Diabetes Insipidus
Print Overview Diabetes insipidus (die-uh-BEE-teze in-SIP-uh-dus) is an uncommon disorder that causes an imbalance of water in the body. This imbalance leads to intense thirst even after drinking fluids (polydipsia), and excretion of large amounts of urine (polyuria). While the names diabetes insipidus and diabetes mellitus sound similar, they're not related. Diabetes mellitus — which can occur as type 1 or type 2 — is the more common form of diabetes. There's no cure for diabetes insipidus, but treatments are available to relieve your thirst and normalize your urine output. Symptoms The most common signs and symptoms of diabetes insipidus are: Extreme thirst Excretion of an excessive amount of diluted urine Depending on the severity of the condition, urine output can be as much as 16 quarts (about 15 liters) a day if you're drinking a lot of fluids. Normally, a healthy adult will urinate an average of less than 3 quarts (about 3 liters) a day. Other signs may include needing to get up at night to urinate (nocturia) and bed-wetting. Infants and young children who have diabetes insipidus may have the following signs and symptoms: Unexplained fussiness or inconsolable crying Trouble sleeping Fever Vomiting Diarrhea Delayed growth Weight loss When to see a doctor See your doctor immediately if you notice the two most common signs of diabetes insipidus: excessive urination and extreme thirst. Causes Diabetes insipidus occurs when your body can't regulate how it handles fluids. Normally, your kidneys remove excess body fluids from your bloodstream. This fluid waste is temporarily stored in your bladder as urine, before you urinate. When your fluid regulation system is working properly, your kidneys conserve fluid and make less urine when your body water is decreased, suc Continue reading >>
How To Do A Water Deprivation Test: Interpretation Of Results
How to do a water deprivation test: interpretation of results Oxford Centre for Diabetes, Churchill Hospital, Oxford, UK. In order to test posterior pituitary function it is important to assess and replace corticotroph function before assessing posterior pituitary hormone production because ACTH deficiency leads to a reduced GFR and the inability to excrete a water load which may therefore mask diabetes insipidus. With diabetes insipidus the urine output is usually >3 l a day. Other causes of osmotic diuresis need to be excluded. The fluid deprivation test assesses the ability of the kidney to concentrate urine under the influence of ADH. Occasionally further investigations are required particularly when only partial forms of the condition are present. The patient is allowed fluids overnight. The patient is deprived of fluids for 8 hours or until 5% of the body mass has been lost. The patient needs to be weighed hourly. Plasma osmolality is measured 4 hourly and urine volume and osmolality every 2 h. At the end of 8 h the patient is given 2 mcg of intramuscular desmopressin and urine and plasma osmolality checked over the next 4 h. If serum osmolality rises to >305 mmol/kg the patient has diabetes insipidus and the test is stopped. With cranial DI the urine osmolality remains below 300 osmols/kg and rises to >800 after desmopressin. With nephrogenetic diabetes insipidus the urine osmolality is <300 both before and after desmopressin. Continue reading >>
Nephrogenic Diabetes Insipidus
In nephrogenic diabetes insipidus, the kidneys produce a large volume of dilute urine because the kidney tubules fail to respond to vasopressin (antidiuretic hormone) and are unable to reabsorb filtered water back into the body. Often nephrogenic diabetes insipidus is hereditary, but it can be caused by drugs or disorders that affect the kidneys. To treat nephrogenic diabetes insipidus, people restrict salt in their diet and sometimes take drugs to reduce the amount of urine excreted. Both diabetes insipidus and the better-known type of diabetes, diabetes mellitus, result in the excretion of large volumes of urine. Otherwise, the two types of diabetes are very different. Two types of diabetes insipidus exist. Nephrogenic diabetes insipidus and diabetes mellitus are very different, except that both cause people to excrete large amounts of urine. Causes Normally, the kidneys adjust the concentration and amount of urine according to the body’s needs. The kidneys make this adjustment in response to the level of vasopressin in the blood. Vasopressin, which is secreted