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Nephrogenic Diabetes Insipidus

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101. Aquaporin-2: new mutations responsible for autosomal-recessive nephrogenic diabetes insipidus—update and epidemiology Full Text available with Trip Pro

Aquaporin-2: new mutations responsible for autosomal-recessive nephrogenic diabetes insipidus—update and epidemiology It is clinically useful to distinguish between two types of hereditary nephrogenic diabetes insipidus (NDI): a 'pure' type characterized by loss of water only and a complex type characterized by loss of water and ions. Patients with congenital NDI bearing mutations in the vasopressin 2 receptor gene, AVPR2, or in the aquaporin-2 gene, AQP2, have a pure NDI phenotype with loss

2012 Clinical kidney journal

102. On the Mechanism of Lithium-Induced Diabetes Insipidus in Man and the Rat Full Text available with Trip Pro

. The normal corticopapillary gradient for sodium was not reduced by lithium treatment. The polyuria was not interrupted by brief intravenous doses of vasopressin (5-10 mU/kg) or dibutyryl cyclic AMP (10-15 mg/kg) capable of reversing water diuresis in normal and hypothalamic diabetes insipidus rats (Brattleboro strain). The present studies suggest that nephrogenic diabetes insipidus is a common finding after lithium treatment and results in part from interference with the mediation of vasopressin (...) On the Mechanism of Lithium-Induced Diabetes Insipidus in Man and the Rat The mechanism of lithium-induced diabetes insipidus was investigated in 96 patients and in a rat model. Polydipsia was reported by 40% and polyuria (more than 3 liter/day) by 12% of patients receiving lithium. Maximum concentrating ability after dehydration and vasopressin was markedly impaired in 10 polyuric patients and was reduced in 7 of 10 nonpolyuric patients studied before and during lithium therapy. Severe

1974 Journal of Clinical Investigation

103. The Clinical Physiology of Water Metabolism: Part II: Renal Mechanisms for Urinary Concentration; Diabetes Insipidus Full Text available with Trip Pro

or the pituitary stalk. Possible causes include idiopathic, familial, trauma, tumor, infection or vascular lesions. Patients present with polyuria, usually beginning over a period of a few days. The diagnosis is made by showing that urinary concentration is impaired after water restriction but that there is a good response to exogenous vasopressin therapy. Nephrogenic diabetes insipidus can be identified by a patient's lack of response to AVP. Nephrogenic diabetes insipidus is caused by a familial defect (...) , although milder forms can be acquired as a result of various forms of renal disease. Central diabetes insipidus is eminently responsive to replacement therapy, particularly with dDAVP, a long lasting analogue of AVP. Nephrogenic diabetes insipidus is best treated with a combination of thiazide diuretics as well as a diet low in sodium and protein.

1979 Western Journal of Medicine

104. Novel mutation in the AVPR2 gene in a Danish male with nephrogenic diabetes insipidus caused by ER retention and subsequent lysosomal degradation of the mutant receptor Full Text available with Trip Pro

Novel mutation in the AVPR2 gene in a Danish male with nephrogenic diabetes insipidus caused by ER retention and subsequent lysosomal degradation of the mutant receptor Mutations in the arginine vasopressin receptor 2 (AVPR2) gene can cause X-linked nephrogenic diabetes insipidus (NDI) characterized by the production of large amounts of urine and an inability to concentrate urine in response to the antidiuretic hormone vasopressin. We have identified a novel mutation in the AVPR2 gene (L170P

2011 NDT Plus

105. Functional characterization of novel loss-of-function mutations in the vasopressin type 2 receptor gene causing nephrogenic diabetes insipidus. Full Text available with Trip Pro

Functional characterization of novel loss-of-function mutations in the vasopressin type 2 receptor gene causing nephrogenic diabetes insipidus. X-linked nephrogenic diabetes insipidus (NDI) is a rare polyuric disorder caused by inactivating mutations in the arginine vasopressin receptor Type 2 (AVPR2) gene.NDI patients from six unrelated families were subjected to mutational analysis of the AVPR2 gene. In-depth in vitro characterization of novel AVPR2 mutants by a combination of functional

