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Nephrogenic Diabetes Insipidus

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61. The soluble (Pro) renin receptor does not influence lithium‐induced diabetes insipidus but does provoke beiging of white adipose tissue in mice Full Text available with Trip Pro

The soluble (Pro) renin receptor does not influence lithium‐induced diabetes insipidus but does provoke beiging of white adipose tissue in mice Earlier we reported that the recombinant soluble (pro) renin receptor sPRR-His upregulates renal aquoporin-2 (AQP2) expression, and attenuates polyuria associated with nephrogenic diabetes insipidus (NDI) induced by vasopressin type 2 receptor (V2R) antagonism. Patients that receive lithium therapy develop polyuria associated NDI that might

2017 Physiological reports

62. A Novel Deletion Mutation of the Arginine Vasopressin Receptor 2 Gene in a Japanese Infant with Nephrogenic Diabetes Insipidus Full Text available with Trip Pro

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

2014 Clinical Pediatric Endocrinology

63. Hydrochorothiazide attenuates lithium-induced Nephrogenic Diabetes Insipidus independently of the sodium-chloride co-transporter. Full Text available with Trip Pro

Hydrochorothiazide attenuates lithium-induced Nephrogenic Diabetes Insipidus independently of the sodium-chloride co-transporter. Lithium is the most common cause of nephrogenic diabetes insipidus (Li-NDI). Hydrochlorothiazide (HCTZ) combined with amiloride is the mainstay treatment in Li-NDI. The paradoxical antidiuretic action of HCTZ in Li-NDI is generally attributed to increased sodium and water uptake in proximal tubules as a compensation for increased volume loss due to HCTZ inhibition

2013 American Journal of Physiology. Renal physiology

64. Evaluation of cellular plasticity in the collecting duct during the recovery of lithium-induced nephrogenic diabetes insipidus. Full Text available with Trip Pro

Evaluation of cellular plasticity in the collecting duct during the recovery of lithium-induced nephrogenic diabetes insipidus. The cellular morphology of the collecting duct is altered by chronic lithium treatment. We have previously shown that lithium increases the fraction of type-A intercalated cells and lowers the fraction of principal cells along the collecting duct. Moreover, type-A intercalated cells acquire a long-row distribution pattern along the tubules. In the present study, we

2013 American Journal of Physiology. Renal physiology

65. Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment. Full Text available with Trip Pro

Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment. The water channel aquaporin-2 (AQP2), expressed in the kidney collecting ducts, plays a pivotal role in maintaining body water balance. The channel is regulated by the peptide hormone arginine vasopressin (AVP), which exerts its effects through the type 2 vasopressin receptor (AVPR2). Disrupted function or regulation of AQP2 or the AVPR2 results in nephrogenic diabetes (...) insipidus (NDI), a common clinical condition of renal origin characterized by polydipsia and polyuria. Over several years, major research efforts have advanced our understanding of NDI at the genetic, cellular, molecular, and biological levels. NDI is commonly characterized as hereditary (congenital) NDI, arising from genetic mutations in the AVPR2 or AQP2; or acquired NDI, due to for exmple medical treatment or electrolyte disturbances. In this article, we provide a comprehensive overview

2013 Endocrine Reviews

66. Inherited secondary nephrogenic diabetes insipidus: Concentrating on humans. Full Text available with Trip Pro

Inherited secondary nephrogenic diabetes insipidus: Concentrating on humans. The study of human physiology is paramount to understanding disease and developing rational and targeted treatments. Conversely, the study of human disease can teach us a lot about physiology. Investigations into primary inherited nephrogenic diabetes insipidus (NDI) have contributed enormously to our understanding of the mechanisms of urinary concentration and identified the vasopressin receptor AVPR2, as well

2013 American Journal of Physiology. Renal physiology

67. Nephrogenic Diabetes Insipidus

Nephrogenic Diabetes Insipidus Nephrogenic Diabetes Insipidus Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Nephrogenic Diabetes (...) Insipidus Nephrogenic Diabetes Insipidus Aka: Nephrogenic Diabetes Insipidus , Nephrogenic DI From Related Chapters II. Definition Deficient response by to Antidiuretic Hormone III. Pathophysiology ADH fails increasing collecting duct water permeability Failed countercurrent mechanism Inadequate generation of hypertonic interstitium IV. Causes Congenital Chronic disease of renal ry cystic disease Protein deficient diet Salt deficient diet Medications Demeclocycline V. Diagnosis No response to water

