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Diabetes Insipidus Journal Articles

Diabetes Insipidus: A Challenging Diagnosis With New Drug Therapies

Diabetes Insipidus: A Challenging Diagnosis With New Drug Therapies

Diabetes Insipidus: A Challenging Diagnosis with New Drug Therapies Chadi Saifan , Rabih Nasr ,* Suchita Mehta , Pranab Sharma Acharya , Isera Perrera , Giovanni Faddoul , Nikhil Nalluri , Mayurakhan Kesavan , Yorg Azzi , and Suzanne El-Sayegh Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Received 2013 Jan 31; Accepted 2013 Feb 21. This is an open access article distributed under the Creati Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

What are the types of diabetes insipidus? Central Diabetes Insipidus The most common form of serious diabetes insipidus, central diabetes insipidus, results from damage to the pituitary gland, which disrupts the normal storage and release of ADH. Damage to the pituitary gland can be caused by different diseases as well as by head injuries, neurosurgery, or genetic disorders. To treat the ADH deficiency that results from any kind of damage to the hypothalamus or pituitary, a synthetic hormone called desmopressin can be taken by an injection, a nasal spray, or a pill. While taking desmopressin, a person should drink fluids only when thirsty and not at other times. The drug prevents water excretion, and water can build up now that the kidneys are making less urine and are less responsive to changes in body fluids. Nephrogenic Diabetes Insipidus Nephrogenic diabetes insipidus results when the kidneys are unable to respond to ADH. The kidneys' ability to respond to ADH can be impaired by drugs-like lithium, for example-and by chronic disorders including polycystic kidney disease, sickle cell disease, kidney failure, partial blockage of the ureters, and inherited genetic disorders. Sometimes the cause of nephrogenic diabetes insipidus is never discovered. Desmopressin will not work for this form of diabetes insipidus. Instead, a person with nephrogenic diabetes insipidus may be given hydrochlorothiazide (HCTZ) or indomethacin. HCTZ is sometimes combined with another drug called amiloride. The combination of HCTZ and amiloride is sold under the brand name Moduretic. Again, with this combination of drugs, one should drink fluids only when thirsty and not at other times. Dipsogenic Diabetes insipidus Dipsogenic diabetes insipidus is caused by a defect in or damage to the thirst Continue reading >>

Diabetes Insipidus: Diagnosis And Treatment Of A Complex Disease

Diabetes Insipidus: Diagnosis And Treatment Of A Complex Disease

Abstract Diabetes insipidus, characterized by excretion of copious volumes of dilute urine, can be life-threatening if not properly diagnosed and managed. It can be caused by two fundamentally different defects: inadequate or impaired secretion of antidiuretic hormone (ADH) from the posterior pituitary gland (neurogenic or central diabetes insipidus) or impaired or insufficient renal response to ADH (nephrogenic diabetes insipidus). The distinction is essential for effective treatment. Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

OBJECTIVES After completing this article, readers should be able to: Describe the simple test that will establish the diagnosis of diabetes insipidus. Explain how to differentiate central diabetes insipidus from nephrogenic diabetes insipidus and compulsive water drinking. Delineate the inheritance pattern of central diabetes insipidus and nephrogenic diabetes insipidus. Describe the treatments of choice for central diabetes insipidus and nephrogenic diabetes insipidus. Definition and Epidemiology Polydipsia and polyuria with dilute urine, hypernatremia, and dehydration are the hallmarks of diabetes insipidus in infants and children. Patients who have diabetes insipidus are unable to conserve water and can become severely dehydrated when deprived of water. The polyuria exceeds 5 mL/kg per hour of dilute urine, with a documented specific gravity of less than 1.010. The hypernatremia is evidenced by a serum sodium concentration in excess of 145 mmol/L (145 mEq/L). Three conditions give rise to polydipsia and polyuria. The most common condition is central or neurogenic diabetes insipidus related to a deficiency of vasopressin. Less common is nephrogenic diabetes insipidus, including the X-linked recessive, autosomal recessive, and autosomal dominant types due to renal tubular resistance to vasopressin. Finally, these conditions can occur in the compulsive water drinker who demonstrates physiologic inhibition of vasopressin secretion. The incidence of diabetes insipidus in the general population is 3 in 100,000, with a slightly higher incidence among males (60%). X-linked nephrogenic diabetes insipidus is very rare, with arginine vasopressin receptor2 (AVPR2) gene mutations among males estimated to be 4 in 1,000,000. The incidence of compulsive water drinking is unknown, bu Continue reading >>