by the pituitary gland, signals the kidneys to conserve water and concentrate the urine. In nephrogenic diabetes insipidus, the kidneys fail to respond to the signal. Nephrogenic diabetes insipidus may be Hereditary nephrogenic diabetes insipidus In hereditary nephrogenic diabetes insipidus, the gene that typically causes the disorder is recessive and carried on the X chromosome, one of the two sex chromosomes, so usually only males develop symptoms. However, females who carry the gene can transmit the disease to their sons. Rarely, another abnormal gene can cause nephrogenic insipidus in both males and females. Acquired nephrogenic diabetes insipidus Symptoms People may pass from 1 to 6 gallons (3 to 20 lite Continue reading >>
Central Diabetes Insipidus Diagnosed After Gynecologic Surgery: A Case Report | Akuzawa | Journal Of Endocrinology And Metabolism
Journal of Endocrinology and Metabolism, ISSN 1923-2861 print, 1923-287X online, Open Access Article copyright, the authors; Journal compilation copyright, J Endocrinol Metab and Elmer Press Inc Volume 3, Number 1-2, April 2013, pages 41-46 Central Diabetes Insipidus Diagnosed After Gynecologic Surgery: A Case Report Nobuhiro Akuzawaa, c, Naoyuki Haradaa, Noriko Hasegawaa, Hidenori Sekia, Yuko Okua, Masayuki Totsukaa, Takashi Hatoria, Atsushi Murakamia, Kunihiko Imaia, Yonosuke Kitaharaa, Masahiko Tashiroa, Masahiko Kurabayashib aDepartment of Internal Medicine, Social Insurance Gunma Chuo General Hospital, 1-7-13 Koun-cho, Maebashi, Gunma 371-0025, Japan bDepartment of Medicine and Biological Science, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan cCorresponding author: Nobuhiro Akuzawa, Social Insurance Gunma Chuo General Hospital, 1-7-13 Koun-cho, Maebashi, Gunma 371-0025, Japan Manuscript accepted for publication January 22, 2013 Short title: Central Diabetes Insipidus Diagnosed A 41-year-old woman with non-alcoholic fatty liver disease and complex endometrial hyperplasia with atypia was admitted to our hospital to undergo hysterectomy. Her weight was 107 kg, having doubled after delivery of her second child. After a routine hysterectomy, unexpected polyuria was observed. Investigation revealed a relatively low plasma vasopressin concentration, and absence of hyperintense signals in the region of the posterior lobe of the pituitary gland on T1-weighted magnetic resonance imaging, suggesting partial central diabetes insipidus. It was concluded that excessive intake of sweetened carbonated beverages due to thirst caused by diabetes insipidus had contributed to her obesity. Keywords: Central diabetes insipidus; Magne Continue reading >>
Management Of Diabetes Insipidus In Children
Go to: Abstract Diabetes Insipidus (DI) is a heterogeneous clinical syndrome of disturbance in water balance, characterized by polyuria (urine output > 4 ml/kg/hr), polydypsia (water intake > 2 L/m2/d) and failure to thrive. In children, Nephrogenic DI (NDI) is more common than Central DI (CDI), and is often acquired. The signs and symptoms vary with etiology, age at presentation and mode of onset. Neonates and infants with NDI are severely affected and difficult to treat. Diagnosis is based on the presence of high plasma osmolality and low urinary osmolality with significant water diuresis. Water deprivation test with vasopressin challenge, though has limitations, is done to differentiate NDI and CDI and diagnose their partial forms. Measurement of urinary aquaporin 2 and serum copeptin levels are being studied and show promising diagnostic potential. Magnetic Resonance Imaging (MRI) pituitary helps in the etiological diagnosis of CDI, absence of posterior pituitary bright signal being the pathognomic sign. If pituitary stalk thickening of < 2 mm is present, these children need to be monitored for evolving lesion. Neonates and young infants are better managed with fluids alone. Older children with CDI are treated with desmopressin. The oral form is safe, highly effective, with more flexibility of dosing and has largely replaced the intranasal form. In NDI besides treatment of the underlying cause, use of high calorie low solute diet and drugs to ameliorate water excretion (thiazide, amelioride, indomethacin) are useful. Children with NDI however well treated, remain short and have mental retardation on follow up. Continue reading >>
Life-threatening Hypernatremia In A Case Of Diabetes Insipidus/panhypopituitarism
