Diabetes Insipidus


Article Author:
Channing Hui


Article Editor:
Jared Radbel


Editors In Chief:
Russell McAllister
Jason Widrich
Daniel Sizemore


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
3/29/2019 12:29:39 AM

Introduction

Diabetes insipidus (DI) is a disease process that results in either decreased release of or response to antidiuretic hormone (ADH, also known as vasopressin or AVP), which can cause electrolyte imbalances. [1][2]There are two types of diabetes insipidus, central and nephrogenic, and each has congenital and acquired causes.

Etiology

Idiopathic central diabetes insipidus is the most common cause, in which no identifiable cause was determined. The congenital form of central diabetes insipidus is rare and is associated with hypothalamus malformations, defects in ADH precursor synthesis, or deficiency in ADH.[3][4]

Acquired forms of central diabetes insipidus include autoimmune and vascular diseases, sarcoidosis, craniopharyngioma, Langerhans Cell Histiocytosis, surgery, trauma, structural malformations, metastasis, hypoxic brain injury, or ischemia.

The congenital form of nephrogenic diabetes insipidus is associated with mutations in either the AVPR2 or AQP2 gene. AVPR2 receptor defects are the source of 90% of congenital nephrogenic diabetes insipidus forms of nephrogenic diabetes insipidus are more common and can stem from multiple drug treatments including lithium, antibiotics, antifungals, and antineoplastic agents. Other acquired causes include renal disease, sickle cell disease, obstructive uropathy, pregnancy, craniopharyngioma surgery, and electrolyte disturbances such as hypokalemia and hypercalcemia.

Epidemiology

Diabetes insipidus is an uncommon disease process with a low prevalence of 1:25,0000. In clinical practice, congenital forms of diabetes insipidus constitute less than 10% of patient cases.

Pathophysiology

Water balance is regulated by ADH, thirst, and kidney function. ADH is produced by the posterior pituitary and released into the blood supply via the inferior hypophyseal arteries. Subsequently, ADH targets the kidney and binds to V2-receptors on the renal collecting tubule. This leads to a signaling cascade of Gs-adenyl cyclase system activation which increases cyclic 3',5'-adenosine monophosphate (cAMP), leading to the phosphorylation of preformed AQP2 water channels. The AQP2 channels translocate to the cell membrane and promote water flow by an osmotic gradient from the lumen into the cells of the collecting duct.[5][6][7]

In central diabetes insipidus, there is a deficiency of ADH. In nephrogenic diabetes insipidus, ADH is available, but there is a lack of response by the kidneys.

Apelin is a diuretic neuropeptide that has shown to counteract ADH and may play a role in regulating fluid balance. In lactating mice, water deprivation demonstrated an increase in ADH release and depletion of hypothalamic stores, in conjunction with decreased apelin concentrations and increased hypothalamic stores.

History and Physical

The most common findings in patients with diabetes insipidus are polydipsia, polyuria, and nocturia.

Polyuria is defined as urine output more than 3 L/day in adults or 2 L/m2 in children. In children, symptoms can be nonspecific, and they may present with severe dehydration, constipation, vomiting, fevers, irritability, failure to thrive, and growth retardation. In patients with central nervous system (CNS) tumors, headaches, and visual defects may present in addition to the classic symptoms.

Additional symptoms in patients with diabetes insipidus may include weakness, lethargy, fatigue, and myalgias.

The differentials for polyuria should include primary polydipsia and uncontrolled diabetes mellitus.

Evaluation

Calculate the plasma osmolality: 2[Na+] + [Glucose]/18 + [BUN]/2.8

Calculate the total 24-hour urine volume to confirm polyuria. Obtain baseline values of plasma electrolytes, random serum, and urine osmolality.[8][9][10][11]

To differentiate central and nephrogenic diabetes insipidus, perform a water deprivation test and desmopressin (DDAVP) trial. Typically a 7-hour deprivation test is adequate to diagnose diabetes insipidus. Primary polydipsia may require longer dehydration periods.

In adults, the water restriction test should be discontinued when one of the following is reached:

  • Urine osmolality reaches normal reference range
  • Urine osmolality stable on two to three consecutive hourly measurements, even with rising plasma osmolality
  • Plasma osmolality greater than 295 mosmol/kg to 300 mosmol/kg
  • Plasma Na greater than 145 mEq

In newborns and young infants, if nephrogenic diabetes insipidus is suspected the diagnostic test of choice is DDAVP (1 mcg subcutaneously or intravenously over 20 minutes, maximum dose 0.4 mcg/kg).