Diabetes Insipidus – Diagnosis And Management

Diabetes Insipidus – Diagnosis And Management

Abstract Central diabetes insipidus (CDI) is the end result of a number of conditions that affect the hypothalamic-neurohypophyseal system. The known causes include germinoma/craniopharyngioma, Langerhans cell histiocytosis (LCH), local inflammatory, autoimmune or vascular diseases, trauma resulting from surgery or an accident, sarcoidosis, metastases and midline cerebral and cranial malformations. In rare cases, the underlying cause can be genetic defects in vasopressin synthesis that are inherited as autosomal dominant, autosomal recessive or X-linked recessive traits. The diagnosis of the underlying condition is challenging and raises several concerns for patients and parents as it requires long-term follow-up. Proper etiological diagnosis can be achieved via a series of steps that start with clinical observations and then progress to more sophisticated tools. Specifically, MRI identification of pituitary hyperintensity in the posterior part of the sella, now considered a clear marker of neurohypophyseal functional integrity, together with the careful analysis of pituitary stalk shape and size, have provided the most striking findings contributing to the diagnosis and understanding of some forms of ‘idiopathic’ CDI. MRI STIR (short-inversion-time inversion recovery sequencing) is a promising technology for the early identification of LCH-dependent CDI. © 2012 S. Karger AG, Basel Definition/Classification Diabetes insipidus is a disease in which large volumes of dilute urine (polyuria) are excreted due to vasopressin (AVP) deficiency [central diabetes insipidus (CDI)], AVP resistance [nephrogenic diabetes insipidus (NDI)], or excessive water intake (primary polydipsia). Polyuria is characterized by a urine volume in excess of 2 l/m2/24 h or approximately 150 ml/k Continue reading >>

Absence Of Pkc-alpha Attenuates Lithium-induced Nephrogenic Diabetes Insipidus

Absence Of Pkc-alpha Attenuates Lithium-induced Nephrogenic Diabetes Insipidus

Absence of PKC-Alpha Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliation: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America Affiliations: Renal Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States of America, Department of Physiology, Emory University School of Medicine, Atlanta, Georgia, United States of America Lithium, an effective antipsychotic, induces nephrogenic diabetes insipidus (NDI) in 40% of patients. The decreased capacity to concentrate urine is likely due to lithium acutely disrupting the cAMP pathway and chronically reducing urea transporter (UT-A1) and water channel (AQP2) expression in the inner medulla. Targeting an alternative signaling pathway, such as PKC-mediated signaling, may be an effective meth Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

Diabetes insipidus (DI) causes frequent urination. You become extremely thirsty, so you drink. Then you urinate. This cycle can keep you from sleeping or even make you wet the bed. Your body produces lots of urine that is almost all water. DI is different from diabetes mellitus (DM), which involves insulin problems and high blood sugar. The symptoms can be similar. However, DI is related to how your kidneys handle fluids. It's much less common than DM. Urine and blood tests can show which one you have. Usually, DI is caused by a problem with your pituitary gland or your kidneys. Treatment depends on the cause of the problem. Medicines can often help. NIH: National Institute of Diabetes and Digestive and Kidney Diseases Continue reading >>

