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Is Diabetes Insipidus Reversible

Clinical Manifestations And Causes Of Nephrogenic Diabetes Insipidus

Clinical Manifestations And Causes Of Nephrogenic Diabetes Insipidus

INTRODUCTION Nephrogenic diabetes insipidus (DI) refers to a decrease in urinary concentrating ability that results from resistance to the action of antidiuretic hormone (ADH). This problem can reflect resistance at the ADH site of action in the collecting tubules, or interference with the countercurrent mechanism due, for example, to medullary injury or to decreased sodium chloride reabsorption in the medullary aspect of the thick ascending limb of the loop of Henle (figure 1) [1]. (See "Diagnosis of polyuria and diabetes insipidus".) Nephrogenic DI, in its mild form, is relatively common since almost all patients who are elderly, sick, or have acute or chronic kidney disease have a reduction in maximum concentrating ability [1]. As an example, the maximum urine osmolality that can be achieved may fall from the normal value of 800 to 1200 mosmol/kg down to 350 to 600 mosmol/kg in these settings [1]. In chronic kidney disease, this defect is due in part to increased solute excretion per functioning nephron and to decreased expression of mRNA for the V2 vasopressin receptor [1,2]. The clinical manifestations and causes of nephrogenic DI will be reviewed here. The treatment of nephrogenic DI, the diagnostic approach to polyuria and diabetes insipidus, and the clinical manifestations and causes of central DI are discussed separately. (See "Treatment of nephrogenic diabetes insipidus" and "Diagnosis of polyuria and diabetes insipidus" and "Clinical manifestations and causes of central diabetes insipidus".) CLINICAL MANIFESTATIONS Patients with moderate to severe nephrogenic or central DI typically present with polyuria, nocturia, and polydipsia. Polyuria is arbitrarily defined as a urine output exceeding 3 L/day in adults or 2 L/m2 in children. Causes of polyuria other than Continue reading >>

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review

In nephrogenic diabetes insipidus (NDI), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone (arginine vasopressin). In settings in which fluid intake cannot be maintained, this may result in severe dehydration and electrolyte imbalances. The risk for conversion of reversible to irreversible NDI seems to be a potential complication. This review summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians.Two reviewers independently searched MEDLINE, Experta Medica (EMBASE), and ISI bibliographic databases. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. To evaluate the causal role of the risk factor, data were abstracted according to Koch's postulates.One hundred fifty-five studies published between 1957 and March 2004 described 30 risk factors. Of 155 studies, 58 studies provided a "definite" diagnosis of NDI; 83 studies, a "probable" diagnosis; and 14 studies, a "possible" diagnosis. Nine factors were considered "definite" causes of NDI; 15 factors, "probable" causes; and 6 factors, "possible" causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure.Most risk factors for reversible NDI were medications, and their identification and removal resulted in resolution of the condition. Long-term treatment with lithium seemed to result in irreversible NDI. Do you want to read the rest of this article? ... Muta Continue reading >>

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review

Causes of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review Causes of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review BACKGROUND: In nephrogenic diabetes insipidus ( NDI ), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone ( arginine vasopressin ). In settings in which fluid intake cannot be maintained, this may result in severe dehydration and electrolyte imbalances. The risk for conversion of reversible to irreversible NDI seems to be a potential complication. This review summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians. METHODS: Two reviewers independently searched MEDLINE, Experta Medica (EMBASE), and ISI bibliographic databases. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. To evaluate the causal role of the risk factor , data were abstracted according to Koch's postulates. RESULTS: One hundred fifty-five studies published between 1957 and March 2004 described 30 risk factors . Of 155 studies, 58 studies provided a "definite" diagnosis of NDI ; 83 studies, a "probable" diagnosis; and 14 studies, a "possible" diagnosis. Nine factors were considered "definite" causes of NDI ; 15 factors, "probable" causes; and 6 factors, "possible" causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure. CONCLUSION: Most risk factors for reversible NDI were medications, and Continue reading >>