2015 FP Notebook

68. Novel compound aquaporin 2 mutations in nephrogenic diabetes insipidus Full Text available with Trip Pro

Novel compound aquaporin 2 mutations in nephrogenic diabetes insipidus 22249485 2012 09 19 2018 11 13 1980-5322 67 1 2012 Clinics (Sao Paulo, Brazil) Clinics (Sao Paulo) Novel compound aquaporin 2 mutations in nephrogenic diabetes insipidus. 79-82 S1807-59322012000100013 Liberatore Junior Raphael D RD Faculdade de Medicina de São José do Rio Preto, Department of Pediatrics, Brazil. Carneiro Juliana G JG Leidenz Franciele B FB Melilo-Carolino Rachel R Sarubi Helena C HC De Marco Luiz L eng Case (...) Reports Journal Article Research Support, Non-U.S. Gov't Brazil Clinics (Sao Paulo) 101244734 1807-5932 0 Aquaporin 2 IM Aquaporin 2 genetics Diabetes Insipidus, Nephrogenic congenital genetics Exons genetics Female Heterozygote Humans Infant Mutation genetics 2012 1 18 6 0 2012 1 18 6 0 2012 9 20 6 0 ppublish 22249485 S1807-59322012000100013 PMC3248606 J Am Soc Nephrol. 2002 Sep;13(9):2267-77 12191971 J Physiol. 2010 Jun 15;588(Pt 12):2205-18 20403973 J Clin Invest. 1994 Mar;93(3):1250-6 7510718

2012 Clinics

69. Congenital nephrogenic diabetes insipidus: the current state of affairs. (Abstract)

Congenital nephrogenic diabetes insipidus: the current state of affairs. The anti-diuretic hormone arginine vasopressin (AVP) is released from the pituitary upon hypovolemia or hypernatremia, and regulates water reabsorption in the renal collecting duct principal cells. Binding of AVP to the arginine vasopressin receptor type 2 (AVPR2) in the basolateral membrane leads to translocation of aquaporin 2 (AQP2) water channels to the apical membrane of the collecting duct principal cells, inducing (...) water permeability of the membrane. This results in water reabsorption from the pro-urine into the medullary interstitium following an osmotic gradient. Congenital nephrogenic diabetes insipidus (NDI) is a disorder associated with mutations in either the AVPR2 or AQP2 gene, causing the inability of patients to concentrate their pro-urine, which leads to a high risk of dehydration. This review focuses on the current knowledge regarding the cell biological aspects of congenital X-linked, autosomal

2012 Pediatric Nephrology

70. Membrane Protein Stability Analyses by Means of Protein Energy Profiles in Case of Nephrogenic Diabetes Insipidus Full Text available with Trip Pro

Membrane Protein Stability Analyses by Means of Protein Energy Profiles in Case of Nephrogenic Diabetes Insipidus Diabetes insipidus (DI) is a rare endocrine, inheritable disorder with low incidences in an estimated one per 25,000-30,000 live births. This disease is characterized by polyuria and compensatory polydypsia. The diverse underlying causes of DI can be central defects, in which no functional arginine vasopressin (AVP) is released from the pituitary or can be a result of defects (...) in the kidney (nephrogenic DI, NDI). NDI is a disorder in which patients are unable to concentrate their urine despite the presence of AVP. This antidiuretic hormone regulates the process of water reabsorption from the prourine that is formed in the kidney. It binds to its type-2 receptor (V2R) in the kidney induces a cAMP-driven cascade, which leads to the insertion of aquaporin-2 water channels into the apical membrane. Mutations in the genes of V2R and aquaporin-2 often lead to NDI. We investigated

2012 Computational and mathematical methods in medicine

71. Vasopressin increases S261 phosphorylation in AQP2-P262L, a mutant in recessive nephrogenic diabetes insipidus. Full Text available with Trip Pro