Prime Pubmed | Endocrinology And Diabetes Insipidus Journal Articles From Pubmed

Prime Pubmed | Endocrinology And Diabetes Insipidus Journal Articles From Pubmed

ADAtten Defic Hyperact Disord 2018 Aug 29 Diabetes insipidus is known to be associated with neurodevelopmental disorders. In this case report, we present a child suffering from a central diabetes insipidus (DI) and an attention-deficit/hyper... Diabetes insipidus is known to be associated with neurodevelopmental disorders. In this case report, we present a child suffering from a central diabetes insipidus (DI) and an attention-deficit/hyperactivity disorder (ADHD). The DI was due to a mutation on the vasopressin gene, impairing its secretion. We discuss the effects of this impairment on the central nervous system and how it might be linked to ADHD symptoms. JEJ Endocr Soc 2018 Sep 01; 2(9):1010-1019 CONCLUSIONS: Pituitary adenoma patients presenting with visual abnormalities, suprasellar extension, or large tumors are at higher risk of developing DI postoperatively. These patients warrant closer postoperative monitoring as well as adequate preoperative counseling to decrease their postsurgical morbidity. Tumor metastasis to the pituitary gland is a life-threatening condition associated with short life span. Pituitary metastasis is rare, however, and not well-documented. A better understanding of its ... Tumor metastasis to the pituitary gland is a life-threatening condition associated with short life span. Pituitary metastasis is rare, however, and not well-documented. A better understanding of its clinical manifestations could lead to earlier diagnosis, appropriate therapy, and potentially improving quality of life. Therefore, we retrospectively studied the charts of patients with pituitary metastases who were treated at the City of Hope National Medical Center in Duarte, California, from 1984 to 2018. We reviewed and analyzed tumor origin, primary pituitary clinical Continue reading >>

Diabetes Insipidus. - Abstract - Europe Pmc

Diabetes Insipidus. - Abstract - Europe Pmc

Service d'endocrinologie et maladies mtaboliques, centre hospitalier rgional universitaire de Lille (CHRU de LIlle), hpital Huriez/Inserm U 859, 1, rue Polonovski, 59000 Lille, France. More 1.Service d'endocrinologie et maladies mtaboliques, centre hospitalier rgional universitaire de Lille (CHRU de LIlle), hpital Huriez/Inserm U 859, 1, rue Polonovski, 59000 Lille, France. Annales D'endocrinologie [25 Nov 2013, 74(5-6):496-507] Diabetes insipidus (DI) is characterized by hypotonic polyuria greater than 3 liters/24 hours in adults and persisting even during water deprivation. It is mostly due to a defect in arginin-vasopressin (AVP) synthesis (central DI); other causes are: AVP resistance (nephrogenic DI), abnormal thirst regulation (primary polydipsia) or early destruction of AVP by placental enzymes (gestational DI). A thorough medical history is warranted to investigate nocturnal persistence of polyuria (night waking being a good sign of its organic nature) to specify the onset and duration of the trouble, the medication use and the potential hereditary nature of the disorder. The next step is based on weight and blood pressure measurements and especially the quantification of beverages and diuresis over a 24-hour cycle. Assessment of signs of dehydration, bladder distention, pituitary hormone hyper- or hyposecretion, tumor chiasmatic syndrome, granulomatosis and cancer is required. The diagnosis is based on biological assessment, pituitary magnetic resonance imaging (MRI) and results of a desmopressin test. In severe forms of DI, urine osmolality remains below 250 mOsmol/kg and serum sodium greater than 145 mmol/L. In partial forms of DI (urine osmolality between 250 and 750), the water deprivation test demonstrating the incapacity to obtain a maximal urine concent Continue reading >>

Diabetes Insipidus: A Review

Diabetes Insipidus: A Review

Moshe Shapiro and Jeffrey P. Weiss* Department of Urology, SUNY Downstate College of Medicine, USA *Corresponding Author: Jeffrey P. Weiss, MD, FACS Department of Urology SUNY Downstate College of Medicine 450 Clarkson Avenue, Box 79, Brooklyn NY, 11203, USA1 Fax: 212-838-323 E-mail: [email protected] Citation: Shapiro M, Weiss JP (2012) Diabetes Insipidus: A Review. J Diabetes Metab S6:009. doi:10.4172/2155-6156.S6-009 Copyright: © 2012 Shapiro M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Introduction Inappropriate secretion or action of serum antidiuretic hormone (ADH) is termed Diabetes Insipidus (DI), characterized by polyuria (defined as 24 hour urine output in excess of 40 ml/kg) and polydipsia [1]. As opposed to Diabetes Mellitus, where the urine is hypertonic and sweet (mellitus means honey in Greek), DI is defined as having urine that is hypotonic and bland, in the setting of polyuria. There are various mechanisms of pathogenesis of DI, all leading to the same clinical manifestation. In cases where the disorder is due to inadequate secretion of ADH, the disorder is termed Central DI, whereas when the disease is a result of renal insensitivity to ADH, the disease is termed Nephrogenic DI [1]. In cases where polyuria is due to vast amounts of ingested fluids driven primarily by behavioral or thirst disorders, it is called Primary Polydipsia (PP). Pregnant women can metabolize ADH in an accelerated manner leading to Gestational DI [2]. Overall, there are 3 cases of DI per 100,000 in the general popula Continue reading >>