Life-Threatening Hypernatremia In A Case Of Diabetes Insipidus/Panhypopituitarism Author links open overlay panel EkamolTantisattamo Thomas B.Francis Open Access funded by The Korean Society of Nephrology Management of diabetes insipidus (DI) accompanied by panhypopituitarism requires understanding of the relationships between ADH and thyroid/glucocorticoid tone. Low thyroid/glucocorticoid tone decreases free water clearance which protects against DI and may lead to hyponatremia while high thyroid/glucocorticoid tone may unmask DI and facilitate hypernatremia. A 31 year-old man with DI/panhypopituitarism was stable until his levothyroxine was incorrectly lowered based on TSH levels. He became hypothyroid and was hospitalized 3 times over 1 month for recurring altered mental status and mild hyponatremia. DDAVP was repeatedly held with rapid onset of polyuria resulting severe hypernatremia. On the last admission, he presented with altered mental status from sepsis. Serum sodium was 135mmol/l. He was made NPO and treated with stress dose hydrocortisone and fludrocortisone. DDAVP was held for the mild hyponatremia. Serum sodium rapidly elevated to 168mmol/l after only 12 hours. DDAVP was restarted with liberalization of diet to unlimited free water access causing rapid downward sodium correction. Hypernatremia almost always results from iatrogenic causes. In our case, holding DDAVP for hyponatremia resulted in rapid onset of hypernatremia and volume depletion. Stress dose glucocorticoids further unmasked DI. Thirst and free access to water which typically protects patients with un-replaced DI were not operational due to his NPO status which contributed to the rapid rise in serum sodium. Water balance is controlled by thyroid, glucocorticoid, and principally ADH working at Continue reading >>
Management Of Electrolyte And Fluid Disorders After Brain Surgery For Pituitary/suprasellar Tumours
Management of Electrolyte and Fluid Disorders after Brain Surgery for Pituitary/Suprasellar Tumours Disturbances in salt and water balances are relatively common in children after brain surgeries for suprasellar and pituitary tumours, presenting diagnostic and therapeutic challenges. Although hypernatraemia associated with central diabetes insipidus is commonly encountered, it is hyponatraemia (HN) that poses more of a diagnostic dilemma. The main differential diagnoses causing HN are the syndrome of inappropriate antidiuretic hormone secretion, marked by inappropriate retention of water, and cerebral salt wasting, characterized by polyuria and natriuresis. Diagnosis and management can be even more difficult when these conditions precede or coexist with each other. These diagnostic and therapeutic dilemmas are discussed in detail in this review. Due to the anatomic location of suprasellar and pituitary tumours, interventional brain surgery can have peri- and postoperative complications related to anterior and posterior pituitary dysfunctions with fluid and electrolyte disorders. Conditions such as central diabetes insipidus (CDI), which can be transient or permanent, partial or complete, the syndrome of inappropriate antidiuretic hormone secretion (SIADH), cerebral salt wasting (CSW) and adipsic diabetes insipidus (ADI) can occur/coexist, making clinical management extremely challenging. Anterior and posterior pituitary dysfunction can also be present at diagnosis. The aim of this article is to review the pre- and postoperative management of electrolyte and fluid disorders after brain surgery for pituitary/suprasellar tumours and to discuss the diagnostic and therapeutic challenges encountered based on the authors' personal experience, as well as a review of the releva Continue reading >>
Polyuria- Diabetes Mellitus Or Diabetes Insipidus Or Both
Abstract: Introduction: Coincident development of Diabetes Mellitus (DM) and Diabetes Insipidus (DI) in adults has rarely been reported. Clinical case: A 54 year old obese white male with no known past medical history was admitted to the hospital with 2 day history of slurred speech, weakness and 1 week history of polyuria. At the time of presentation, he was found to be in Hyperosmolar Hyperglycemic state [Blood Glucose 792 mg/dl, Anion Gap 23, HCO3: 20mEq/L , ABG pH:7.35, Serum Osmolality: 395mOsm/kg, Serum Sodium: 149 mEq/L] which was treated with insulin infusion and iv fluids and transitioned in 10 hours to subq basal-bolus insulin regimen. However, his polyuria [urine output 4-5 L/day] persisted and serum sodium (Na+) rose to 