2011 Transplantation

106. Why Do Thiazides Decrease Polyuria in Diabetes Insipidus?

Why Do Thiazides Decrease Polyuria in Diabetes Insipidus? Renal Fellow Network: Why Do Thiazides Decrease Polyuria in Diabetes Insipidus? | | | | | Tuesday, September 4, 2012 Why Do Thiazides Decrease Polyuria in Diabetes Insipidus? I was reviewing the treatment of diabetes insipidus the other day, and was reminded of the paradoxical effect of thiazide diuretics on urine output in diabetes insipidus. How does this work? The traditional thinking is that thiazide-induced blockade of the Na-Cl (...) explain how a thiazide can serve to decrease polyuria in patients with diabetes insipidus. Posted by lisajcohen at Labels: , 4 comments: said... There are also studies that show thiazides DO decrease plasma volume on the long-run. So this is still controversial. Actually, research in mice shows that this is the mechanism for thiazide-induced hypocalciuria. said... I think, that the problem with Thiazides use in treating Diabetes Indipidus(DI or NDI) is that you loose more H2O(water) than Na+(sodium

2012 Renal Fellow Network

107. Central Diabetes Insipidus

Endocrine System Video Overview of Buffering and the Henderson-Hasselbalch Equation SOCIAL MEDIA Add to Any Platform Loading , MBBS, PhD, University of Adelaide, Royal Adelaide Hospital Click here for Patient Education NOTE: This is the Professional Version. CONSUMERS: Topic Resources Diabetes insipidus (DI) results from a deficiency of vasopressin (ADH) due to a hypothalamic-pituitary disorder (central DI [CDI]) or from resistance of the kidneys to vasopressin (nephrogenic DI [NDI]). Polyuria (...) Water deprivation test Sometimes vasopressin levels Central diabetes insipidus must be differentiated from other causes of polyuria, particularly psychogenic polydipsia (see Table: ) and nephrogenic diabetes insipidus. All tests for CDI (and for NDI) are based on the principle that increasing the plasma osmolality in normal people will lead to decreased excretion of urine with increased urine osmolality. Table Common Causes of Polyuria Mechanism Example Vasopressin -sensitive polyuria Decreased

2013 Merck Manual (19th Edition)

108. Nephrogenic Syndrome of Inappropriate Antidiuresis Full Text available with Trip Pro

Nephrogenic Syndrome of Inappropriate Antidiuresis Mutations in the vasopressin V2 receptor gene are responsible for two human tubular disorders: X-linked congenital nephrogenic diabetes insipidus, due to a loss of function of the mutant V2 receptor, and the nephrogenic syndrome of inappropriate antidiuresis, due to a constitutive activation of the mutant V2 receptor. This latter recently described disease may be diagnosed from infancy to adulthood, as some carriers remain asymptomatic for many

2012 International journal of pediatrics

109. A Study of Minirin Melt in Japanese Patients With Central Diabetes Insipidus (CDI).

specific gravity, and serum sodium (mEq/L) maintained at a normal level by desmopressin nasal administration Outpatient The participant is, in the investigator's opinion, otherwise healthy Be willing and able to comply with the protocol requirements including restriction of water intake Exclusion Criteria: Presence or a history of nephrogenic diabetes insipidus or diabetes mellitus Presence of uncorrected hypothyroidism, hypoadrenalism or hypogonadism Abnormalities or disease of the oral cavity (...) A Study of Minirin Melt in Japanese Patients With Central Diabetes Insipidus (CDI). A Study of Minirin Melt in Japanese Patients With Central Diabetes Insipidus (CDI). - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before

2011 Clinical Trials

110. Management of diabetes insipidus in children Full Text available with Trip Pro

Management of diabetes insipidus in children 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/m(2)/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