Diabetes Insipidus After Traumatic Brain Injury

Diabetes Insipidus After Traumatic Brain Injury

Open Access Cristina Capatina 1, Alessandro Paluzzi 2, Rosalid Mitchell 2 and Niki Karavitaki 3,* 3 Centre for Endocrinology, Diabetes, and Metabolism, Institute for Biomedical Research, School of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT, UK Abstract : Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI. 1. Introduction Diabetes insipidus (DI) is caused by decreased secretion (central/neurogenic DI) or action (nephrogenic DI) of antidiuretic hormone (ADH, vasopressin). ADH is produced by the hypothalamic neurons in the supraop Continue reading >>

Diabetes Insipidus | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic

Diabetes Insipidus | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic

Diabetes insipidus, also called DI, is a rare condition that leads to frequent urination (passing a lot of clear urine) and excessive thirst. The condition may be caused by problems with your pituitary gland and/or your kidneys. DI is not related to diabetes mellitus (type 1 and type 2 diabetes), which is when your levels of blood sugar (glucose) are too high. Antidiuretic hormone (ADH): A hormone that helps the kidneys work well and keeps blood levels of sodium (salt) and water in the normal range. ADH is also called vasopressin. Hypothalamus: An area of the brain that makes ADH. Pituitary gland: A tiny gland found at the base of the brain; it stores and releases ADH and other hormones into the bloodstream. TYPES OF DI, THEIR CAUSES, AND TREATMENTS There are four types of DI. The goal of treatment for all types of DI is to relieve thirst and to decrease the amount of urine being made. The specific treatment depends on the type. Damage to your pituitary gland or hypothalamus from head injury, surgery, or tumors. This can lead to a lack of ADH. Synthetic ADH: desmopressin, given by injection, nasal spray, or pill In mild cases, treatment is increased water intake The pituitary releases enough ADH into the body but your kidneys can't respond to it. This can result from the prescription drug lithium, sickle cell disease, or genetic problems. Medications such as water pills (HCTZ and amiloride) Damage to your pituitary gland or hypothalamus from head injury, surgery, or tumors. This can lead to a lack of ADH. Synthetic ADH: desmopressin, given by injection, nasal spray, or pill In mild cases, treatment is increased water intake The pituitary releases enough ADH into the body but your kidneys can't respond to it. This can result from the prescription drug lithium, sickle ce Continue reading >>

Diabetes Insipidus In Pregnancy: How To Advice The Patient? - Minerva Endocrinologica 2018 Feb 19 - Minerva Medica - Journals

Diabetes Insipidus In Pregnancy: How To Advice The Patient? - Minerva Endocrinologica 2018 Feb 19 - Minerva Medica - Journals

Diabetes insipidus in pregnancy: how to advice the patient? Diabetes insipidus, characterized by polyuria and polydipsia, is a rare disease during pregnancy. Nevertheless, its recognition is important to avoid complications due to dehydration and hypernatremia. Its manifestation during pregnancy ranges from exacerbation of pre-existing central or nephrogenic diabetes insipidus to transient pregnancy-induced diabetes insipidus due to the increased metabolism of the antidiuretic hormone vasopressin by the placental vasopressinase. Diagnosis can be challenging, as urinary frequency is common during pregnancy and primary polydipsia also needs to be excluded. Also the standard water deprivation test is not recommended during pregnancy due to the increased risk of complications. Treatment depends upon the final diagnosis, with desmopressin (DDAVP) being the medication of choice in AVP-deficient diabetes insipidus, whereas nephrogenic diabetes insipidus requires treatment of the underlying disease and supportive measures. KEY WORDS: Diabetes insipidus - Pregnancy - Desmopressin (DDAVP) Continue reading >>