152mEq/L over the next 3 days despite aggressive free water replacement and adequate control of DM. In view of polyuria and Hypernatremia, adiagnosis of DI was considered. This was supported by the finding of hypo-osmolar urine [Urine Osmolality: 214mOsm/kg] with hyperosmolar serum [Serum Osmolality: 321mOsm/kg]. Thyroid function and serum cortisol were normal. He was given a dose of Desmopressin acetate 1 microgram nasal spray with decrease in urine output and 300% increase in Urine Osmolality [from 214 to 671 mOsm/kg] over the next 8 hours. He was diagnosed with Central Diabetes Insipidus (CDI) and Desmopressin was continued with normalization of the serum Na: 138 mEq/L and Serum Osmolality: 295 mOsm/kg. Imaging of the brain did not show pituitary stalk thickening or absence of bright spot. Pt was discharged on Desmopressin, Insulin and Sitagliptin-Metformin. On a follow up outpatient visit, his DDAVP dose was titrated down and DM remained well controlled. Discussion: Co-existence of DM and DI has been reported in pediatric population as a Continue reading >>
Diabetes Insipidus
Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst.[1] The amount of urine produced can be nearly 20 liters per day.[1] Reduction of fluid has little effect on the concentration of the urine.[1] Complications may include dehydration or seizures.[1] There are four types of DI, each with a different set of causes.[1] Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone).[1] This can be due to damage to the hypothalamus or pituitary gland or genetics.[1] Nephrogenic diabetes insipidus (NDI) occurs when the kidneys do not respond properly to vasopressin.[1] Dipsogenic DI is due to abnormal thirst mechanisms in the hypothalamus while gestational DI occurs only during pregnancy.[1] Diagnosis is often based on urine tests, blood tests, and the fluid deprivation test.[1] Diabetes mellitus is a separate condition with an unrelated mechanism, though both can result in the production of large amounts of urine.[1] Treatment involves drinking sufficient fluids to prevent dehydration.[1] Other treatments depend on the type.[1] In central and gestational disease treated is with desmopressin.[1] Nephrogenic disease may be treated by addressing the underlying cause or the use of a thiazide, aspirin, or ibuprofen.[1] The number of new cases of diabetes insipidus each year is 3 in 100,000.[4] Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally.[2] Nephrogenic DI can begin at any age.[3] The term "diabetes" is derived from the Greek word meaning siphon.[5] Signs and symptoms[edit] Excessive urination and extreme thirst and increased fluid intake (especially for cold water and sometimes ice or ice water) are typical for DI.[6] The symptoms of excessive urination Continue reading >>
Treatment Of Central Diabetes Insipidus
INTRODUCTION The major symptoms of central diabetes insipidus (DI) are polyuria, nocturia, and polydipsia due to the concentrating defect. Treatment of this disorder is primarily aimed at decreasing the urine output, usually by increasing the activity of antidiuretic hormone (ADH, also called arginine vasopressin or AVP). Replacement of previous and ongoing fluid losses is also important. Most patients with central DI have a normal or only mildly elevated plasma sodium concentration because concurrent stimulation of thirst minimizes the degree of net water loss. However, hypernatremia can occur if thirst is impaired or the patient has no access to water [1-3]. Correction of the hypernatremia requires repair of this free water deficit. (See "Treatment of hypernatremia".) The treatment of central DI will be reviewed here. The causes of this disorder and the approach to the patient with polyuria are discussed separately. (See "Clinical manifestations and causes of central diabetes insipidus" and "Diagnosis of polyuria and diabetes insipidus".) CHOICE OF THERAPY There are three main options for the treatment of polyuria in patients with central DI: Desmopressin, which is an ADH analog and is the preferred drug in almost all patients. Continue reading >>
Central Diabetes Insipidus Diagnosed After Gynecologic Surgery: A Case Report | Akuzawa | Journal Of Endocrinology And Metabolism
