruction of the pars nervosa, infundibular stalk, or supraoptic nucleus in the hypothalamus. The lesions responsible for the disruption of ADH synthesis or secretion in hypophyseal diabetes insipidus include large pituitary neoplasms (endocrinologically active or inactive), a dorsally expanding cyst or inflammatory granuloma, and traumatic injury to the skull with hemorrhage and glial proliferation in the neurohypophyseal system.

Clinical Findings:

Affected animals excrete large volumes of hypotonic urine and drink equally large amounts of water. Urine osmolality is decreased below normal plasma osmolality (

300 mOsm/kg) in both hypophyseal and nephrogenic forms, even if the animal is deprived of water. The increase of urine osmolality above that of plasma in response to exogenous ADH in the hypophyseal form, but not in the nephrogenic form, is useful in the clinical differentiation of the two forms of the disease.

The posterior lobe, infundibular stalk, and hypothalamus are compressed or disrupted by neoplastic cells. This interrupts the nonmyelinated axons that transport ADH from its site of production (hypothalamus) to its site of release (pars nervosa).

This is based on chronic polyuria that does not respond to dehydration and is not due to primary renal disease. To evaluate the ability to concentrate urine, a water deprivation test should be done if the animal is not dehydrated and does not have renal disease. The bladder is emptied, and water and food are withheld (usually 3–8 hr) to provide a maximum stimulus for ADH secretion. The animal should be monitored carefully to prevent a loss of >5% body wt and severe dehydration. Urine and plasma osmolality should be determined; however, because these tests are not readily available to most practitioners, urine specific gravity is frequently used instead. At the end of the test, urine specific gravity is >1.025 in those animals with only a partial ADH deficiency or with antagonism to ADH action caused by hypercortisolism. There is little change in specific gravity in those animals with a complete lack of ADH activity, whether due to a primary loss of ADH or to unresponsiveness of the kidneys.

An ADH response test should follow to differentiate among conditions that may result in large volumes of urine that is chronically low in specific gravity but otherwise normal. These include nephrogenic diabetes insipidus (an inability of the kidneys to respond to ADH), psychogenic diabetes insipidus (a polydipsia in response to some psychological disturbance but a normal response to ADH), and hypercortisolism (which results in a partial deficiency of ADH activity due to the antagonistic effect of cortisol on ADH activity in the kidneys). This test also can be used to evaluate animals in which a water deprivation test could not be performed. Urine specific gravity is determined at the start of the test, desmopressin acetate is administered (2–4 drops in the conjunctival sac), the bladder is emptied at 2 hr, and urine specific gravity is measured at set intervals (4, 8, 12, 18, and 24 hr) after ADH administration. Specific gravity peaks at >1.026 in animals with a primary ADH deficiency, is significantly increased above the level induced with water deprivation in those with a partial deficiency in ADH activity, and shows little change in those with nephrogenic diabetes insipidus.

If osmolality is measured, the ratio of urine to plasma osmolality after water deprivation is >3 in healthy animals, 1.8–3 in those with moderate ADH deficiency, and 2 in animals with primary ADH deficiency, between 1.1 and 2 in those with inhibitors to ADH action, and 50%) during the first treatment day strongly suggests an ADH deficiency and a diagnosis of central diabetes insipidus or partial nephrogenic diabetes insipidus.

Diabetes insipidus also needs to be distinguished from other diseases with polyuria. The most common are diabetes mellitus with glycosuria and high urine specific gravity, and chronic nephritis with a urine specific gravity that is usually low and shows evidence of renal failure (protein, casts, etc).

Polyuria may be controlled using desmopressin acetate, a synthetic analogue of ADH. The initial dose is 2 drops applied to the nasal mucosae or conjunctivae; this is gradually increased until the minimal effective dose is determined. Maximal effect usually occurs in 2–6 hr and lasts for 10–12 hr. Water should not be restricted. Treatment should be continued once or twice daily for the life of the animal.

The Pituitary Gland

Overview of the Pituitary Gland

Cushing Disease (Hyperadrenocorticism)

Nonfunctional Pituitary Tumors

Hirsutism Associated with Adenomas of the Pars Intermedia

Adult-onset Panhypopituitarism

Juvenile-onset Panhypopituitarism

Was This Page Helpful?

Also of Interest

Test your knowledge

Which of the following serum biochemical abnormalities is most likely to occur in a dog with primary hypothyroidism?

Merck and the Merck Veterinary Manual

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Diabetes insipidus

Diabetes insipidus is an endocrine disease characterized by vasopressin dysregulation [1] , excessive polyuria, polydipsia, and the absence of hyperglycemia and glucosuria.