Diabetes Insipidus: Causes, Symptoms And Treatment

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 >>

Pediatric Diabetes Insipidus

Pediatric Diabetes Insipidus

Author: Karl S Roth, MD; Chief Editor: Robert P Hoffman, MD more... Diabetes insipidus (DI) is part of a group of hereditary or acquired polyuria and polydipsia diseases in which the kidneys pass large amounts of water irrespective of the body's hydration state. DI is due either to (1) deficient secretion of ADH by the pituitary gland (central or neurogenic DI) or to (2) renal tubular unresponsiveness to vasopressin (nephrogenic DI). The hallmarks of centralDI(CDI) arepolyuria(urine volume in excess of 150 ml/kg/24 hr at birth, 100-110 ml/kg/24 hr until the age of 2 years, and 40-50 ml/kg/24 hr in older children and adults), dilute urine (osmolality <300 mOsm/L), and polydipsia (water intake of up to 20 L/day). [ 1 ] NephrogenicDI (NDI) is characterized by polyuria with polydipsia, recurrent bouts of fever, constipation, and acute hypernatremic dehydration after birth that may cause neurologic sequelae. Acquired CDI can occur at any age and is usually secondary to a condition damaging the central nervous system. Typical injuries include head trauma , tumor, and neurosurgical procedures. CDI is considered idiopathic in 20-50% of cases. [ 2 ] Central DI with an autosomal dominant pattern inheritance is due to a mutation in the prepro-arginine vasopressin (prepro-AVP2) gene, mapped to locus 20p13. Central DI with diabetes mellitus, optic atrophy, and mental retardation (Wolfram syndrome) may be inherited in an autosomal recessive pattern (locus 4p16) or may be due to mitochondrial deletions. [ 1 ] In most cases, NDI is caused by mutations in the gene located on Xq28 coding for the V2 receptor of antidiuretic hormone (AVPR2). [ 3 , 4 , 5 ] In cases of autosomal recessive or dominant transmission, NDI is caused by mutations in theAQP2gene (located on chromosome 12) that cod Continue reading >>

Diabetes Insipidus: A Challenging Diagnosis With New Drug Therapies

Diabetes Insipidus: A Challenging Diagnosis With New Drug Therapies

ISRN Nephrology Volume 2013 (2013), Article ID 797620, 7 pages Division of Nephrology, Department of Medicine, Staten Island University Hospital, 475 Seaview Avenue, Staten Island, NY 10305, USA Academic Editors: M. Léone and D. Malhotra Copyright © 2013 Chadi Saifan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Diabetes Insipidus (DI) is either due to deficient secretion of arginine vasopressin (central) or to tubular unresponsiveness (nephrogenic). Drug induced DI is a well-known entity with an extensive list of medications. Polyuria is generally defined as urine output exceeding 3 liters per day in adults. It is crucial to identify the cause of diabetes insipidus and to implement therapy as early as possible to prevent the electrolyte disturbances and the associated mortality and morbidity. It is very rare to have an idiosyncratic effect after a short use of a medication, and physicians should be aware of such a complication to avoid volume depletion. The diagnosis of diabetes insipidus is very challenging because it relies on laboratory values, urine output, and the physical examination of the patient. A high clinical suspicion of diabetes insipidus should be enough to initiate treatment. The complications related to DI are mostly related to the electrolyte imbalance that can affect the normal physiology of different organ systems. 1. Background Though it is a rare disorder, diabetes insipidus was first described in the 18th century [1]. Diabetes insipidus (DI) is either due to deficient secretion of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH) by the pitu 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 >>

Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects Of Amiloride

Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects Of Amiloride

Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects of Amiloride Departments of *Medical and Surgical Sciences and Physiology, University of Otago, Dunedin, New Zealand; and Department of Psychological Medicine, University of Otago, Christchurch, New Zealand Prof. Robert J. Walker, Department of Medical & Surgical Sciences, University of Otago, PO Box 913, Dunedin, New Zealand. Phone: (643) 474 0999, 8045; Fax: (643) 474 7641; E-mail: rob.walker{at}stonebow.otago.ac.nz Background and objectives: Polyuria, polydipsia, and nephrogenic diabetes insipidus have been associated with use of psychotropic medications, especially lithium. Design, setting, participants, & measurements: The impact of psychotropic medications on urinary concentrating ability and urinary aquaporin 2 (AQP2) excretion was investigated after overnight fluid deprivation, and over 6 h after 40 g of desmopressin (dDAVP), in patients on lithium (n = 45), compared with those on alternate psychotropic medications (n = 42). Results: Those not on lithium demonstrated normal urinary concentrating ability (958 51 mOsm/kg) and increased urinary excretion of AQP2 (98 21 fmol/mol creatinine) and cAMP (410 15 pmol/mol creatinine). Participants taking lithium were divided into tertiles according to urinary concentrating ability: normal, >750 mOsm/kg; partial nephrogenic diabetes insipidus (NDI), 750 to 300 mOsm/kg; full NDI, <300 mOsm/kg. Urinary AQP2 concentrations were 70.9 13.6 fmol/mol creatinine (normal), 76.5 10.4 fmol/mol creatinine (partial NDI), and 27.3 fmol/mol creatinine (full NDI). Impaired urinary concentrating ability and reduced urinary AQP2, cAMP excretion correlated with duration of lithium therapy. Other psychotropic agents did not impair urinary concentrating ability. Eleven patients on Continue reading >>

