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Nephrogenic Diabetes Insipidus

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161. Thirsty Phursty: The Polydipsia Workup

with low solute intake. A 4-hour water restriction test began and was followed by DDAVP 2 mcg IV with results in Table 2. Table 2. Serum and Urine osmolarities during the water restriction test with DDAVP Final results of the water restriction test and administration of DDAVP revealed normal response with increased urine osmolarity to appropriate high levels. This ruled out a Central Diabetes Insipidus (CDI) and Nephrogenic Diabetes Insipidus (NDI) respectively. Osmotic Diuresis was excluded as her (...) in middle-aged women and is common in those with psychiatric disorders. Hypothalamic disorders have been reported to alter the thirst regulation center and systemic infiltrative disorders such as sarcoidosis can lead to this. A large number of medications can lead to dry mouth and thirst and must be ruled out as a cause prior to PP diagnosis. Differentiating PP from CDI and NDI is paramount on the urine studies. Central Diabetes Insipidus is lack of partial or complete ADH production. Nephrogenic

2017 Renal Fellow Network

162. Bartter's and Gitelman's syndrome. (Abstract)

syndrome best fits in the group with the loop and DCT combination.Besides secondary hyperaldosteronism, loop disorders present a whole spectrum of (secondary) pathophysiologic characteristics with significant diagnostic and therapeutic impact, such as polyhydramnios, hyperprostaglandinuria, nephrogenic diabetes insipidus, and nephrocalcinosis. Recent reports indicate that neonatal hyperparathyroidism has also to be added to the clinical presentation of isolated loop disorders.As long as gene therapy

2016 Current Opinion in Pediatrics

163. Demonstration of the functional impact of vasopressin signalling in thick ascending limb by a targeted transgenic rat approach. (Full text)

diabetes insipidus (NDI), which has chiefly been related with impaired aquaporin 2-mediated water reabsorption in the collecting ducts. Previous work also suggested the AVP-V2R-mediated activation of Na(+)-K(+)-2Cl(-)-cotransporters (NKCC2) along the thick ascending limb (TAL) in the context of urine concentration, but its individual contribution to NDI or, more generally, to overall renal function was unclear. We hypothesized that V2R-mediated effects in TAL essentially determine its reabsorptive (...) Demonstration of the functional impact of vasopressin signalling in thick ascending limb by a targeted transgenic rat approach. The antidiuretic hormone vasopressin (AVP) regulates renal salt and water reabsorption along the distal nephron and collecting duct system. These effects are mediated by vasopressin 2 receptors (V2R) and release of intracellular Gs-mediated cAMP to activate epithelial transport proteins. Inactivating mutations in the V2R gene lead to the X-linked form of nephrogenic

2016 American Journal of Physiology. Renal physiology PubMed abstract

164. Metformin, an AMPK activator, stimulates the phosphorylation of Aquaporin 2 and Urea Transporter A1 in Inner Medullary Collecting Ducts. (Full text)

Metformin, an AMPK activator, stimulates the phosphorylation of Aquaporin 2 and Urea Transporter A1 in Inner Medullary Collecting Ducts. Nephrogenic diabetes insipidus (NDI) is characterized by production of very large quantities of dilute urine due to an inability of the kidney to respond to vasopressin. Congenital NDI results from mutations in the type 2 vasopressin receptor (V2R) in ∼90% of families. These patients do not have mutations in aquaporin-2 (AQP2) or urea transporter UT-A1 (UT-A1

2016 American Journal of Physiology. Renal physiology PubMed abstract

165. Plasma Apelin concentrations in Patients with Polyuria-Polydipsia Syndrome. (Full text)

analysis of a prospective study performed in tertiary care hospitals in Switzerland and Germany and 113 healthy volunteers as a control group.Plasma apelin and copeptin levels were measured in 15 patients with complete central diabetes insipidus (DI), seven patients with complete nephrogenic DI, 19 patients with primary polydipsia (PP), and 113 healthy volunteers.Plasma apelin levels were highest in patients with complete nephrogenic DI (413 pmol/L; interquartile range, 332-504 pmol/L; P = .01 (...) ) and lower in patients with PP (190 [172-215] pmol/L; P < .001) or complete central DI (209 [174-241] pmol/L; P = .02) as compared to healthy volunteers (254 [225-311] pmol/L). Plasma apelin to copeptin ratio in patients with PP (53 [38-92] pmol/pmol; P > .9) was similar to healthy volunteers (57 [37-102] pmol/pmol). In contrast, the apelin to copeptin ratio was higher in patients with complete central DI (89 [73-135] pmol/pmol; P = .02) and lower in patients with complete nephrogenic DI (7 [6-10] pmol

