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Nephrogenic Diabetes Insipidus

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41. A novel AVPR2 gene mutation of X-linked congenital nephrogenic diabetes insipidus in an Asian pedigree Full Text available with Trip Pro

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

2016 The Journal of international medical research

42. Metformin improves urine concentration in rodents with nephrogenic diabetes insipidus Full Text available with Trip Pro

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

2016 JCI insight

43. Identification of Potential Pharmacoperones Capable of Rescuing the Functionality of Misfolded Vasopressin 2 Receptor Involved in Nephrogenic Diabetes Insipidus Full Text available with Trip Pro

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

2016 Journal of biomolecular screening

44. Atorvastatin for the Treatment of Lithium-Induced Nephrogenic Diabetes Insipidus

Atorvastatin for the Treatment of Lithium-Induced Nephrogenic Diabetes Insipidus Atorvastatin for the Treatment of Lithium-Induced 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. Atorvastatin for the Treatment of Lithium-Induced Nephrogenic Diabetes Insipidus The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. of clinical studies and talk to your health care provider before participating. Read our for details. ClinicalTrials.gov Identifier: NCT02967653 Recruitment Status : Recruiting First Posted : November 18, 2016 Last Update

2016 Clinical Trials

45. Physiological insights into novel therapies for nephrogenic diabetes insipidus. Full Text available with Trip Pro

Physiological insights into novel therapies for nephrogenic diabetes insipidus. Fundamental kidney physiology research can provide important insight into how the kidney works and suggest novel therapeutic opportunities to treat human diseases. This is especially true for nephrogenic diabetes insipidus (NDI). Over the past decade, studies elucidating the molecular physiology and signaling pathways regulating water transport have suggested novel therapeutic possibilities. In patients

2016 American Journal of Physiology. Renal physiology

46. Pemetrexed-Induced Nephrogenic Diabetes Insipidus. Full Text available with Trip Pro

Pemetrexed-Induced Nephrogenic Diabetes Insipidus. Pemetrexed is an approved antimetabolite agent, now widely used for treating locally advanced or metastatic nonsquamous non-small cell lung cancer. Although no electrolyte abnormalities are described in the prescribing information for this drug, several case reports have noted nephrogenic diabetes insipidus with associated acute kidney injury. We present a case of nephrogenic diabetes insipidus without severely reduced kidney function

2016 American Journal of Kidney Diseases

47. Defective Store-Operated Calcium Entry Causes Partial Nephrogenic Diabetes Insipidus. Full Text available with Trip Pro

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.

2015 Journal of the American Society of Nephrology

48. Acetazolamide Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus. Full Text available with Trip Pro

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

2015 Journal of the American Society of Nephrology

49. Partial nephrogenic diabetes insipidus caused by a novel AQP2 variation impairing trafficking of the aquaporin-2 water channel. Full Text available with Trip Pro

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

2015 BMC Nephrology

50. 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

51. Water, Water Everywhere: A New Cause and a New Treatment for Nephrogenic Diabetes Insipidus Full Text available with Trip Pro

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

2015 Journal of the American Society of Nephrology : JASN

52. Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus Full Text available with Trip Pro

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

2015 Scientific reports

53. X-Linked Recessive form of Nephrogenic Diabetes Insipidus in a 7-Year-Old Boy Full Text available with Trip Pro

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.

2015 Balkan Journal of Medical Genetics

54. P2Y12 Receptor Localizes in the Renal Collecting Duct and Its Blockade Augments Arginine Vasopressin Action and Alleviates Nephrogenic Diabetes Insipidus. Full Text available with Trip Pro

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

2015 Journal of the American Society of Nephrology

55. Evolutionary Influenced Interaction Pattern as Indicator for the Investigation of Natural Variants Causing Nephrogenic Diabetes Insipidus Full Text available with Trip Pro

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

2015 Computational and mathematical methods in medicine

56. Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus. Full Text available with Trip Pro

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

2015 Nature reviews. Nephrology

57. Novel autosomal recessive gene mutations in aquaporin-2 in two Chinese congenital nephrogenic diabetes insipidus pedigrees Full Text available with Trip Pro

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

2015 International journal of clinical and experimental medicine

58. Resolution of Diabetes Insipidus after Pyeloplasty: a Case Report and Review of the Literature. Full Text available with Trip Pro

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

59. 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

60. Soluble (Pro)Renin Receptor as a Potential Therapy for Diabetes Insipidus. Full Text available with Trip Pro

signaling pathway can result in polyuria, polydipsia, and hypotonic urine, collectively termed diabetes insipidus (DI). A lack of VP production precipitates central diabetes insipidus (CDI), which can be managed effectively by VP supplementation. A majority of cases of nephrogenic diabetes insipidus (NDI) result from V2R mutations that impair receptor sensitivity. No specific therapy is currently available for management of NDI. Evidence is evolving that (pro)renin receptor (PRR), a newly identified (...) Soluble (Pro)Renin Receptor as a Potential Therapy for Diabetes Insipidus. The antidiuretic hormone vasopressin (VP) is produced by the hypothalamus and is stored and secreted from the posterior pituitary. VP acts via VP type 2 receptors (V2Rs) on the basolateral membrane of principal cells of the collecting duct (CD) to regulate fluid permeability. The VP-evoked endocrine pathway is essential in determining urine concentrating capability. For example, a defect in any component of the VP

2018 American Journal of Physiology. Renal physiology

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