Lithium-induced Diabetes Insipidus: Prevention And Management

Lithium-induced Diabetes Insipidus: Prevention And Management

Lithium-induced diabetes insipidus: Prevention and management Current Psychiatry. 2013 July;12(7):42-45 John Gideon Searle Professor of Clinical and Translational Pharmacy University of Michigan College of Pharmacy and School of Medicine 1. Ecelbarger CA. Lithium treatment and remodeling of the collecting duct. Am J Physiol Renal Physiol. 2006;291(1):F37-38. 2. Christensen BM, Kim YH, Kwon TH, et al. Lithium treatment induces a marked proliferation of primarily principal cells in rat kidney inner medullary collecting duct. Am J Physiol Renal Physiol. 2006;291(1):F39-48. 3. Francis SG, Gardner DG. Basic and clinical endocrinology. 7th ed. New York, NY: McGraw Hill; 2003:154-158. 4. Stone KA. Lithium-induced nephrogenic diabetes insipidus. J Am Board Fam Pract. 1999;12(1):43-47. 5. Grnfeld JP, Rossier BC. Lithium nephrotoxicity revisited. Nat Rev Nephrol. 2009;5(5):270-276. 6. Wesche D, Deen PM, Knoers NV. Congenital nephrogenic diabetes insipidus: the current state of affairs. Pediatr Nephrol. 2012;27(12):2183-2204. 7. Rose BD, Post TW. Clinical physiology of acid-base and electrolyte disorders. 5th ed. New York, NY: McGraw-Hill; 2001:754-759,782-783. 8. Batlle DC, von Riotte AB, Gaviria M, et al. Amelioration of polyuria by amiloride in patients receiving long-term lithium therapy. N Engl J Med. 1985;312(7):408-414. 9. Earley LE, Orloff J. The mechanism of antidiuresis associated with the administration of hydrochlorothiazide to patients with vasopressin-resistant diabetes insipidus. J Clin Invest. 1962;41(11):1988-1997. 10. Kim GH, Lee JW, Oh YK, et al. Antidiuretic effect of hydrochlorothiazide in lithium-induced nephrogenic diabetes insipidus is associated with upregulation of aquaporin-2, Na-Cl co-transporter, and epithelial sodium channel. J Am Soc Nephrol. 2004;1 Continue reading >>

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review.

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review.

Causes of reversible nephrogenic diabetes insipidus: a systematic review. Division of Nephrology, Walkerton Health Study, London Health Science Centre, Westminster Campus, Canada. In nephrogenic diabetes insipidus (NDI), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone (arginine vasopressin). In settings in which fluid intake cannot be maintained, this may result in severe dehydration and electrolyte imbalances. The risk for conversion of reversible to irreversible NDI seems to be a potential complication. This review summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians. Two reviewers independently searched MEDLINE, Experta Medica (EMBASE), and ISI bibliographic databases. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. To evaluate the causal role of the risk factor, data were abstracted according to Koch's postulates. One hundred fifty-five studies published between 1957 and March 2004 described 30 risk factors. Of 155 studies, 58 studies provided a "definite" diagnosis of NDI; 83 studies, a "probable" diagnosis; and 14 studies, a "possible" diagnosis. Nine factors were considered "definite" causes of NDI; 15 factors, "probable" causes; and 6 factors, "possible" causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure. Most risk factors for reversible NDI were medications, and their identifica Continue reading >>

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review - Sciencedirect

Causes Of Reversible Nephrogenic Diabetes Insipidus: A Systematic Review - Sciencedirect