2016 Journal of Clinical Endocrinology and Metabolism PubMed abstract

166. Mutations of vasopressin receptor 2 including novel L312S have differential effects on trafficking. (Full text)

L312S mutation as well as for previously described V2R gain-of-function mutants (NSIAD; R137C and R137L), loss-of-function mutants (nephrogenic diabetes insipidus; R137H, R181C, and M311V), and a putative silent V266A V2R polymorphism. In doing so, we describe differences in trafficking between unique V2R substitutions, even at the same amino acid position, therefore highlighting the value of full and thorough characterization of receptor function beyond simple signaling pathway analysis. (...) Mutations of vasopressin receptor 2 including novel L312S have differential effects on trafficking. Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is a genetic disease first described in 2 unrelated male infants with severe symptomatic hyponatremia. Despite undetectable arginine vasopressin levels, patients have inappropriately concentrated urine resulting in hyponatremia, hypoosmolality, and natriuresis. Here, we describe and functionally characterize a novel vasopressin type 2

2016 Molecular Endocrinology PubMed abstract

167. A 4-year-old boy presenting with persistent urinary incontinence: Questions. (Abstract)

) associated with partial nephrogenic diabetes insipidus. He was started on daily desmopressin. Within 3 days the urinary incontinence resolved as did the polyuria and faecal incontinence. His grandmother was referred to the geneticist and eventually the adult nephrologist. This case highlights the importance of being thorough when confronted with a difficult diagnosis. It also emphasizes that a test result does not necessarily equate to the presence or absence of a condition since the test with 100 (...) A 4-year-old boy presenting with persistent urinary incontinence: Questions. A 4-year-old boy was referred to the nephrologist with daytime urinary incontinence and suspicion of an overactive bladder. At the age of 17 months he had been referred to the pediatric endocrinologist because of polyuria and polydipsia in order to exclude diabetes insipidus. Repeated water deprivation tests and a magnetic resonance imaging scan of the brain were normal. Diabetes insipidus was excluded, and primary

2016 Pediatric Nephrology

168. What we need to know about the effect of lithium on the kidney. (Full text)

What we need to know about the effect of lithium on the kidney. Lithium has been a valuable treatment for bipolar affective disorders for decades. Clinical use of lithium, however, has been problematic due to its narrow therapeutic index and concerns for its toxicity in various organ systems. Renal side effects associated with lithium include polyuria, nephrogenic diabetes insipidus, proteinuria, distal renal tubular acidosis, and reduction in glomerular filtration rate. Histologically, chronic

2016 American Journal of Physiology. Renal physiology PubMed abstract

169. Copeptin in the diagnosis of vasopressin-dependent disorders of fluid homeostasis. (Abstract)

pmol/l identify patients with nephrogenic diabetes insipidus. Conversely, copeptin levels measured upon osmotic stimulation differentiate primary polydipsia from partial central diabetes insipidus. In patients with hyponatraemia, low levels of copeptin together with low urine osmolality identify patients with primary polydipsia, and the ratio of copeptin to urinary sodium can distinguish the syndrome of inappropriate antidiuretic hormone secretion from other AVP-dependent forms of hyponatraemia.

2016 Nature reviews. Endocrinology

170. Antihypertensive therapy in patients on chronic lithium treatment for bipolar disorders. (Full text)

Antihypertensive therapy in patients on chronic lithium treatment for bipolar disorders. Bipolar disorders are chronic conditions treated with lithium, which exerts deleterious effects on the kidney, among which nephrogenic diabetes insipidus, tubular acidosis and ultimately chronic kidney disease. Conversely, drugs that alter renal function can modify its serum levels and lead to the potentially fatal lithium intoxication. A search in the main library databases from 1975 to 2015 to identify

2016 Journal of Hypertension PubMed abstract

171. Altered Nitric Oxide System in Cardiovascular and Renal Diseases (Full text)

. A pressure-overload may cause severer left ventricular hypertrophy and dysfunction in eNOS null mice than in wild-type mice. iNOS-derived NO has detrimental effects on the myocardium. NO plays an important role in regulating the angiogenesis and slowing the interstitial fibrosis of the obstructed kidney. In unilateral ureteral obstruction, the expression of eNOS was decreased in the affected kidney. In triply n/i/eNOS null mice, nephrogenic diabetes insipidus developed along with reduced aquaporin-2

2016 Chonnam medical journal PubMed abstract

172. Functional Recovery of AQP2 Recessive Mutations Through Hetero-Oligomerization with Wild-Type Counterpart (Full text)

Functional Recovery of AQP2 Recessive Mutations Through Hetero-Oligomerization with Wild-Type Counterpart Aquaporin-2 (AQP2) is a homotetrameric water channel responsible for the final water reuptake in the kidney. Mutations in the protein induce nephrogenic diabetes insipidus (NDI), which challenges the water balance by producing large urinary volumes. Although recessive AQP2 mutations are believed to generate non-functional and monomeric proteins, the literature identifies several mild

2016 Scientific reports PubMed abstract

173. Receptor Antagonism/Agonism Can Be Uncoupled from Pharmacoperone Activity (Full text)

Receptor Antagonism/Agonism Can Be Uncoupled from Pharmacoperone Activity Pharmacoperones rescue misrouted mutants of the vasopressin receptor type 2 (V2R) and enable them to traffic to the correct biological locus where they function. Previously, a library of nearly 645,000 structures was interrogated with a high throughput screen; pharmacoperones were identified for V2R mutants with a view toward correcting the underlying mutational defects in nephrogenic diabetes insipidus. In the present