In children, water deprivation test should be closely monitored. If one of the following endpoints are reached discontinue the trial:

  • Urine osmolality reaches normal reference range
  • Plasma osmolality greater than 295 mosmol/kg to 300 mosmol/kg
  • Plasma sodium greater than 145 meq/L
  • Loss of 5% of body weight or signs of volume depletion

The water deprivation trial is most accurate when DDAVP is not given. After water deprivation, studies have demonstrated DDAVP can increase urine osmolality greater than 100% incomplete central diabetes insipidus and up to 50% in partial central diabetes insipidus.

In cases of nephrogenic diabetes insipidus, water deprivation suboptimally increases urine osmolality. DDAVP minimally increases urine osmolality in partial nephrogenic diabetes insipidus, with no increase urine osmolality in complete nephrogenic diabetes insipidus.

Central diabetes insipidus is diagnosed when there is evidence of plasma hyperosmolality (greater than 300 mosm/l), urine hyperosmolality (less than 300 mosm/l or urine/plasma osmolality less than 1), with polyuria (urinary volume greater than 4 mL/kg/hr to 5 mL/kg/hr for two consecutive hours after surgery).

Copeptin and AQP2 have also been utilized to differentiate nephrogenic and central diabetes insipidus. In central diabetes insipidus, AQP2 increases with DDAVP administration. On the contrary, in patients with nephrogenic diabetes insipidus, the AQP2 excretion does not increase after DDAVP administration.

When suspecting a structural cause of diabetes insipidus, MRI imaging can identify malformations of the posterior pituitary.

Treatment / Management

DDAVP, an ADH analog, can be administered orally, intranasally, subcutaneously, or intravenously. In adults, the dose is ten mcg by nasal insufflation or 4 mcg subcutaneously or intravenously. In newborns or very young infants, the dose is one mcg subcutaneously or intravenously over 20 minutes with a maximum dose of 0.4 mcg/kg.

It is essential to replete fluid losses in diabetes insipidus, as some patients may have thirst impairment and will not respond adequately to water intake.[12][13][14]

Central Diabetes Insipidus

The preferred therapy is DDAVP. Typically, therapy is maintained for the duration of central diabetes insipidus, which varies depending on the cause. The minimum dose should be administered to control polyuria adequately.

It is important to monitor for hyponatremia, as water retention can lead to sodium concentration changes that may cause brain injury. The patients and families should be educated to observe for symptoms of nausea, vomiting, lethargy, headaches, confusion, seizures, and coma.

Other treatment options for central diabetes insipidus include low-solute diet (low salt, low protein), thiazide diuretics, chlorpropamide, carbamazepine, and non-steroidal anti-inflammatory drugs (NSAID).

DDAVP is considered safe the pregnancy.

Nephrogenic Diabetes Insipidus

The first step is correct the underlying cause. If possible, discontinue the offending agent such as lithium.

Low-solute diet may decrease the urine output. The lower amount of total solutes ingested, the lower the urine volume that will be excreted.

Thiazide diuretics may be used in conjunction with dietary changes. The mechanism of administering a diuretic in the setting of polyuria is to promote the reduction of urine volume, which triggers the endogenous release of aldosterone. By having less water delivered distally, there would be less water loss in the collecting tubule, where ADH targets its effects.

Other treatment options include DDAVP and NSAIDs. NSAIDs inhibit prostaglandin synthesis, which has antagonistic the effects of ADH.

Pearls and Other Issues

Patients with significant electrolyte abnormalities should be closely monitored and admitted to the hospital.

Enhancing Healthcare Team Outcomes

There are many causes of DI and it is best managed by a multidisciplinary team that includes the primary care provider, nurse practitioner, internist, and a pharmacist. The key is to hydrate and replace the electrolytes and then manage the primary condition causing DI. The pharmacist should keep track of all medications that can cause DI and make the appropriate recommendations to the physician.

The outlook for patients with DI depends on the cause. For benign causes, the prognosis is good, but if the cause if a malignancy, then the prognosis is guarded.[15][5]


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Diabetes Insipidus - Questions

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A 65-year-old man with a history of bitemporal hemianopsia is sent for surgical evaluation. An MRI of the head and neck revealed a craniopharyngioma. Transsphenoidal hypophysectomy is performed without apparent complications. Two hours after surgery she develops polyuria (375 mL/h) and hypernatremia (155 mmol/L). The patient describes severe thirst and seems lethargic and disoriented. Which of the following pharmaceutical interventions is the best next step in this patient?