Diabetes insipidus is entirely different to diabetes mellitus and has two presentations:

Central diabetes insipidus - due to hypothalamic-pituitary trauma [2] , post-transsphenoidal surgery for correction of hyperadrenocorticism[3] , dorsally expanding cysts, inflammatory granuloma, lymphocytic hypophysitis [4] , congenital malformation and neoplasms such as craniopharyngioma, pituitary chromophobe adenoma[5] , pituitary chromophobe adenocarcinoma [6] and metastatic tumors such as metastatic mammary carcinoma, lymphoma[7] , malignant melanoma and pancreatic carcinoma

- results in lack of vasopressin (antidiuretic hormone) production

Nephrogenic diabetes insipidus - due to nephron impairment as a result of genetic or acquired disease

- results in lack of vasopressin sensitivity by nephrons

Central diabetes insipidus (CDI) results in absolute or partial loss of vasopressin (antidiuretic hormone; ADH) production by the central nervous system, causing persistent hyposthenuria (urine specific gravities ≤ 1.006) and severe diuresis, even with severe dehydration.

Nephrogenic diabetes insipidus (NDI), which may be primary (familial; X-link in humans [8] ) or secondary (acquired), results from impaired responsiveness of the nephron to the actions of vasopressin. Plasma vasopressin concentrations are normal or increased in animals with this disorder. Primary NDI is a rare congenital disorder of dogs resulting from a congenital defect involving the cellular mechanisms responsible for insertion of aquaporin-2 water channels into the luminal cell membrane.

Acquired secondary NDI includes a variety of renal and metabolic disorders which interfere with the normal interaction between vasopressin and its renal tubular receptors, affect renal tubular cell function, or decrease the hypertonic renal medullary interstitium, resulting in a loss of the normal osmotic gradient. These disorders are listed below as differential causes od secondary nephrogenic diabetes insipidus.

Clinical signs

Common clinical signs in dogs with diabetes insipidus is polyuria and polydipsia.

In dogs with primary (familial) NDI, clinical signs typically become apparent by the time the dog is 8 to 12 weeks of age, with symptoms of excessive thirst, urination and difficulty in house-breaking [9] .

Neurological signs have been reported, due to electrolyte disturbances or pituitary neoplasia, with depression and seizures observed in rare cases [10] .

Water consumption can often be extreme, sometimes exceeding 800 ml/kg/day, with compensatory urine production exceeding 50 mL/kg/day, .

Blood tests are usually within normal limits apart from a polydipsia-induced hyponatremia.

Urinalysis usually shows hyposthenuria or isosthenuria, and hematuria is not regularly observed unless underlying concurrent nephropathy present. Urine culture and sensitivity is required to eliminate underlying cystitis or pyelonephritis.

Diagnosis is initially one of exclusion of other diseases (see list below), followed by low dose dexamethasone suppression test, water-deprivation tests, vasopressin therapy and central nervous imaging studies to diagnose central diabetes insipidus. The main diagnostic dilemma is differentiating between central diabetes insipidus, psychogenic polydipsia and nephrogenic diabetes insipidus.

Standard hematology and biochemistry assessments are usually unrewarding and in most cases, plasma concentrations of thyroid-stimulating hormone, thyroxine, growth hormone, insulin-like growth factor-1, adrenocorticotropic hormone and plasma α-melanocyte-stimulating hormone are within normal reference levels.

A response to synthetic vasopressin therapy (desmopressin; 0.1 - 0.2 mg orally every 8 hours) or urinary aquaporin-2 excretion testing may help clarify nephrogenic from central diabetes insipidus [11] . Other tests include vasopressin measurements during hypertonic saline infusion [12] . However, the occurrence of spontaneous vasopressin pulses may hamper the interpretation of the curve describing the relationship between plasma osmolality and plasma vasopressin concentration during osmotic stimulation [13] .

An increase in urine specific gravity by 50% or more, compared with pre-treatment specific gravities, supports the diagnosis of CDI, especially if urine specific gravity exceeds 1.030. There should be only minimal improvement in dogs with primary NDI. Dogs with psychogenic water consumption may exhibit a mild decline in urine output and water intake because the chronically low plasma osmolality tends to depress vasopressin production.

Pituitary or hypothalamic neoplasia should be considered in older dogs diagnosed with CDI. A renal biopsy may be warranted in the older dog tentatively considered to have primary NDI.

A differential diagnosis would include:

Diabetes mellitus - osmotic diuresis

Chronic renal disease osmotic diuresis

Primary renal glycosuria - osmotic diuresis

Post-urolithiasis diuresis - osmotic diuresis, down-regulation of aquaporin-2

Pyometra - bacterial endotoxin-induced reduced tubular sensitivity to vasopressin

Escherichia coli septicemia - bacterial endotoxin-induced reduced tubular sensitivity to vasopressin

Hypercalcemia - interference with action of vasopressin on renal tubules

Hepatitis - loss of medullary hypertonicity, impaired hormone metabolism

Hyperadrenocorticism - impaired tubular response to vasopressin

Hyperaldosteronism - impaired tubular response to vasopressin

Pyelonephritis - bacterial endotoxin-induced reduced tubular sensitivity to vasopressin, damaged countercurrent mechanism

Fanconi's syndrome - osmotic diuresis

Hypokalemia - down-regulation of aquaporin-2, loss of medullary hypertonicity

Hyponatremia - loss of medullary hypertonicity

Hypoadrenocorticism - loss of medullary hypertonicity

Hyperthyroidism - loss of medullary hypertonicity

Leptospirosis - action unknown

Polycythemia - action of natriuretic peptide

Pheochromocytoma - excessive catecholamines

Portosystemic shunt - loss of medullary hypertonicity, increased GFR

Dwarfism - action unknown [14]