2011 Indian journal of endocrinology and metabolism

111. George Thomas: Diabetes mellitus—the need for better terminology

is “dysglycemic metabolism” syndrome and not dysglycemic “metabolic syndrome,” although the latter comes under the domain of the definition. Similarly, the term dysglycemia is automatically included in the ambit of the new terminology. Type 1 diabetes mellitus and should be called “hypoinsulinism.” This term will be similar to hypothyroidism or hypopituitarism. Similarly, diabetes insipidus should be termed “hypovasopressinism.” Nephrogenic diabetes insipidus should be plain “nephrogenic polyuria (...) George Thomas: Diabetes mellitus—the need for better terminology George Thomas: Diabetes mellitus—the need for better terminology - The BMJ ---> Diabetes is . However, the term “diabetes” connotes archaic concepts and needs to be reviewed. The ancient Greek physician Aretaeus of Cappadocia is often recorded as the first person to use the term “diabetes” (meaning “excessive discharge of urine”) in the first century CE. Later, the word “mellitus” (sweet) after he noted the sweetness of patients

2015 The BMJ Blog

112. Diabetes insipidus Full Text available with Trip Pro

Diabetes insipidus Diabetes insipidus - Wikipedia Diabetes insipidus From Wikipedia, the free encyclopedia Not to be confused with . Diabetes insipidus Pronunciation "Diabetes: or Symptoms Large amounts of dilute urine, increased thirst , Usual onset Any age Types Central, nephrogenic, dipsogenic, gestational Causes Depends on the type , , Treatment Drinking sufficient fluids Medication , , Prognosis Good with treatment Frequency 3 per 100,000 per year Diabetes insipidus ( DI (...) DI occurs only during . Diagnosis is often based on , , and the . is a separate condition with an unrelated mechanism, though both can result in the production of large amounts of urine. Treatment involves drinking sufficient fluids to prevent dehydration. Other treatments depend on the type. In central and gestational DI treatment is with . Nephrogenic DI may be treated by addressing the underlying cause or the use of a , , or . The number of new cases of diabetes insipidus each year is 3

2012 Wikipedia

113. Lack of MRI neurohypophyseal bright signal in a child with congenital nephrogenic diabetes insipidus Full Text available with Trip Pro

Lack of MRI neurohypophyseal bright signal in a child with congenital nephrogenic diabetes insipidus 25984077 2015 05 18 2018 11 13 1753-0784 3 5 2010 Oct NDT plus NDT Plus Lack of MRI neurohypophyseal bright signal in a child with congenital nephrogenic diabetes insipidus. 511-2 10.1093/ndtplus/sfq120 Chehade Hassib H Children's Hospital of Geneva . Pediatric Nephrology, 6 Rue Willy-Donzé, 1211 Geneva 14 , Switzerland. Parvex Paloma P Children's Hospital of Geneva . Pediatric Nephrology, 6 Rue

2010 NDT Plus

114. A de novo novel missense mutation in AVPR2 with severe nephrogenic diabetes insipidus Full Text available with Trip Pro

A de novo novel missense mutation in AVPR2 with severe nephrogenic diabetes insipidus We describe a paediatric case of nephrogenic diabetes insipidus (NDI) with a novel mutation in the arginine vasopressin receptor 2 gene (AVPR2) in the absence of a family history of congenital polyuria. The patient, a 5-month-old Caucasian boy, had failure to thrive and hypernatraemia. On admission to hospital, he had a plasma sodium of 171 mEq/L with a concomittant urine osmolality of 131 mOsm/kg. Molecular

2010 NDT Plus

115. {alpha}ENaC-Mediated Lithium Absorption Promotes Nephrogenic Diabetes Insipidus. Full Text available with Trip Pro

{alpha}ENaC-Mediated Lithium Absorption Promotes Nephrogenic Diabetes Insipidus. Lithium-induced nephrogenic diabetes insipidus (NDI) is accompanied by polyuria, downregulation of aquaporin 2 (AQP2), and cellular remodeling of the collecting duct (CD). The amiloride-sensitive epithelial sodium channel (ENaC) is a likely candidate for lithium entry. Here, we subjected transgenic mice lacking αENaC specifically in the CD (knockout [KO] mice) and littermate controls to chronic lithium treatment