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Which of the following drugs typically is used first in the treatment of central diabetes insipidus?



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A patient diagnosed is diagnosed with diabetes insipidus. Appropriate fluids are started. Which of the following medications is given?



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Infection of any type is LEAST likely in a patient with which of the following?



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Which of the following will be seen in a patient with diabetes insipidus?



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What is the best treatment for central diabetes insipidus?



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A craniopharyngioma is surgically removed under general anesthesia. Halothane is used and the patient is fully awake in the recovery room and sent to the intensive care unit. The patient becomes comatose four hours later. Laboratories show sodium 152 mEq/L, osmolarity 310 mOsm/L, pH 7.50, PCO2 29 mm Hg, bicarbonate 23 mEq/L. Which of the following is responsible for the coma?



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Diabetes insipidus (DI) is usually treated with which medication?



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What hormone is deficient in central diabetes insipidus?



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What is false about diabetes insipidus findings?



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In patients with diabetes insipidus, what parameter is of least concern?



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Which is true about a patient with diabetes insipidus?



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Which of the following is not seen in central diabetes insipidus?



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Which is not used to treat diabetes insipidus?



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What parameter is most important to monitor in a patient with diabetes insipidus?



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A patient presents complaining of dehydration despite drinking a gallon of water, lethargy, morning headaches, occasional double vision, and polyuria. An MRI reveals a pituitary mass and you decide to administer desmopressin as your next step after a failed fluid restriction test. If this patient has central diabetes insipidus, what changes should occur a few hours after desmopressin administration?



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A 32-year-old African American female with sarcoidosis complains of polyuria which is found to be secondary to the sarcoidosis. Which of the following is most likely true?



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Which of the following causes hypernatremic dehydration?



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A patient undergoes a transsphenoidal approach to remove a pituitary tumor. On the first postoperative day, his urine output is increased, serum osmolality and sodium are increased, and urine specific gravity is decreased. The patient complains of thirst. What is the most likely diagnosis?



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Which of the following lab findings are NOT characteristic of diabetes insipidus?



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Which of the following medications is indicated in central diabetes insipidus?



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Which of the following is a potential cause of central diabetes insipidus?



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Which of the following conditions does not impair the ability of the kidney to concentrate urine?



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A 60-year-old female is brought to the emergency department for confusion. Her serum sodium is 160 meq/L with creatine of 2.3 mg/dL. Intravenous hydration causes improvement of her mentation and she reports that she drinks large amounts but is always thirsty. The next day the sodium is 152 meq/L and urine osmolality is 80 mosmol/kg. The patient is fluid restricted and the patient is given 10 TG of desmopressin intranasally. The urine osmolality increases to 90 mosmol/kg. Select the most likely diagnosis.



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What is the proper long term treatment for nephrogenic diabetes insipidus?



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A 17-year-old female has concerns about excessive thirst and urination. The exam is normal. Urine HCG is negative. Laboratories show (meq/L): Na+ 143, K+ 4.1, Cl 108, HCO3 25, BUN 18 mg/dL, Blood glucose 102 mg/dL. Urine electrolytes (mmol/L): Na+ 30, K+ 30 Urine osmolality: 190 mmol/kg water. Fluid restriction causes a 7 percent drop in weight with resulting hypernatremia but no change in urine osmolality. Five units of subcutaneous arginine vasopressin do not change the urine electrolytes or osmolality. Which of the following is the most likely diagnosis?



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Select the true statement about diabetes insipidus (DI).



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Which is true regarding diabetes insipidus (DI)?



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Which does not correctly explain the pathophysiology of diabetes insipidus?



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Which is true regarding central diabetes insipidus (DI)?



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What is the most common indicator of diabetes insipidus in patients without an underlying diagnosis of physical or mental illness?



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What two diagnoses does the water deprivation test with the administration of intravenous vasopressin differentiate?



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Which of the following is a common cause of pregnancy-induced diabetes insipidus?



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A 10-month-old is admitted for the third time for dehydration without any gastrointestinal losses. There is a failure to thrive and the patient is unable to concentrate his urine. Family history shows others with similar symptoms. Select the most likely diagnosis.



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What would be the probable lab values for a 13-year-old female with central diabetes insipidus (DI)?



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Select the most probable lab values for a 3-year-old with nephrogenic diabetes insipidus (DI).



