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Nephrogenic Diabetes Insipidus

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41. Partial Nephrogenic Diabetes Insipidus in a Burned Patient Receiving Sevoflurane Sedation With an Anaesthetic Conserving Device-A Case Report. (PubMed)

Partial Nephrogenic Diabetes Insipidus in a Burned Patient Receiving Sevoflurane Sedation With an Anaesthetic Conserving Device-A Case Report. To describe a case of partial nephrogenic diabetes insipidus in a burned patient after prolonged delivery of low inspired concentrations of sevoflurane via an Anesthetic Conserving Device.Clinical observation.Case report.Relevant clinical information.A 34-year-old man was admitted with burns covering 52% of his total body surface area. Mechanical (...) concentrating ability. After cessation of sevoflurane, all variables returned to normal within 5 days. The results of further investigations (cerebral computed tomographic scan, cerebral magnetic resonance imaging, and serum arginine vasopressin concentration) were compatible with a diagnosis of partial nephrogenic diabetes insipidus. The temporal sequence of clinical findings in relation to sevoflurane administration suggests that the sevoflurane was the probable underlying cause.Clinicians should be aware

2016 Critical Care Medicine

42. 4-PBA Improves Lithium-induced Nephrogenic Diabetes Insipidus by Attenuating ER Stress. (PubMed)

4-PBA Improves Lithium-induced Nephrogenic Diabetes Insipidus by Attenuating ER Stress. Endoplasmic reticulum (ER) stress has been implicated in some types of glomerular and tubular disorders. The objectives of this study were to elucidate the role of ER stress in lithium-induced nephrogenic diabetes insipidus (NDI) and to investigate whether attenuation of ER stress by 4-phenylbutyric acid (4-PBA) improves urinary concentrating defect in lithium-treated rats. Wistar rats received lithium (40

2016 American Journal of Physiology. Renal physiology

43. Identification of Potential Pharmacoperones Capable of Rescuing the Functionality of Misfolded Vasopressin 2 Receptor Involved in Nephrogenic Diabetes Insipidus (PubMed)

Identification of Potential Pharmacoperones Capable of Rescuing the Functionality of Misfolded Vasopressin 2 Receptor Involved in Nephrogenic Diabetes Insipidus Pharmacoperones correct the folding of otherwise misfolded protein mutants, restoring function (i.e., providing "rescue") by correcting their trafficking. Currently, most pharmacoperones possess intrinsic antagonist activity because they were identified using methods initially aimed at discovering such functions. Here, we describe (...) an ultra-high-throughput homogeneous cell-based assay with a cAMP detection system, a method specifically designed to identify pharmacoperones of the vasopressin type 2 receptor (V2R), a GPCR that, when mutated, is associated with nephrogenic diabetes insipidus. Previously developed methods to identify compounds capable of altering cellular trafficking of V2R were modified and used to screen a 645,000 compound collection by measuring the ability of library compounds to rescue a mutant hV2R [L83Q

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2016 Journal of biomolecular screening

44. A novel AVPR2 gene mutation of X-linked congenital nephrogenic diabetes insipidus in an Asian pedigree (PubMed)

A novel AVPR2 gene mutation of X-linked congenital nephrogenic diabetes insipidus in an Asian pedigree Polyuria and polydipsia are the characteristics of congenital nephrogenic diabetes insipidus (CNDI). Approximately 90% of all patients with CNDI have X-linked hereditary disease, which is due to a mutation of the arginine vasopressin receptor 2 ( AVPR2) gene. This case report describes a 54-year-old male with polyuria and polydipsia and several male members of his pedigree who had the same (...) symptoms. The proband was diagnosed with diabetes insipidus using a water-deprivation and arginine vasopressin stimulation test. Genomic DNA from the patient and his family members was extracted and the AVPR2 gene was sequenced. A novel missense mutation of a cytosine to guanine transition at position 972 (c.972C > G) was found, which resulted in the substitution of isoleucine for methionine at amino acid position 324 (p.I324M) in the seventh transmembrane domain of the protein. The proband's mother

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2016 The Journal of international medical research

45. Metformin improves urine concentration in rodents with nephrogenic diabetes insipidus (PubMed)

Metformin improves urine concentration in rodents with nephrogenic diabetes insipidus Urine concentration is regulated by vasopressin. Congenital nephrogenic diabetes insipidus (NDI) is caused by vasopressin type 2 receptor (V2R) mutations. We studied whether metformin could improve urine concentration in rodent models of congenital NDI by stimulating AMPK. To block the V2R in rats, tolvaptan (10 mg/kg/d) was given by oral gavage with or without metformin (800 mg/ kg/d). Control rats received