Volume 45, Issue 4 , April 2005, Pages 626-637 Causes of reversible nephrogenic diabetes insipidus: A systematic review Get rights and content Background: In nephrogenic diabetes insipidus (NDI), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone (arginine vasopressin). In settings in which fluid intake cannot be maintained, this may result in severe dehydration and electrolyte imbalances. The risk for conversion of reversible to irreversible NDI seems to be a potential complication. This review summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians. Methods: Two reviewers independently searched MEDLINE, Experta Medica (EMBASE), and ISI bibliographic databases. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. To evaluate the causal role of the risk factor, data were abstracted according to Kochs postulates. Results: One hundred fifty-five studies published between 1957 and March 2004 described 30 risk factors. Of 155 studies, 58 studies provided a definite diagnosis of NDI; 83 studies, a probable diagnosis; and 14 studies, a possible diagnosis. Nine factors were considered definite causes of NDI; 15 factors, probable causes; and 6 factors, possible causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure. Conclusion: Most risk factors for reversible NDI were medications, and their identification and Continue reading >>

Nephrogenic Diabetes Insipidus

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 >>

Idiopathic Hypoparathyreoidism, Reversible Cardiomyopathy And Nephrogenic Diabetes Insipidus Case Report

Idiopathic Hypoparathyreoidism, Reversible Cardiomyopathy And Nephrogenic Diabetes Insipidus Case Report

We are presenting a case of a 36-year-old patient with idiopathic hypoparathyroidism and reversible dilated cardiomyopathy as a result of hypocalcaemia. Twelve years later, the patient presented a picture of nephrogenic diabetes insipidus, which according to available literature has so far not yet been described. Key words: hypoparathyreoidism, cardiomyopathy, nephrogenic diabetes insipidus Idiopathic hypoparathyroidism manifests with signs of hypocalcaemia. Dilated cardiomyopathy caused by hypocalcaemia is rare. Association between idiopathic hypoparathyroidism and nephrogenic diabetes insipidus is also rare. A thirty-sixyear-old patient was transferred to the intensive care unit from the department of cardiology because of deterioration of cardiac decompensation. This was a patient who was treated for alcoholism seven years ago and has been abstinent since. Four years ago he was hospitalized for acute psychosis. He was already treated at the Department of Cardiology 2.5 months earlier for recurrent pulmonary oedema and dilated cardiomyopathy. The patient was of medium height, conscious, afebrile and eupneic. Lung auscultation showed rales on both sides of the lungs. The action of the heart was rhythmic with quiet tones, and blood pressure was 135/80 mm Hg. The extremities were without oedema. A phenomenon of gear and gynecological hand were found in neurological status with the tongue and left hand tremor and increased muscle tone. The psychiatrist stated that the patient had signs of psychotic anxiety that occasionally had the proportions of panic and fear of immediate death. Attacks were mostly present at night, lasting about five minutes, accompanied by hyperventilation with the worsening of extrapyramidal side effects. He was treated with biperiden, clozapine, fl 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 >>

Reversible Diabetes Insipidus In A Patient With Multiple Myeloma

Reversible Diabetes Insipidus In A Patient With Multiple Myeloma

Reversible diabetes insipidus in a patient with multiple myeloma 3rd July 2015, Volume 128 Number 1417 A 64-year-old man presented with bone pain and weight loss. Blood tests revealed serum IgA 12.8 g/L (normal range 0.84.0), serum free lambda light chains 857 mg/L (626), beta-2 microglobulin 7.5 mg/L (0.03.2), corrected calcium 3.41 mmol/L (2.102.55), albumin 41 g/L (3852) and creatinine 134 umol/L (60105). X-rays demonstrated multiple long bone lytic lesions. A diagnosis of advanced IgA lambda multiple myeloma (MM) was made and the patient commenced chemotherapy with cyclophosphamide, dexamethasone and bortezomib. On the day of his third weekly dose of the first cycle of chemotherapy, he required hospital admission with profound dehydration and hypotension. He reported that he had been passing six litres of urine per day and drinking copious fluids. In retrospect, he had noticed increased thirst and urine output for six months, but had not mentioned it previously. His regular medications at this time were aciclovir, trimethoprim/sulfamethoxazole, ezetimibe, allopurinol, aspirin, cilazapril and dexamethasone. Admitting blood tests showed a creatinine of 152 umol/L (60105), corrected calcium of 2.22 mmol/L (2.102.55) and a sodium of 137 mmol/L (135145). His anti-hypertensive agent (cilazapril) was discontinued and he was rehydrated with IV fluids. An overnight water deprivation test was suggestive of diabetes insipidus (DI), with a urine osmolality of 288 mOsm/kg (normal >750) and a matched serum osmolality of 293 mOsm/kg (normal urine/serum osmolality >2.4). He then underwent a formal 7-hour water deprivation test, as per the local protocol.1 Despite being nil by mouth he continued to produce 75200mL urine per hour. At the end of the test his urine osmolality was inap Continue reading >>

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