Acromegaly - osmotic diuresis due to diabetes mellitus [15]

Psychogenic polydipsia - loss of medullary hypertonicity

Intestinal leiomyosarcoma - impaired tubular response to vasopressin [16]

Very low protein diet - loss of medullary hypertonicity

Gastrointestinal disease (e.g. ulcerative colitis) [17]

X-link hereditary nephropathy - loss of medullary hypertonicity, increased GFR

Renal dysplasia - loss of medullary hypertonicity, increased GFR

With hypophyseal tumors, a transsphenoidal hypophysectomy is usually recommended. In dogs which develop CDI secondary to hypophysectomy may spontaneously resolve within 2 - 4 weeks [18] [19] .

Prophylactic use of desmopressin at 4 μg twice daily has been shown effective at minimizing onset of CDI [20] .

In dogs with primary NDI, long-term therapy with low sodium diet, unlimited water access, hydrochlorothiazide (used to increase urine osmolality) [21] or desmopressin tablets or nasal spray.

Vad är diabetes insipidus hos hundar?

Det finns två typer av diabetes insipidus: central diabetes insipidus (CDI) och nephrogenic diabetes insipidus (NDI). CDI uppstår när hundens hypofysen i hjärnan inte producerar tillräckligt anti diuretic hormon (ADH), medan NDI uppstår när anti diuretic hormon produceras normalt men njurarna inte kan svara ordentligt på deras insatser.

På grund av anti diuretic hormon, hundar drabbats av diabetes insipidus kommer att ha mycket utspädd urin, överdriven urinering och en nästan omättlig törst.

Även i de flesta fall är orsaken till diabetes insipidus okänd, eftersom ADH hormonet produceras i hjärnan, kan en hjärnskada eller en hjärntumör vara en potentiell brottsling. När det gäller nephrogenic diabetes insipidus är orsaken genetisk.

Behandling

Behandling av hundar drabbats av diabetes insipidus består av förvaltning av en syntetisk form av ADH hormonet kallas desmopressin acetat, ofta förkortat DDAVP. Andra former av behandling inkluderar en minskning av salt i hundens kost och administrationen av chlorpropamide och thiazide diuretika.

Management

Om ägarna kan se till att vatten är tillgänglig hela tiden och om de är klara överflödigt vattenintaget och behovet av att kissa ofta och rikligt, kan medicinsk behandling vara valfritt. Det är dock bäst att rådgöra med en veterinär.

Så länge vattnet är alltid tillgängliga och villkoret är välskött, har hundar med diabetes insipidus en god prognos. Följa upp vård och rutinmässig tentor rekommenderas. En ägare måste lära sig att känna igen tecken på uttorkning och rådfråga en veterinär omedelbart vid behov.

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Practical Matters: Desmopressin is safer than water deprivation to identify the cause of polyuria and polydipsia in dogs

Marjorie L. Chandler, DVM, MS, MACVSc, DACVN, DACVIM, DECVIM, MRCVS

Measuring the basal serum cortisol concentration may help rule out hypoadrenocorticism since this disorder is unlikely if the value is > 2 μg/dl (

70 mmol/L). If the value is ≤ 2 μg/dl, hypoadrenocorticism must be confirmed with an ACTH stimulation test. If hyperadrenocorticism is suspected, perform ACTH stimulation and low-dose dexamethasone suppression tests, imaging, and other diagnostic tests as needed.

Table 1: Differential Diagnoses in Dogs with Polyuria and Polydipsia

To conduct this trial, the owner measures the patient's free-choice 24-hour water intake for two or three days and collects and labels daily urine samples. The specific gravity of the urine samples should be checked. The owner then administers 0.05 to 0.2 mg desmopressin orally every eight hours or 1 to 4 drops of the 100 μg/ml desmopressin nasal spray in one conjunctival sac every 12 hours for five to seven days. The owner monitors the dog's water consumption and collects and labels urine samples during the treatment period. Dogs with central diabetes insipidus should respond well to this treatment, forming more concentrated urine and drinking much less water than they were previously drinking. A moderate response may occur in dogs with partial central diabetes insipidus or with hyperadrenocorticism.

Even with a desmopressin trial, caution should be exercised in geriatric patients and those having isosthenuria since these patients are more likely to have early-stage chronic kidney disease, and excessive dehydration could be damaging. Further, if an animal with unexplained polyuria and polydipsia presents to the hospital in a dehydrated state and its urine specific gravity is < 1.030, a water deprivation test is unnecessary and is contraindicated.

1. Feldman EC, Nelson RW. Water metabolism and diabetes insipidus. In: Canine and feline endocrinology and reproduction. 3rd ed. St Louis, Mo: Saunders, 2004;2-44.

Marjorie L. Chandler, DVM, MS, MACVSc, DACVN, DACVIM, DECVIM, MRCVS

Hospital for Small Animals

University of Edinburgh

Roslin, Midlothian, Scotland

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