Diabetes Insipidus: Causes, Symptoms And Treatment
Diabetes insipidus is a condition where the body loses too much fluid through urination, causing a significant risk of dangerous dehydration as well as a range of illnesses and conditions. There are two forms of the disease: nephrogenic diabetes insipidus and central diabetes insipidus (also known as neurogenic diabetes insipidus). A number of factors have been linked to the development of diabetes insipidus, which may also occur in pregnancy or with the use of certain medications. Establishing the cause of the problem can help determine the most appropriate treatment to support the regulation of water balance in the body. Diabetes insipidus is a condition that can be managed successfully. Contents of this article: What is diabetes insipidus? An uncommon condition, diabetes insipidus is a disorder affecting the regulation of body fluid levels. Two key symptoms resemble those of the more common forms of diabetes that affect blood sugar levels (diabetes mellitus types 1 and 2).1-5 People with diabetes insipidus produce excessive amounts of urine (polyuria), resulting in frequent urination and, in turn, thirst (polydipsia). However, the underlying cause of these two symptoms is quite different from the causes in types 1 and 2 diabetes. In diabetes mellitus, elevated blood sugar prompts the production of large volumes of urine to help remove the excess sugar from the body. In diabetes insipidus, it is the body's water balance system itself that is not working properly. Here are some key points about diabetes insipidus. More detail and supporting information is in the body of this article. Diabetes insipidus is a condition where the body fails to properly control water balance, resulting in excessive urination. Diabetes insipidus can be caused by low or absent secretion of t Continue reading >>
Diagnosis
Print Since the signs and symptoms of diabetes insipidus can be caused by other conditions, your doctor will perform a number of tests. If your doctor determines you have diabetes insipidus, he or she will need to determine which type of diabetes insipidus you have, because the treatment is different for each form of the disease. Some of the tests doctors commonly use to diagnose and determine the type of diabetes insipidus and in some cases, its cause, include: Water deprivation test. This test confirms the diagnosis and helps determine the cause of diabetes insipidus. Under medical supervision, you'll be asked to stop drinking fluids for a time so that your doctor can measure changes in your body weight, urine output and the concentration of your urine and blood when fluids are withheld. Your doctor may also measure blood levels of ADH or administer synthetic ADH during this test. The water deprivation test is performed under close supervision in children and pregnant women to make sure no more than 5 percent of body weight is lost during the test. Urinalysis. Urinalysis is the physical and chemical examination of urine. If your urine is less concentrated — meaning the amount of water is high relative to other excreted substances — it could be due to diabetes insipidus. Magnetic resonance imaging (MRI). An MRI of the head is a noninvasive procedure that uses a powerful magnetic field and radio waves to construct detailed pictures of brain tissues. Your doctor may want to perform an MRI to look for abnormalities in or near the pituitary gland. Genetic screening If your doctor suspects an inherited form of diabetes insipidus, he or she will look at your family history of polyuria and may suggest genetic screening. Treatment Treatment of diabetes insipidus depends on Continue reading >>
Treatment Of Nephrogenic Diabetes Insipidus With Hydrochlorothiazide And Amiloride
Nephrogenic diabetes insipidus (NDI) is characterised by the inability of the kidney to concentrate urine in response to arginine vasopressin. The consequences are severe polyuria and polydipsia, often associated with hypertonic dehydration. Intracerebral calcification, seizures, psychosomatic retardation, hydronephrosis, and hydroureters are its sequelae. In this study, four children with NDI were treated with 3 mg/kg/day hydrochlorothiazide and 0.3 mg/kg/day amiloride orally three times a day for up to five years. While undergoing treatment, none of the patients had signs of dehydration or electrolyte imbalance, all showed normal body growth, and there was no evidence of cerebral calcification or seizures. All but one had normal psychomotor development and normal sonography of the urinary tract. However, normal fluid balance was not attainable (fluid intake, 3.8-7.7 l/m2/day; urine output, 2.2-7.4 l/m2/day). The treatment was well tolerated and no side effects could be detected. Prolonged treatment with hydrochlorothiazide/amiloride appears to be more effective and better tolerated than just hydrochlorothiazide. Its efficacy appears to be similar to that of hydrochlorothiazide/indomethacin but without their severe side effects. Full Text Selected References These references are in PubMed. This may not be the complete list of references from this article. Continue reading >>
Nephrogenic Diabetes Insipidus: Essential Insights Into The Molecular Background And Potential Therapies For Treatment
Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Address all correspondence and requests for reprints to: Hanne B. Moeller, Department of Biomedicine, Aarhus University, Wilhelm Meyers Alle 3, Building 1234, Aarhus 8000, Denmark., E-mail: [email protected] ; or Robert A. Fenton. E-mail: [email protected] . Received 2012 Jul 11; Accepted 2012 Dec 7. Copyright 2013 by The Endocrine Society This article has been cited by other articles in PMC. The water channel aquaporin-2 (AQP2), expressed in the kidney collecting ducts, plays a pivotal role in maintaining body water balance. The channel is regulated by the peptide hormone arginine vasopressin (AVP), which exerts its effects through the type 2 vasopressin receptor (AVPR2). Disrupted function or regulation of AQP2 or the AVPR2 results in nephrogenic diabetes insipidus (NDI), a common clinical condition of renal origin characterized by polydipsia and polyuria. Over several years, major research efforts have advanced our understanding of NDI at the genetic, cellular, molecular, and biological levels. NDI is commonly characterized as hereditary (congenital) NDI, arising from genetic mutations in the AVPR2 or AQP2; or acquired NDI, due to for exmple medical treatment or electrolyte disturbances. In this article, we provide a comprehensive overview of the genetic, cell biological, and pathophysiological causes of NDI, with emphasis on the congenital forms and the acquired forms arising from lithium and other drug therapies, acute and chronic renal failure, and di Continue reading >>
Treatment Of Nephrogenic Diabetes Insipidus
INTRODUCTION Nephrogenic diabetes insipidus (nephrogenic DI) results from partial or complete resistance of the kidney to the effects of antidiuretic hormone (ADH). As a result, patients with this disorder are not likely to have a good response to hormone administration (as desmopressin [dDAVP]) or to drugs that increase either the renal response to ADH or ADH secretion. Nephrogenic DI can be hereditary or acquired. In adults, a concentrating defect severe enough to produce polyuria due to nephrogenic DI is most often due to chronic lithium use or hypercalcemia and less frequently to other conditions that impair tubular function, such as Sjögren's syndrome [1]. Release of ureteral obstruction is often associated with a diuresis, but this is short lived and does not require specific therapy other than maintenance fluids. (See "Clinical manifestations and causes of nephrogenic diabetes insipidus" and "Clinical manifestations and diagnosis of urinary tract obstruction and hydronephrosis", section on 'Prognosis and recovery of renal function'.) Hereditary nephrogenic DI, which is largely an X-linked disease, may also be seen by internists since early recognition and treatment in infancy has led to survival to adulthood [2,3]. In addition, affected women may be carriers with few or no symptoms until pregnancy or other stress. In infants with hereditary nephrogenic DI, treatment is aimed at minimizing the polyuria and avoiding hypernatremia and volume depletion. In adults, therapy is usually aimed at correcting the underlying disorder or discontinuing an offending drug. In hypercalcemic patients, for example, normalization of the plasma calcium concentration usually leads to amelioration of polyuria. By contrast, lithium-induced nephrogenic DI may be irreversible if the pati Continue reading >>
Diabetes Insipidus: Causes & Symptoms + 5 Natural Treatments
Diabetes insipidus, is a debilitating and rare disease, with a prevalence of 1 out of 25,000 people. Often referred to as “water diabetes,” it is a condition characterized by frequent and heavy urination, excessive thirst and an overall feeling of weakness. It’s caused by a defect in the pituitary gland or in the kidneys. (1) The term insipidus means “without taste” in Latin, while diabetes mellitus involves the excretion of “sweet” urine. People with diabetes insipidus pass urine that is diluted, odorless and relatively low in sodium content. Diabetes insipidus and diabetes mellitus (which includes both type 1 and type 2 diabetes) are unrelated. Both conditions do cause frequent urination and constant thirst. People with diabetes insipidus have normal blood sugar levels, but their kidneys cannot balance fluid in the body. Although the symptoms of diabetes insipidus can be bothersome and sometimes even life-changing, the condition doesn’t increase future health risks when it is managed properly. It’s important to find the right treatment plan, which typically involves taking measures to avoid dehydration. What is Diabetes Insipidus? Diabetes insipidus is a condition that disrupts normal life due to increased thirst and passing of large volumes or urine, even at night. It is a part of a group of hereditary or acquired polyuria (when large amounts of urine is produced) and polydipsia (excessive thirst) diseases. It’s associated with inadequate vasopressin or antidiuretic hormone secretion. Vasopressin, which includes arginine vasopressin (AVP) and antidiuretic hormone (ADH), is a peptide hormone formed in the hypothalamus. It then travels to the posterior pituitary where it releases into the blood. In order to fully understand the cause of diabetes ins 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 >>
Nephrogenic Diabetes Insipidus