Familial Forms Of Diabetes Insipidus: Clinical And Molecular Characteristics

Familial Forms Of Diabetes Insipidus: Clinical And Molecular Characteristics

Familial forms of diabetes insipidus: clinical and molecular characteristics Muriel Babey is a postdoctoral research fellow at the Division of Endocrinology, University of California, San Francisco in San Francisco. She received her MD degree from the University of Berne, Switzerland. She undertook postgraduate training in Neurosurgery for one year at the same institution. Following this, she completed a research fellowship in Dr. Kopp's laboratory at the Division of Endocrinology, Northwestern University in Chicago. Her research work focused understanding the genetic basis of X-linked familial neurohypophyseal DI and characterizing mutations in a transcription factor involved in anterior pituitary gland development. She received research fellowships from the Swiss National Research Foundation, Janggen-Phn-Foundation and Novartis Foundation. Peter Kopp is an Associate Professor in the Division of Endocrinology, Metabolism and Molecular Medicine, and he serves as Director ad interim of the Center for Genetic Medicine at the Feinberg School of Medicine of Northwestern University in Chicago. Dr. Kopp received his MD degree from the University of Berne, Switzerland. He completed his training in Internal Medicine and Endocrinology at the same institution. He then joined the Division of Endocrinology at Northwestern University. His research interests focus primarily on the molecular basis of endocrine disorders such as congenital thyroid disorders and disorders of water balance. He has published more than 110 publications in the field of endocrinology and endocrine genetics. He is a member of the Board of Directors of the American Thyroid Association, Associate Editor of the Journal Thyroid, and a member of the Editorial Board of the Journal of Clinical Endocrinology and Met Continue reading >>

Diabetes Insipidus: Practice Essentials, Background, Etiology

Diabetes Insipidus: Practice Essentials, Background, Etiology

Diabetes insipidus (DI) is defined as the passage of large volumes (>3 L/24 hr) of dilute urine (< 300 mOsm/kg). It has the following 2 major forms: Central (neurogenic, pituitary, or neurohypophyseal) DI, characterized by decreased secretion of antidiuretic hormone (ADH; also referred to as arginine vasopressin [AVP]) Nephrogenic DI, characterized by decreased ability to concentrate urine because of resistance to ADH action in the kidney [ 1 ] Two other forms are gestational DI and primary polydipsia (dipsogenic DI); both are caused by deficiencies in AVP, but the deficiencies do not result from a defect in the neurohypophysis or kidneys. The predominant manifestations of DI are as follows: Polyuria: The daily urine volume is relatively constant for each patient but is highly variable between patients (3-20 L) The most common form is central DI after trauma or surgery to the region of the pituitary and hypothalamus, which may exhibit 1 of the following 3 patterns: Earley LE, Orloff J. The mechanism of antidiuresis associated with the administration of hydrochlorothiazide to patients with vasopressin-resistant diabetes insipidus. J Clin Invest. Nov 1962;41(11):1988-97. Babey M, Kopp P, Robertson GL. Familial forms of diabetes insipidus: clinical and molecular characteristics. Nat Rev Endocrinol. 2011 Jul 5. 7(12):701-14. [Medline] . Bockenhauer D, van't Hoff W, Dattani M, Lehnhardt A, Subtirelu M, Hildebrandt F, et al. Secondary nephrogenic diabetes insipidus as a complication of inherited renal diseases. Nephron Physiol. 2010. 116(4):p23-9. [Medline] . Los EL, Deen PM, Robben JH. Potential of nonpeptide (ant)agonists to rescue vasopressin V2 receptor mutants for the treatment of X-linked nephrogenic diabetes insipidus. J Neuroendocrinol. 2010 May. 22(5):393-9. [Medlin Continue reading >>

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