2016 Molecular and cellular endocrinology PubMed abstract

174. Lithium toxicity after Roux-en-Y bariatric surgery (Full text)

Lithium toxicity after Roux-en-Y bariatric surgery A 61-year-old woman with medical history significant for morbid obesity, type II diabetes mellitus, nephrogenic diabetes insipidus and bipolar disorder, had been stable on lithium carbonate therapy for several years. She had undergone a Roux-en-Y bypass surgery and, at the time of her surgery, her lithium level was found to be 0.61 mEq/L on a maintenance dose of 600 mg orally twice per day. She was discharged 8 days postoperatively on the same

2016 BMJ case reports PubMed abstract

175. Prorenin Receptor, a Necessary Component in Urine Concentration Mechanism (Full text)

. Gov't Comment 2016 04 20 United States J Am Soc Nephrol 9013836 1046-6673 0 Aquaporin 2 0 Receptors, Cell Surface 0 Receptors, Vasopressin 0 prorenin receptor IM J Am Soc Nephrol. 2016 Oct;27(10):3022-3034 27000064 Aquaporin 2 Diabetes Insipidus, Nephrogenic Humans Receptors, Cell Surface Receptors, Vasopressin aquaporin diabetes insipidus prorenin prostaglandin vasopressin 2016 4 22 6 0 2018 8 21 6 0 2016 4 22 6 0 ppublish 27098238 ASN.2016030344 10.1681/ASN.2016030344 PMC5042682 Hypertension. 2009

2016 Journal of the American Society of Nephrology : JASN PubMed abstract

176. Wnt5a induces renal AQP2 expression by activating calcineurin signalling pathway (Full text)

Wnt5a induces renal AQP2 expression by activating calcineurin signalling pathway Heritable nephrogenic diabetes insipidus (NDI) is characterized by defective urine concentration mechanisms in the kidney, which are mainly caused by loss-of-function mutations in the vasopressin type 2 receptor. For the treatment of heritable NDI, novel strategies that bypass the defective vasopressin type 2 receptor are required to activate the aquaporin-2 (AQP2) water channel. Here we show that Wnt5a regulates

2016 Nature communications PubMed abstract

177. Trial of Desmopressin Orally Disintegrating Tablets (ODT) for Nocturia Due to Nocturnal Polyuria in Japanese Male Subjects

, or neoplasia at Visit 1 History of any neurological disease affecting bladder function or muscle strength at Visit 1 Habitual or psychogenic polydipsia based on medical history at Visit 1 or 24 hour urine output of >2.8 L based on the voiding diary at Visit 2 Central or nephrogenic diabetes insipidus at Visit 1 Syndrome of inappropriate antidiuretic hormone secretion at Visit 1 Suspicion or evidence of cardiac failure at Visit 1 Uncontrolled hypertension at Visit 1 Uncontrolled diabetes mellitus at Visit 1

2016 Clinical Trials

178. Trial of Desmopressin Orally Disintegrating Tablets (ODT) for Nocturia Due to Nocturnal Polyuria in Japanese Female Subjects

of >2.8 L based on the voiding diary at Visit 2 Central or nephrogenic diabetes insipidus at Visit 1 Syndrome of inappropriate antidiuretic hormone secretion at Visit 1 Suspicion or evidence of cardiac failure at Visit 1 Uncontrolled hypertension at Visit 1 Uncontrolled diabetes mellitus at Visit 1 Hyponatraemia (serum sodium level <135 mmol/L) at Visit 1 Renal insufficiency at Visit 1 Hepatic and/or biliary diseases at Visit 1 Known or suspected hypersensitivity to desmopressin ODTs or previous

2016 Clinical Trials

179. Effects of GLP-1 Analogues on Fluid Intake in Patients With Primary Polydipsia (The GOLD-Study)

or probable central or nephrogenic Diabetes insipidus, expected from patient's history Polyuria secondary to diabetes mellitus, hypokalemia, hypercalcemia Pregnancy Previous treatment with GLP-1 agonists within the last 3 month History of pancreatitis Severe renal insufficiency (eGFR (CKD EPI) <30 ml/min/1,73 m2) Cancer Contacts and Locations Go to Information from the National Library of Medicine To learn more about this study, you or your doctor may contact the study research staff using the contact (...) : Layout table for MeSH terms Polydipsia Polydipsia, Psychogenic Diabetes Insipidus Pathologic Processes Signs and Symptoms Behavioral Symptoms Neurobehavioral Manifestations Kidney Diseases Urologic Diseases Pituitary Diseases Endocrine System Diseases Dulaglutide Hypoglycemic Agents Physiological Effects of Drugs

2016 Clinical Trials

180. Molecular mechanisms in lithium-associated renal disease: a systematic review. (Abstract)

English-language original research articles published prior to November 2015 that specifically investigated lithium's effects on nephrogenic diabetes insipidus (NDI) and chronic kidney disease (CKD), using molecular markers.From a total of 3510 records, 71 pre-clinical studies and two relevant clinical studies were identified. Molecular alterations were reported in calcium signaling, inositol monophosphate, extracellular-regulated, prostaglandin, sodium/solute transport, G-protein-coupled receptors

2016 International urology and nephrology

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