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Nephrogenic Diabetes Insipidus

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Nephrogenic diabetes insipidus is a long name for an uncommon condition. Nephrogenic diabetes insipidus is not the same as diabetes mellitus. Diabetes mellitus causes elevated blood sugar levels. But nephrogenic diabetes insipidus is due to a problem in the kidneys.

In nephrogenic diabetes insipidus, the kidneys can't respond to a hormone that regulates fluid balance. Excessive urination and thirst are the results. Nephrogenic diabetes insipidus can be challenging to treat.

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

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

In animals, the middle zone of the adrenal cortex, called the zona fasciculata, produces glucocorticoids. Which one of the following effects is LEAST likely to be caused by the release of endogenous glucocorticoids?

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 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.

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

In animals, the middle zone of the adrenal cortex, called the zona fasciculata, produces glucocorticoids. Which one of the following effects is LEAST likely to be caused by the release of endogenous glucocorticoids?

Merck and the Merck Veterinary Manual

Merck & Co., Inc., Kenilworth, NJ, USA 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 Merck 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 Manual outside of North America.

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

Camilla Stefansdotter - Hundtränarblogg

Lyckliga hundar lyder gärna!

fredag 8 februari 2013

Diabetes hos hund

I januari skrev jag om sköldkörtelsjukdomar hos hund. Den här månadens reportage handlar om en annan sjukdom som ökar bland både katter och hundar - och människor - nämligen Diabetes. Den absolut vanligaste orsaken till att hundar får diabetes är övervikt. Det vanligaste symptomet är såna som man i vardagen ser hos hundar med just övervikt; trötthet. Andra symtpom är ökad törst och därmed ökad kissning (ökad urinmängd och frekvens av "toabesök"). Övervikt är ju ofta boven vid diabetes och ironiskt nog ökar även aptiten hos en hund med diabetes och hunden får också svårare att bli av med övervikten (enligt Agria) eller avmagrat rejält (enligt SLU).

Symptomen kan också vara varningstecken på andra sjukdomar än diabetes. Som hos människan kan ofta diabetes och ämnesomsättningsstörningar gå hand i hand. Hunden riskerar också gråstarr, njursvikt och ökad infektionsrisk.

Enligt Agria (som baserar sin information på de hundar som är försäkrade hos de) så är det oftast äldre eller medelålders hundar som får diabetes. Diabetes är vanligast hos tikar och tikar med diabetes måste alltid kastreras.

SLU:s hemsida har en bra beskrivning för nybörjare och ett avsnitt för vanliga frågor och svar där det bl.a. finns svar om ärftliget, ögonbesvär, livslängs och kostnader vid diabetesbehandling. Där finns även ett diabeteslexikon.

På Agrias hemsida kan man läsa om vad som täcks och vad som inte täcks av just deras försäkringar. T.ex. så täcks kastrationen av tikar med diabetes.

1 kommentar:

Som diabetiker själv tycker jag att det är bra skrivet. Men eftersom jag vet vilken svår sjukdom det är, så skulle jag också välja att avliva min hund. Det låter så lätt: Äta rätt på bestämda tider och ta sina sprutor. Men det är det inte. En liten extra sväng upp för trapporna kan ställa till det. En liten förkylning likaså. Och jag har lärt mig känna tecknen på både för högt och för lågt blodsocker. Men en hund kommer aldrig att kunna det. Och gå med den oron i magen varje dag som hundägare skulle inte jag mäkta med.

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.

opheimblog

blandt andet om at have hund med diabetes

Emneord: hund og diabetes

Sådan måler du blodsukker på hund

5 gode tips til måling af blodsukker på hund

Jeg gjorde mig nogle erfaringer med at måle blodsukker på Ciewie. Det fungerede også. MEN vi nåede at stikke så mange små huller i hendes ører, at det blev svært at finde steder at stikke. Her viser jeg hvordan jeg stak:

Dyrlægen havde desværre glemt at fortælle mig, at der var andre muligheder.

F. eks den tynde hud bag skulderen. Jeg har samlet links til alternative måder/steder at måle blodsukker på hunden.

Jeg tror især metode 3 ville have fungeret for os, men vi slap jo heldigvis for at fortsætte med at måle blodsukker.