Journal of Endocrinology and Metabolism, ISSN 1923-2861 print, 1923-287X online, Open Access Article copyright, the authors; Journal compilation copyright, J Endocrinol Metab and Elmer Press Inc Volume 3, Number 1-2, April 2013, pages 41-46 Central Diabetes Insipidus Diagnosed After Gynecologic Surgery: A Case Report Nobuhiro Akuzawaa, c, Naoyuki Haradaa, Noriko Hasegawaa, Hidenori Sekia, Yuko Okua, Masayuki Totsukaa, Takashi Hatoria, Atsushi Murakamia, Kunihiko Imaia, Yonosuke Kitaharaa, Masahiko Tashiroa, Masahiko Kurabayashib aDepartment of Internal Medicine, Social Insurance Gunma Chuo General Hospital, 1-7-13 Koun-cho, Maebashi, Gunma 371-0025, Japan bDepartment of Medicine and Biological Science, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan cCorresponding author: Nobuhiro Akuzawa, Social Insurance Gunma Chuo General Hospital, 1-7-13 Koun-cho, Maebashi, Gunma 371-0025, Japan Manuscript accepted for publication January 22, 2013 Short title: Central Diabetes Insipidus Diagnosed A 41-year-old woman with non-alcoholic fatty liver disease and complex endometrial hyperplasia with atypia was admitted to our hospital to undergo hysterectomy. Her weight was 107 kg, having doubled after delivery of her second child. After a routine hysterectomy, unexpected polyuria was observed. Investigation revealed a relatively low plasma vasopressin concentration, and absence of hyperintense signals in the region of the posterior lobe of the pituitary gland on T1-weighted magnetic resonance imaging, suggesting partial central diabetes insipidus. It was concluded that excessive intake of sweetened carbonated beverages due to thirst caused by diabetes insipidus had contributed to her obesity. Keywords: Central diabetes insipidus; Magne Continue reading >>
Diabetes Insipidus: A Few Clinical Pearls
Diabetes Insipidus: A few clinical pearls From Lewis Blevins. MD Polyuria in the setting of thirst and increased water intake, with a dilute urine, and a high or high normal serum sodium (>141-142 mEq/L) is usually recognizable as DI. Some occasional patients require water deprivation tests. DI can occur in 5-20% of people after pituitary surgery. It goes away in about two-thirds of people. The longest report of time to recovery to normal function from DI that I can recall is 8 years. In most cases, if it is not better by 6-12 months it is not going to get better. Polyuria is defined as 30 mL of urine per kilogram of body weight in a 24 hr period. This is useful to determine thresholds for DI in children and small adults. For example, 2 L of urine out per day is normal for some adults but too much urine for someone weighing less than 66 kg or about 147 pounds. dDAVP doesnt work as well if you have a cold or are pregnant as there are vasopressinases in the nose that can destroy the drug. Also, it may not work as well within a few weeks after transsphenoidal pituitary surgery. dDAVP that doesnt work may have expired. The bright spot of the posterior pituitary gland on MRI is due to AVP and its neurophysin protein. Patients with DI often lack this bright spot on MRI. When a patient with DI does becomes hyponatremic its, unfortunately, common practice to stop the dDAVP and to restrict fluid intake. The problem comes when the vasopressin starts to wear off. As you know, it wears off quickly. Urine output increases and the sodium rises quickly. Too quickly!!!! To compound matters, fluid restriction is in place and patients are not allowed to drink in response to thirst until the nurse gets an order from the doctorand this can be too late! The sodium rises more quickly as deh Continue reading >>
Polyuria- Diabetes Mellitus Or Diabetes Insipidus Or Both
Abstract: Introduction: Coincident development of Diabetes Mellitus (DM) and Diabetes Insipidus (DI) in adults has rarely been reported. Clinical case: A 54 year old obese white male with no known past medical history was admitted to the hospital with 2 day history of slurred speech, weakness and 1 week history of polyuria. At the time of presentation, he was found to be in Hyperosmolar Hyperglycemic state [Blood Glucose 792 mg/dl, Anion Gap 23, HCO3: 20mEq/L , ABG pH:7.35, Serum Osmolality: 395mOsm/kg, Serum Sodium: 149 mEq/L] which was treated with insulin infusion and iv fluids and transitioned in 10 hours to subq basal-bolus insulin regimen. However, his polyuria [urine output 4-5 L/day] persisted and serum sodium (Na+) rose to 152mEq/L over the next 3 days despite aggressive free water replacement and adequate control of DM. In view of polyuria and Hypernatremia, adiagnosis of DI was considered. This was supported by the finding of hypo-osmolar urine [Urine Osmolality: 214mOsm/kg] with hyperosmolar serum [Serum Osmolality: 