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2016 JCI insight

46. A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus. (PubMed)

of 144 patients underwent both tests. The final diagnosis was primary polydipsia in 82 patients (57%), central diabetes insipidus in 59 (41%), and nephrogenic diabetes insipidus in 3 (2%). Overall, among the 141 patients included in the analysis, the indirect water-deprivation test determined the correct diagnosis in 108 patients (diagnostic accuracy, 76.6%; 95% confidence interval [CI], 68.9 to 83.2), and the hypertonic saline infusion test (with a copeptin cutoff level of >4.9 pmol per liter (...) A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus. The indirect water-deprivation test is the current reference standard for the diagnosis of diabetes insipidus. However, it is technically cumbersome to administer, and the results are often inaccurate. The current study compared the indirect water-deprivation test with direct detection of plasma copeptin, a precursor-derived surrogate of arginine vasopressin.From 2013 to 2017, we recruited 156 patients with hypotonic polyuria

2018 NEJM

47. Metformin and Congenital Nephrogenic Diabetes Insipidus

Metformin and Congenital Nephrogenic Diabetes Insipidus Metformin and Congenital Nephrogenic Diabetes Insipidus - 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 adding more. Metformin and Congenital Nephrogenic Diabetes (...) University Study Details Study Description Go to Brief Summary: The purpose of this study is to determine whether metformin can increase urine concentration (osmolality) and decrease the amount of urine in patients with congenital nephrogenic diabetes insipidus (NDI). Condition or disease Intervention/treatment Phase Diabetes Insipidus Drug: Metformin Phase 1 Detailed Description: Nephrogenic diabetes insipidus (NDI) is a genetic disease. Patients with this disease make large amounts of urine because

2015 Clinical Trials

48. Partial nephrogenic diabetes insipidus caused by a novel AQP2 variation impairing trafficking of the aquaporin-2 water channel. (PubMed)

Partial nephrogenic diabetes insipidus caused by a novel AQP2 variation impairing trafficking of the aquaporin-2 water channel. Autosomal dominant inheritance of congenital nephrogenic diabetes insipidus (CNDI) is rare and usually caused by variations in the AQP2 gene. We have investigated the genetic and molecular background underlying symptoms of diabetes insipidus (DI) in a Swedish family with autosomal dominant inheritance of the condition.The proband and her father were subjected to water (...) -GFP protein and AQP2 variant protein phosphorylation levels were assessed by Western blotting analysis.Clinical and genetic data suggest that the proband and her father suffer from partial nephrogenic DI due to a variation (g.4807C > T) in the AQP2 gene. The variation results in substitution of arginine-254 to tryptophan (p.R254W) in AQP2. Analysis of MDCK cells stably expressing AQP2 variant proteins revealed disabled phosphorylation, impaired trafficking and intracellular accumulation of AQP2

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2015 BMC Nephrology

49. Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus (PubMed)

Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus 26712528 2018 08 20 2018 12 02 1533-3450 27 7 2016 07 Journal of the American Society of Nephrology : JASN J. Am. Soc. Nephrol. Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus. 1872-4 10.1681/ASN.2015111223 Sands Jeff M JM Renal Division, Department of Medicine and Department of Physiology, Emory University School of Medicine, Atlanta, Georgia jsands@emory.edu (...) . eng R01 DK041707 DK NIDDK NIH HHS United States R01 DK089828 DK NIDDK NIH HHS United States Editorial Research Support, N.I.H., Extramural Comment 2015 12 28 United States J Am Soc Nephrol 9013836 1046-6673 0 Aquaporin 2 0 Aquaporins 0 Receptors, Vasopressin 059QF0KO0R Water IM J Am Soc Nephrol. 2016 Jul;27(7):2035-48 26574044 J Am Soc Nephrol. 2016 Jul;27(7):2082-91 26574046 Aquaporin 2 genetics Aquaporins genetics Diabetes Insipidus, Nephrogenic Humans Mutation Receptors, Vasopressin genetics

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2015 Journal of the American Society of Nephrology : JASN

50. Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus (PubMed)

Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus Hypokalemia (low serum potassium level) is a common electrolyte imbalance that can cause a defect in urinary concentrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular mechanism is unknown. We employed proteomic analysis of inner medullary collecting ducts (IMCD) from rats fed with a potassium-free diet for 1 day. IMCD protein quantification was performed

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2015 Scientific reports

51. Defective Store-Operated Calcium Entry Causes Partial Nephrogenic Diabetes Insipidus. (PubMed)

Defective Store-Operated Calcium Entry Causes Partial Nephrogenic Diabetes Insipidus. Store-operated calcium entry (SOCE) is the mechanism by which extracellular signals elicit prolonged intracellular calcium elevation to drive changes in fundamental cellular processes. Here, we investigated the role of SOCE in the regulation of renal water reabsorption, using the inbred rat strain SHR-A3 as an animal model with disrupted SOCE. We found that SHR-A3, but not SHR-B2, have a novel truncating (...) STIM1. Overall, these results identify a novel mechanism of nephrogenic diabetes insipidus and uncover a role of SOCE in renal water handling.Copyright © 2016 by the American Society of Nephrology.

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2015 Journal of the American Society of Nephrology

52. Acetazolamide Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus. (PubMed)

Acetazolamide Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus. To reduce lithium-induced nephrogenic diabetes insipidus (lithium-NDI), patients with bipolar disorder are treated with thiazide and amiloride, which are thought to induce antidiuresis by a compensatory increase in prourine uptake in proximal tubules. However, thiazides induced antidiuresis and alkalinized the urine in lithium-NDI mice lacking the sodium-chloride cotransporter, suggesting that inhibition of carbonic

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2015 Journal of the American Society of Nephrology

53. Novel autosomal recessive gene mutations in aquaporin-2 in two Chinese congenital nephrogenic diabetes insipidus pedigrees (PubMed)

Novel autosomal recessive gene mutations in aquaporin-2 in two Chinese congenital nephrogenic diabetes insipidus pedigrees Recent evidence has linked novel mutations in the arginine vasopressin receptor 2 gene (AVPR2) and aquaporin-2 gene (AQP2) present in Southeast Asian populations to congenital nephrogenic diabetes insipidus (NDI). To investigate mutations in 2 distinct Chinese pedigrees with NDI patients, clinical data, laboratory findings, and genomic DNA sequences from peripheral blood

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2015 International journal of clinical and experimental medicine

54. X-Linked Recessive form of Nephrogenic Diabetes Insipidus in a 7-Year-Old Boy (PubMed)

X-Linked Recessive form of Nephrogenic Diabetes Insipidus in a 7-Year-Old Boy Nephrogenic diabetes insipidus (NDI) is caused by the inability of renal collecting duct cells to respond to arginine vasopressin (AVP)/antidiuretic hormone (ADH). We present the case of a 7-year-old boy with a history of excretion of large amounts of dilute urine and polydipsia since infancy. The boy had several vomiting episodes with mild dehydration during the first 3 years of life. There was no evidence (...) desmopressin administration. This indicated a nephrogenic form of diabetes insipidus. Molecular analyses revealed a P286L [p.Pro(CCC)286Leu(CTC)] mutation in the AVPR2 gene, that was inherited from his mother. This patient is the first case with genetically confirmed X-linked inherited form of NDI in the Republic of Macedonia. Molecular analysis confirmed the clinical diagnosis and enabled genetic advice for this family.

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2015 Balkan Journal of Medical Genetics

55. Evolutionary Influenced Interaction Pattern as Indicator for the Investigation of Natural Variants Causing Nephrogenic Diabetes Insipidus (PubMed)

Evolutionary Influenced Interaction Pattern as Indicator for the Investigation of Natural Variants Causing Nephrogenic Diabetes Insipidus The importance of short membrane sequence motifs has been shown in many works and emphasizes the related sequence motif analysis. Together with specific transmembrane helix-helix interactions, the analysis of interacting sequence parts is helpful for understanding the process during membrane protein folding and in retaining the three-dimensional fold. Here we (...) present a simple high-throughput analysis method for deriving mutational information of interacting sequence parts. Applied on aquaporin water channel proteins, our approach supports the analysis of mutational variants within different interacting subsequences and finally the investigation of natural variants which cause diseases like, for example, nephrogenic diabetes insipidus. In this work we demonstrate a simple method for massive membrane protein data analysis. As shown, the presented in silico

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2015 Computational and mathematical methods in medicine

56. Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus. (PubMed)

Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus. Healthy kidneys maintain fluid and electrolyte homoeostasis by adjusting urine volume and composition according to physiological needs. The final urine composition is determined in the last tubular segment: the collecting duct. Water permeability in the collecting duct is regulated by arginine vasopressin (AVP). Secretion of AVP from the neurohypophysis is regulated by a complex signalling network that involves (...) osmosensors, barosensors and volume sensors. AVP facilitates aquaporin (AQP)-mediated water reabsorption via activation of the vasopressin V2 receptor (AVPR2) in the collecting duct, thus enabling concentration of urine. In nephrogenic diabetes insipidus (NDI), inability of the kidneys to respond to AVP results in functional AQP deficiency. Consequently, affected patients have constant diuresis, resulting in large volumes of dilute urine. Primary forms of NDI result from mutations in the genes that encode

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2015 Nature reviews. Nephrology

57. P2Y12 Receptor Localizes in the Renal Collecting Duct and Its Blockade Augments Arginine Vasopressin Action and Alleviates Nephrogenic Diabetes Insipidus. (PubMed)

P2Y12 Receptor Localizes in the Renal Collecting Duct and Its Blockade Augments Arginine Vasopressin Action and Alleviates Nephrogenic Diabetes Insipidus. P2Y12 receptor (P2Y12-R) signaling is mediated through Gi, ultimately reducing cellular cAMP levels. Because cAMP is a central modulator of arginine vasopressin (AVP)-induced water transport in the renal collecting duct (CD), we hypothesized that if expressed in the CD, P2Y12-R may play a role in renal handling of water in health (...) and in nephrogenic diabetes insipidus. We found P2Y12-R mRNA expression in rat kidney, and immunolocalized its protein and aquaporin-2 (AQP2) in CD principal cells. Administration of clopidogrel bisulfate, an irreversible inhibitor of P2Y12-R, significantly increased urine concentration and AQP2 protein in the kidneys of Sprague-Dawley rats. Notably, clopidogrel did not alter urine concentration in Brattleboro rats that lack AVP. Clopidogrel administration also significantly ameliorated lithium-induced polyuria

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2015 Journal of the American Society of Nephrology

58. A Novel Deletion Mutation of the Arginine Vasopressin Receptor 2 Gene in a Japanese Infant with Nephrogenic Diabetes Insipidus (PubMed)

A Novel Deletion Mutation of the Arginine Vasopressin Receptor 2 Gene in a Japanese Infant with Nephrogenic Diabetes Insipidus 25374441 2014 11 06 2018 11 13 0918-5739 23 4 2014 Oct Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology Clin Pediatr Endocrinol A novel deletion mutation of the arginine vasopressin receptor 2 gene in a Japanese infant with nephrogenic diabetes insipidus. 115-7 10.1297/cpe

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2014 Clinical Pediatric Endocrinology

59. Resolution of Diabetes Insipidus after Pyeloplasty: a Case Report and Review of the Literature. (PubMed)

Resolution of Diabetes Insipidus after Pyeloplasty: a Case Report and Review of the Literature. Nephrogenic diabetes insipidus (NDI), a rare cause of polyuria and polydipsia in children, is usually managed with medications and careful monitoring of water intake. We present a child who was incidentally found to have right hydronephrosis secondary to ureteropelvic junction obstruction, and was subsequently also diagnosed with NDI. After being medically managed, he underwent open right pyeloplasty

2018 Urology

60. Use of Copeptin Measurement After Arginine Infusion for the Differential Diagnosis of Diabetes Insipidus

, hypercalcemia or hypokalemia Nephrogenic diabetes insipidus (defined as baseline copeptin level >21.4pmol/L) Evidence of any acute illness Epilepsy requiring treatment Uncontrolled arterial hypertension (blood pressure >160/100mmHg at baseline) Cardiac failure (NYHA III-IV) Liver cirrhosis (Child B-C) Uncorrected adrenal or thyroidal deficiency Patients refusing or unable to give written informed consent Pregnancy or breast feeding End of life care Contacts and Locations Go to Information from the National (...) Use of Copeptin Measurement After Arginine Infusion for the Differential Diagnosis of Diabetes Insipidus Use of Copeptin Measurement After Arginine Infusion for the Differential Diagnosis of Diabetes Insipidus - the CARGOx Study - 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

2018 Clinical Trials

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