2010 Journal of the American Society of Nephrology

116. Severe hydramnios and preterm delivery in association with transient maternal diabetes insipidus. (Abstract)

Severe hydramnios and preterm delivery in association with transient maternal diabetes insipidus. Diabetes insipidus is rare in pregnancy. It is characterized by hypoosmolar polyuria and may be central, nephrogenic, or transient in etiology; the latter is presumably related to excess placental vasopresinase production. In theory, fetal effects of this endocrine condition may include hydramnios secondary to fetal polyuria.A pregnant patient developed rapid-onset second-trimester hydramnios (...) that prompted a thorough fetal and maternal evaluation. She ultimately was diagnosed with transient diabetes insipidus of pregnancy because of an abrupt change in her voiding pattern at 20 weeks of gestation, significant polydipsia, and laboratory studies that revealed a hypoosmolar polyuria with normal serum and urine electrolytes. Transient neonatal polyuria also was confirmed in association with this unique maternal endocrine syndrome.The most likely cause of hydramnios in this case is transient maternal

2010 Obstetrics and Gynecology

117. Management of Chronic Kidney Disease

syndrome, liver disease, or accompanying heart failure. Regardless of the etiology of hypervolemia, some practical issues occur for diuretic management in patients with CKD: • Dietary sodium restriction should, in general, be emphasized, unless one suspects salt-wasting nephropathy, which is relatively rare. • Loop diuretics are preferred when GFR is 4 L of fluid and a high salt diet. • Central and nephrogenic diabetes insipidus: fluid intake of > 5 L daily may be needed. Secondary Preventive Care (...) conditions such as cardiovascular disease and diabetes, emphasizing the importance of aggressive management of these conditions to potentially decrease morbidity and mortality among patients with CKD. Key points Background • Despite increasing prevalence of CKD, it is often under-recognized and under-treated. [A]* • Evidence for screening and management of early stage CKD is limited due to absence of large randomized controlled trials. Definition and Staging (Tables 1 and 2) • Kidney damage for = 3

2020 University of Michigan Health System

118. Chronic Kidney Disease - Identification, Evaluation and Management of Adult Patients

/ persistent muscle pain. No Phenytoin Risk of accumulation and toxicity Monitor levels and also adjust level for serum albumin No Lithium Accumulation and increased risk of side effects Risk of nephrogenic diabetes insipidus Risk of chronic interstitial nephritis Monitor lithium and electrolyte levels Encourage hydration Refer to a nephrologist if eGFR declines. No Hypoglycemics (sulfonylureas, insulin, meglitinides, thiazolidinediones) Accumulation can increase risk of hypoglycaemia Avoid long acting (...) . 2009 Jul;20(7):1614–22. Diabetes Control and Complications Trial Research Group, Nathan DM, Genuth S, Lachin J, Cleary P, Crofford O, et al. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med. 1993 30;329(14):977–86. Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek JW, et al. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal

2019 Clinical Practice Guidelines and Protocols in British Columbia

119. Assessment of hypercalcaemia

renal function may be severely damaged. Taniegra ED. Hyperparathyroidism. Am Fam Physician. 2004;69:333-339. http://www.aafp.org/afp/2004/0115/p333.html http://www.ncbi.nlm.nih.gov/pubmed/14765772?tool=bestpractice.com Hypercalcaemia also causes dehydration by inducing renal resistance to vasopressin, leading to nephrogenic diabetes insipidus. Dehydration, in turn, leads to a corresponding further increase in serum calcium concentration. Pathophysiology Phosphate solubility is closely related

2018 BMJ Best Practice

120. Assessment of hypernatraemia

is diagnosed in males and females in equal numbers. Differentials Central diabetes insipidus Hyperosmolar hyperglycaemic state (HHS) Nephrogenic diabetes insipidus Severe diarrhoea Vomiting Limited access to water Primary hypodipsia Cushing's syndrome Primary aldosteronism Post-obstructive diuresis Laxative and bowel cleansing agent use Enteric fistulae Diuretics Heat exposure Exercise Fever Severe burns Inadequate breastfeeding of infants Salt ingestion High-protein diet Use of intravenous sodium chloride

2018 BMJ Best Practice

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