Måle blodsukker, give insulin

Der gik ikke mange dage, før vi begyndte at overveje sterilisation.

Vi skulle stikke Ciewie med en lille nål inde i øret, så vi fik en bloddråbe, vi kunne måle blodsukker i. I begyndelsen skulle vi gøre det hver anden time døgnet rundt, for at man kunne finde ud af, hvor meget insulin hun skulle have.

Det almindelige hverdagsforløb ville være, at hun skulle have målt blodsukker, have mad og 1/2 time efter skulle hun have insulin. Men hun skulle have spist sin mad. Ciewie gad ikke spise, og jeg måtte ikke friste med lækkerier, fordi hun skulle følge en diæt – det var et mareridt.

Hun begyndte også at være ked af, at vi nærmede os, for hun viste godt vi sikkert ville stikke i hendes øre. Vi følte os rigtig onde.

Det letteste var faktisk at give hende insulin. Det var der ingen problemer med.

Efter en lille uge, var jeg klar til at lytte til dyrlægens snak om sterilisation.

Hvad dyrlægen sagde

Vores dyrlæge forklarede, at hvis diabetes kommer kort efter en tæve har været i løbetid, kan den være hormonelt betinget.

Aftalen med dyrlægen blev, at Ciewie først skulle have styr på stofskiftet via medicin og derefter skulle vi have styr på sukkersygen.

I løbet af 1-2 uger, hvor vi afventede hendes reaktion på stofskifte-medicn, blev hendes diabetes meget tydelig. Et tydeligt tegn på diabetes hos dyr er (som hos mennesker), at de drikker og tisser meget. De sidste dage stod hun op og, rent ud sagt, “pisse som en hest”. Det var tydeligt hun skulle i behandling.

1. Første dag blev hun indlagt til opservation.
2. Vi blev instrueret i at måle blodsukker og give hende insulin. Vi fik hende med hjem og skulle desuden sørge for at hun passede en omhyggelig diæt.
3. Dyrlægen forklarede at en sterillisation kunne bedre diabetes, fordi den nok var udløst af hormoner. – men vi overvejede det end ikke. Ciewie var jo en ældre hund og bange for dyrlæger – så vi ville ikke have at hun skulle opereres.

Den dag jeg opdagede, at hunde kan få diabetes

Ved du, at hunhunde kan få hormonelt betinget diabetes? Jeg vidste det ikke, men jeg fandt ud af det da Ciewie, min ene border collie, fik det.

Sommeren 2012 – En søndag eftermiddag da vi var på vej i skoven med hundene, ville Ciewie pludselig ikke gå mere. Vi var lige kommet ind i skoven, 500 meter fra vores hjem, så det var ikke distancen, der var problemet. Hun lagde sig ned og nægtede simpelthen at gå længere. Min mand måtte bære hende hjem. Vi regnede med at hun måske var lidt overanstrengt i benene, hun var jo trods alt 9 1/2 år. Men humør og energi var bare væk.

Næste dag blev hun undersøgt af dyrlægen, som konstaterede for lavt stofskifte og voldsom diabetes. Med rigtig dårlig samvittighed fandt vi nu ud af, at flere af de skavanker, vi havde forklaret med høj alder og almindeligt slid pga agility var relateret til stofskiftesygdom.

Hun fik stofskiftemedicin, så var der sådan set styr på den del. Så manglede vi bare at få styr på det med diabetes…

Diabetes 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 in Dogs

By Ernest Ward, DVM & Robin Downing, DVM, DAAPM, DACVSMR, CVPP

What is Diabetes insipidus?

There are two types of diabetes in dogs. Diabetes mellitus (DM) is also called “sugar diabetes” and results from a disruption of pancreas function and abnormal regulation of blood sugar. The term, meaning “sweetened with honey,” originated from the fact that the urine of these patients was “sweet” due to high amounts of sugar excreted from the body. Diabetes insipidus (DI) gets its name from the fact that the urine of these patients is dilute enough to be “tasteless” or “insipid.” Diabetes insipidus (DI) is rare in dogs, and is characterized by excessive thirst/drinking and the production of enormous volumes of extremely dilute urine. Some dogs may produce so much urine that they become incontinent (incapable of controlling their urine outflow). The irony of this disease is that despite drinking large volumes of water, the dog can become dehydrated from urinating so much.