321mOsm/kg]. Thyroid function and serum cortisol were normal. He was given a dose of Desmopressin acetate 1 microgram nasal spray with decrease in urine output and 300% increase in Urine Osmolality [from 214 to 671 mOsm/kg] over the next 8 hours. He was diagnosed with Central Diabetes Insipidus (CDI) and Desmopressin was continued with normalization of the serum Na: 138 mEq/L and Serum Osmolality: 295 mOsm/kg. Imaging of the brain did not show pituitary stalk thickening or absence of bright spot. Pt was discharged on Desmopressin, Insulin and Sitagliptin-Metformin. On a follow up outpatient visit, his DDAVP dose was titrated down and DM remained well controlled. Discussion: Co-existence of DM and DI has been reported in pediatric population as a Continue reading >>
Diabetes Insipidus Treatment & Management: Approach Considerations, Postoperative Setting, Consultations
Diabetes InsipidusTreatment & Management Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD more... Most patients with diabetes insipidus (DI) can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, replace losses with dextrose and water or an intravenous (IV) fluid that is hypo-osmolar with respect to the patients serum. Do not administer sterile water without dextrose intravenously, as it can cause hemolysis. To avoid hyperglycemia, volume overload, and overly rapid correction of hypernatremia, fluid replacement should be provided at a rate no greater than 500-750 mL/h. A good rule of thumb is to reduce serum sodium by 0.5 mmol/L (0.5 mEq/L) every hour. The water deficit may be calculated on the basis of the assumption that body water is approximately 60% of body weight. In patients with central DI, desmopressin is the drug of choice. [ 31 , 32 ] A synthetic analogue of antidiuretic hormone (ADH), desmopressin is available in subcutaneous, IV, intranasal, and oral preparations. [ 33 ] Generally, it can be administered 2-3 times per day. Patients may require hospitalization to establish fluid needs. Frequent electrolyte monitoring is recommended during the initial phase of treatment. Alternatives to desmopressin as pharmacologic therapy for DI include synthetic vasopressin and the nonhormonal agents chlorpropamide, carbamazepine, clofibrate (no longer on the US market), thiazides, and nonsteroidal anti-inflammatory drugs (NSAIDs). Because of side effects, carbamazepine is rarely used, being employed only when all other measures prove unsatisfactory. NSAIDs (eg, indomethacin) may be used in nephrogenic DI, but only when no better options exist. In central DI, the primary problem is a ho Continue reading >>
Diabetes Insipidous - Cancer Therapy Advisor
Diabetes insipidus (DI) is a disease characterized by polyuria (greater than 3 liters a day) and polydipsia, due to congenital or acquired absence of, or resistance to, vasopressin (or antidiuretic hormone, ADH) action, leading to failure to concentrate urine. Countercurrent exchange mechanisms in the kidney allow for regulation of water reabsorption in the collecting duct by vasopressin. Upon release from the anterior hypothalamus in response to changes in plasma osmolality or to decreased effective circulating volume, ADH binds to vasopressin 2 (V2) receptors in the collecting duct, activating signaling pathways that result in the insertion of aquaporin-2 (AQP-2) water channels in the luminal membrane. In the presence of an intact medullary interstitial osmotic gradient, water is reabsorbed into the cell through AQP-2 channels and exits via AQP-3 and AQP-4 channels into the systemic circulation. Partial or complete absence of vasopressin release from the hypothalamus leads to central diabetes insipidus, whereas nephrogenic diabetes insipidus occurs when ADH is present in the circulation, but the collecting duct cells are unable to respond due to failure at any of the steps in the signaling pathway. Congenital or hereditary forms of central and nephrogenic DI have been described, but are rare. Mutations in the arginine vasopressin (AVP) gene, encoding vasopressin, have been associated with autosomal dominant or autosomal recessive forms of central DI, typically diagnosed after the first year of life when polyuria and polydipsia are noted. X-linked nephrogenic DI has been reported in males carrying mutations in the arginine vasopressin receptor 2 (AVPR2) gene, which codes for the V2 receptor. Finally, mutations in the aquaporin 2 (collecting duct)(AQP2) gene lead to mu Continue reading >>