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Which urine specific gravity is most likely in a patient with poorly controlled diabetes insipidus, DI?



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Which is most likely to be found in a patient with diabetes insipidus (DI)?



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Which is not used to treat diabetes insipidus (DI)?



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A normal serum value for which of the following is most indicative of adequate treatment of a patient with diabetes insipidus?



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Which of the following is not a symptom associated with diabetes insipidus?



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What can be administered to differentiate central from peripheral diabetes insipidus?



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Which of the following is not associated with diabetes insipidus (DI)?



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A patient is admitted to a progressive care unit with a diagnosis of severe dehydration from diabetes insipidus. Which of the following are expected findings in a patient with diabetes insipidus? Select all that apply.



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Which of the following would be expected signs and symptoms in a patient with diabetes insipidus? Select all that apply.



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Diabetes Insipidus - References

References

Guerrero-Pérez F,Marengo AP,Vidal N,Iglesias P,Villabona C, Primary tumors of the posterior pituitary: A systematic review. Reviews in endocrine     [PubMed]
Calina D,Docea AO,Golokhvast KS,Sifakis S,Tsatsakis A,Makrigiannakis A, Management of Endocrinopathies in Pregnancy: A Review of Current Evidence. International journal of environmental research and public health. 2019 Mar 4;     [PubMed]
Tabibzadeh N,Vrtovsnik F,Serrano F,Vidal-Petiot E,Flamant M, [Chronic metabolic and renal disorders related to lithium salts treatment]. La Revue de medecine interne. 2019 Feb 28;     [PubMed]
Ranieri M,Di Mise A,Tamma G,Valenti G, Vasopressin-aquaporin-2 pathway: recent advances in understanding water balance disorders. F1000Research. 2019;     [PubMed]
Harrois A,Anstey JR, Diabetes Insipidus and Syndrome of Inappropriate Antidiuretic Hormone in Critically Ill Patients. Critical care clinics. 2019 Apr;     [PubMed]
Atallah-Yunes SA,Clark J,Samanani S,Soe M, Small Cell Lung Cancer with Pituitary Metastasis Presenting as Secondary Adrenal Insufficiency: A Case Report and Literature Review. The American journal of case reports. 2019 Feb 17;     [PubMed]
Meyfroidt G,Gunst J,Martin-Loeches I,Smith M,Robba C,Taccone FS,Citerio G, Management of the brain-dead donor in the ICU: general and specific therapy to improve transplantable organ quality. Intensive care medicine. 2019 Feb 11;     [PubMed]
Davis J,Desmond M,Berk M, Lithium and nephrotoxicity: a literature review of approaches to clinical management and risk stratification. BMC nephrology. 2018 Nov 3;     [PubMed]
Baldeweg SE,Ball S,Brooke A,Gleeson HK,Levy MJ,Prentice M,Wass J, SOCIETY FOR ENDOCRINOLOGY CLINICAL GUIDANCE: Inpatient management of cranial diabetes insipidus. Endocrine connections. 2018 Jul;     [PubMed]
Lobatto DJ,de Vries F,Zamanipoor Najafabadi AH,Pereira AM,Peul WC,Vliet Vlieland TPM,Biermasz NR,van Furth WR, Preoperative risk factors for postoperative complications in endoscopic pituitary surgery: a systematic review. Pituitary. 2018 Feb;     [PubMed]
Andrysiak-Mamos E,Sagan K,Sagan L,Sowińska-Przepiera E,Syrenicz A, Cystic lesions of the sellar-suprasellar region - diagnosis and treatment. Endokrynologia Polska. 2018;     [PubMed]
Hunter JD,Calikoglu AS, Etiological and clinical characteristics of central diabetes insipidus in children: a single center experience. International journal of pediatric endocrinology. 2016;     [PubMed]
Arambewela MH,Somasundaram NP,Garusinghe C, Extreme hypernatremia as a probable cause of fatal arrhythmia: a case report. Journal of medical case reports. 2016 Oct 1;     [PubMed]
Lamas C,del Pozo C,Villabona C, Clinical guidelines for management of diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion after pituitary surgery. Endocrinologia y nutricion : organo de la Sociedad Espanola de Endocrinologia y Nutricion. 2014 Apr;     [PubMed]
Asemota AO,Gallia GL, Impact of frailty on short-term outcomes in patients undergoing transsphenoidal pituitary surgery. Journal of neurosurgery. 2019 Feb 22;     [PubMed]

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