My dog is drinking and urinating a lot. Is DI the likely cause?

There are many causes of increased thirst (polydipsia) and increased urine production (polyuria), including diabetes insipidus, diabetes mellitus, liver problems, and kidney disease, to name a few. It is essential that several diagnostic tests be performed to determine the cause of your dog’s problem.

How is DI diagnosed?

Part of diagnosing DI involves first eliminating other potential explanations for increased drinking and increased urinating. Typical laboratory testing will include a complete blood count (CBC), blood chemistry panel to evaluate liver and kidney parameters and blood sugar, and a urinalysis. The urine concentration (specific gravity) is quite low in these dogs. A more advanced test involves calculating normal daily water intake, measuring how much the dog is truly drinking in 24 hours, depriving him of a portion of the volume he is consuming (closer to the normal volume), and then measuring the urine concentration to assess whether or not the urine can be concentrated.

Your veterinarian may recommend a CT or MRI if there is any suspicion of a tumor in the pituitary gland. Likewise, your veterinarian may recommend a trial treatment with a medication to assess his response to this therapy.

What causes DI?

Part of kidney function is to continually filter the blood that passes through them and to maintain the balance of the body's water by excreting or reabsorbing fluid as required.

Efficient re-absorption requires an adequate level of a hormone called “antidiuretic hormone” (ADH), or vasopressin, which is produced by the pituitary gland at the base of the brain, and which has its effects in the kidneys. DI may be caused by inadequate production of ADH – this is called Central DI (CDI) – or by kidney resistance to the hormone – this is called Nephrogenic DI (NDI).

Inadequate production of ADH, as in CDI, can be caused by a birth defect, brain trauma, a tumor in the pituitary gland, or there may be no specific cause found (idiopathic).

Lack of kidney response to ADH, as in NDI, can result from a birth defect, an adverse reaction to certain medications, or secondary to certain diseases (like severe infection, metabolic disorders, or advancing kidney disease).

How is DI treated?

CDI is treated using a synthetic formulation of ADH that is applied either as eye drops or by injection under the skin. NDI is treated using oral hydrochlorothiazide and a low-salt diet. The treatment depends upon the definitive diagnosis.

Can DI be cured?

Diabetes insipidus cannot be cured except in the rare patient whose DI is caused by trauma. It can, however, usually be successfully controlled. Without treatment, this disease results in dehydration leading to stupor, coma, and death.

Dog - Cushing's Syndrome

Cushing's disease or hyperadrenocorticism, is more accurately described as a syndrome than a disease, since it produces a much wider variety of signs or symptoms than are normally associated…

Kidney Failure - Acute in Cats

Acute renal failure (ARF) or acute kidney failure refers to the sudden failure of the kidneys to perform normal filtration duties. This is not the same as the much more common form of kidney failure, chronic renal failure (CRF).

Heart Disease - Cardiomyopathy in Cats

Cardiomyopathy is a term used to describe diseases of the heart muscle. In cats, three classes of cardiomyopathy have been described: hypertrophic, dilated, and intermediate or restrictive cardiomyopathy. In all classes, the heart disease usually results in clinical signs of heart failure.

©Copyright VCA Hospitals all rights reserved.

Canine and feline diabetes

Diabetes can be managed successfully with insulin therapy and attention to diet and exercise. Effective diabetes treatment of pets, will restore the quality of life of dogs and cats with diabetes mellitus.

This web site is intended for owners of dogs and cats with diabetes. The site provides disease information on diabetes mellitus. Advice about insulin treatment and suitable diets for managing canine and feline diabetes can also be found.

Answers to questions about diabetes in dogs, canine diabetes treatment and the use of insulin.

Answers to questions about diabetes in cats, feline diabetes treatment and the use of insulin.

In some cases in cats, diabetes may no longer need treatment with insulin but can eventually be stabilised with careful monitoring of diet.

Videos and diagrams describing how to give an insulin injection for the treatment of canine or feline diabetes.