Nephrogenic diabetes insipidus is a disorder of water balance. The body normally balances fluid intake with the excretion of fluid in urine. However, people with nephrogenic diabetes insipidus produce too much urine (polyuria), which causes them to be excessively thirsty (polydipsia). Affected individuals can quickly become dehydrated if they do not drink enough water, especially in hot weather or when they are sick. Nephrogenic diabetes insipidus can be either acquired or hereditary. The acquired form is brought on by certain drugs and chronic diseases and can occur at any time during life. The hereditary form is caused by genetic mutations, and its signs and symptoms usually become apparent within the first few months of life. Infants with hereditary nephrogenic diabetes insipidus may eat poorly and fail to gain weight and grow at the expected rate (failure to thrive). They may also be irritable and experience fevers, diarrhea, and vomiting. Recurrent episodes of dehydration can lead to slow growth and delayed development. If the condition is not well-managed, over time it can damage the bladder and kidneys leading to pain, infections, and kidney failure. With appropriate treatment, affected individuals usually have few complications and a normal lifespan. Nephrogenic diabetes insipidus should not be confused with diabetes mellitus, which is much more common. Diabetes mellitus is characterized by high blood sugar levels resulting from a shortage of the hormone insulin or an insensitivity to this hormone. Although nephrogenic diabetes insipidus and diabetes mellitus have some features in common, they are separate disorders with different causes. Continue reading >>
Treatment
Treatments for diabetes insipidus aim to reduce the amount of urine your body produces. Depending on the type of diabetes insipidus you have, there are several ways of treating your condition and controlling your symptoms. Cranial diabetes insipidus Mild cranial diabetes insipidus may not require any medical treatment. Cranial diabetes insipidus is considered mild if you produce approximately 3-4 litres of urine over 24 hours. If this is the case, you may be able to ease your symptoms by increasing the amount of water you drink, to avoid dehydration. Your GP or endocrinologist (specialist in hormone conditions) may advise you to drink a certain amount of water every day, usually at least 2.5 litres. However, if you have more severe cranial diabetes insipidus, drinking water may not be enough to control your symptoms. As your condition is due to a shortage of vasopressin (AVP), your GP or endocrinologist may prescribe a treatment that takes the place of AVP, known as desmopressin (see below). Desmopressin Desmopressin is a manufactured version of AVP that's more powerful and more resistant to being broken down than the AVP naturally produced by your body. It works just like natural AVP, stopping your kidneys producing urine when the level of water in your body is low. Desmopressin can be taken as a nasal spray, in tablet form or as a form that melts in your mouth, between your gum and your lip. If you're prescribed desmopressin as a nasal spray, you'll need to spray it inside your nose once or twice a day, where it's quickly absorbed into your bloodstream. If you're prescribed desmopressin tablets, you may need to take them more than twice a day. This is because desmopressin is absorbed into your blood less effectively through your stomach than through your nasal passage Continue reading >>
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Diabetes Insipidus Treatment & Management
Approach Considerations Fluid replacement 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 patient’s 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. Desmopressin and other drugs 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 hormone deficiency; therefore, physiologic replacement with Continue reading >>
Nephrogenic Diabetes Insipidus (ndi)
Nephrogenic diabetes insipidus (NDI) is a rare disorder that occurs when the kidneys are unable to concentrate urine. In most people, the body balances the fluids you drink with the amount of urine you excrete, or expel, from your body. However, people with NDI produce excessive amounts of urine. This is a condition known as polyuria and it causes insatiable thirst, or polydipsia. NDI occurs when the balance between fluid intake and urine excretion is disrupted. NDI can cause dehydration, among other complications, so it’s important to talk to a doctor if you’re experiencing symptoms. NDI can be fatal if you don’t get treatment for it. The earlier you receive the diagnosis, the better your outlook will be. NDI is unrelated to diabetes mellitus, which is more commonly known as diabetes. The symptoms of NDI vary with age. Infants are severely affected, but the symptoms can resemble many other disorders. As children age, the symptoms become more recognizable. If a diagnosis isn’t made, the symptoms can become severe enough to be life-threatening. You should visit your doctor as soon as possible if you’re experiencing symptoms of NDI. Symptoms in infants The symptoms in infants can include: excessive wet diapers vomiting recurring fevers that have no known cause constipation Symptoms in young children The symptoms in young children can include: bedwetting difficulties in toilet training a failure to thrive mental confusion due to dehydration Symptoms in older children Older children and teenagers can display symptoms that include: high urine output disturbed sleep and fatigue from urinating at night low body weight due to preferring water to food a failure to thrive Symptoms in adults The most common symptoms experienced by adults include: excessive thirst excessi Continue reading >>
Treatment Of Nephrogenic Diabetes Insipidus With Prostaglandin Synthesisinhibitors.
Treatment of nephrogenic diabetes insipidus with prostaglandin synthesisinhibitors. The antidiuretic effect of two prostaglandin synthetase inhibitors, ibuprofen (25mg/kg/day) and indomethacin (2 mg/kg/day), was studied in patients aged 8 to 18years with hereditary nephrogenic diabetes insipidus. Ibuprofen (studied in five patients) did not have demonstrable effects on urine volume, free waterclearance, or osmolar clearance, but fractional excretion of sodium decreasedfrom a mean of 0.38% to 0.19% (P less than 0.05). In contrast, indomethacin(studied in three patients) was associated with a decrease in mean urine volumefrom 5.8 to 2.8 mL/min and a decrease in mean free water clearance from 3.1 to1.1 mL/min (both P less than 0.05). Fractional excretion of sodium decreased from0.77% to 0.27% (P less than 0.01) and was accompanied by an increase in serumurea nitrogen level (P less than 0.01) and a decrease in urea nitrogen clearance (P less than 0.025). Thus, prostaglandin synthetase inhibitors are not uniformly effective in treatment of nephrogenic diabetes insipidus. The inhibitory effectof indomethacin on urine volume and free water clearance in our patients may havebeen mediated by an enhancement of antidiuretic hormone (ADH)-stimulated cyclicadenosine monophosphate generation, or by increased ADH-independent waterreabsorption resulting from an increase in solute reabsorption and consequentmedullary hypertonicity. Continue reading >>
Nephrogenic Diabetes Insipidus
Not to be confused with Neurogenic diabetes insipidus. Nephrogenic diabetes insipidus (also known as renal diabetes insipidus) is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central/neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (ADH, that is, arginine vasopressin or AVP). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to ADH, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water. Signs and symptoms[edit] The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with excessive thirst and excretion of a large amount of dilute urine. Dehydration is common, and incontinence can occur secondary to chronic bladder distension.[1] On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, ADH levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then hypernatremia will ensue with its neurologic symptoms.[citation needed] Causes[edit] Acquired[edit] Nephrogenic DI (NDI) is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis,[2] polycystic kidney disease,[3] electrolyte imbalance,[4][5] or some other kidney defect.[2] The major causes of acquired NDI that produce clinical symptoms (e.g. polyuria) in the adult are lithium toxicity and high blood calcium. Chronic lithium ingestion – appears to affect the tubules by enterin Continue reading >>
Nephrogenic Diabetes Insipidus: Essential Insights Into The Molecular Background And Potential Therapies For Treatment
Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Address all correspondence and requests for reprints to: Hanne B. Moeller, Department of Biomedicine, Aarhus University, Wilhelm Meyers Alle 3, Building 1234, Aarhus 8000, Denmark. Search for other works by this author on: Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Search for other works by this author on: Department of Biomedicine, Aarhus University, Department of Pediatrics, Aarhus University Hospital, and Center for Interactions of Proteins in Epithelial Transport, Aarhus University, Aarhus 8000, Denmark Search for other works by this author on: Endocrine Reviews, Volume 34, Issue 2, 1 April 2013, Pages 278301, Hanne B. Moeller, Sren Rittig, Robert A. Fenton; Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment, Endocrine Reviews, Volume 34, Issue 2, 1 April 2013, Pages 278301, The water channel aquaporin-2 (AQP2), expressed in the kidney collecting ducts, plays a pivotal role in maintaining body water balance. The channel is regulated by the peptide hormone arginine vasopressin (AVP), which exerts its effects through the type 2 vasopressin receptor (AVPR2). Disrupted function or regulation of AQP2 or the AVPR2 results in nephrogenic diabetes insipidus (NDI), a common clinical condition of renal origin characterized by polyd Continue reading >>
Nephrogenic Diabetes Insipidus
Nephrogenic diabetes insipidus is a disorder in which a defect in the small tubes (tubules) in the kidneys causes a person to produce a large amount of urine. Nephrogenic diabetes insipidus occurs when the kidney tubules, which allow water to be removed from the body or reabsorbed, do not respond to a chemical in the body called antidiuretic hormone (ADH) or vasopressin.[1] ADH normally tells the kidneys to make the urine more concentrated. As a result of the defect, the kidneys release an excessive amount of water into the urine, producing a large quantity of very dilute urine.[2] The most common symptoms are frequent urination (polyuria), especially during nighttime (nocturia), and drinking too much liquids (polydipsia). It can be either acquired or hereditary. The acquired form is brought on by certain drugs and chronic diseases and can occur at any time during life. About 90% of all cases of hereditary nephrogenic diabetes insipidus result from mutations in the AVPR2 gene, and about 10% of cases are caused by mutations in the AQP2 gene.[3][4] Treatment consists of plenty of water intake; medication, such as thiazide diuretics and NSAIDs; and a low-salt, low-protein diet.[5] Continue reading >>