Vasopressin increases S261 phosphorylation in AQP2-P262L, a mutant in recessive nephrogenic diabetes insipidus. Mutations in the aquaporin-2 (AQP2) gene cause nephrogenic diabetes insipidus (NDI), a renal disorder characterized by polyuria due to a lacking antidiuretic response to vasopressin. While most AQP2 mutants in recessive NDI are misfolded and retained in the endoplasmic reticulum, AQP2-P262L in NDI was impaired in its vasopressin-dependent translocation from vesicles to the plasma

2012 Transplantation

72. Two new large deletions of the AVPR2 gene causing nephrogenic diabetes insipidus and a review of previously published deletions. Full Text available with Trip Pro

Two new large deletions of the AVPR2 gene causing nephrogenic diabetes insipidus and a review of previously published deletions. In this paper, we report two new original deletions and present an extended review of the previously characterized AVPR2 gene deletions to better understand the underlying deletion mechanisms.The two novel deletions were defined using polymerase chain reaction mapping and junction fragment sequencing. Bioinformatic analysis was performed on both the previously mapped (...) deletions and the novel ones through several web tools.In our two patients with nephrogenic diabetes insipidus, we found a 23 755 bp deletion and a 9264 bp deletion both comprising the entire AVPR2 gene and part of the ARHGAP4 gene. Through bioinformatic studies, the smallest overlapping region as well as several motifs and repeats that are known to promote rearrangements were confirmed.Through this study, it was determined that the deletion mechanisms in the AVPR2 region do not follow the rules of non

2012 Transplantation

73. Fanconi's Syndrome and Nephrogenic Diabetes Insipidus in an Adult Treated with Ifosfamide. (Abstract)

Fanconi's Syndrome and Nephrogenic Diabetes Insipidus in an Adult Treated with Ifosfamide. Fanconi's syndrome is a serious condition characterized by type II proximal renal tubular dysfunction, with urinary loss of glucose, amino acids, phosphate, bicarbonate, and potassium. Ifosfamide-induced Fanconi's syndrome is reported in about 1.4-5% of children being treated for solid tumors, yet only a few cases have been reported in adults. We describe a 54-year-old man who came to the hospital (...) with symptoms of neutropenic fever 4 days after his fourth cycle of ifosfamide and doxorubicin treatment for recurrent sarcoma with metastases to the lung. During admission, he was noted to have severe renal tubular dysfunction; ifosfamide-induced nephrogenic diabetes insipidus and Fanconi's syndrome were suspected. He received supportive therapy that resulted in incomplete resolution of signs and symptoms. The patient was discharged after a 5-day hospital stay when his white blood cell count increased from

2012 Pharmacotherapy

74. Inheritance of nephrogenic diabetes insipidus Full Text available with Trip Pro

Inheritance of nephrogenic diabetes insipidus 13197364 2003 05 01 2018 12 01 0002-9297 6 3 1954 Sep American journal of human genetics Am. J. Hum. Genet. Inheritance of nephrogenic diabetes insipidus. 354-8 WALKER N F NF RANCE C P CP eng Journal Article United States Am J Hum Genet 0370475 0002-9297 OM Databases, Genetic Diabetes Insipidus etiology Diabetes Insipidus, Nephrogenic Heredity Humans 5527:8998:137:216 DIABETES INSIPIDUS/etiology and pathogenesis HEREDITY 1954 9 1 1954 9 1 0 1 1954 9

1954 American Journal of Human Genetics

75. A Case of Nephrogenic Diabetes Insipidus Full Text available with Trip Pro

A Case of Nephrogenic Diabetes Insipidus 13572903 2000 07 01 2018 12 01 0007-1447 2 5099 1958 Sep 27 British medical journal Br Med J A case of nephrogenic diabetes insipidus. 780-1 GLASER L H LH eng Case Reports Journal Article England Br Med J 0372673 0007-1447 OM Diabetes Insipidus Diabetes Insipidus, Nephrogenic Diabetes Insipidus, Neurogenic Humans Medical Records 5935:2233:172 DIABETES INSIPIDUS/case reports 1958 9 27 1958 9 27 0 1 1958 9 27 0 0 ppublish 13572903 PMC2026293 Lancet. 1956

1958 British medical journal

76. Nephrogenic diabetes insipidus: absence of close linkage with Xg. Full Text available with Trip Pro

Nephrogenic diabetes insipidus: absence of close linkage with Xg. 5309332 1970 05 05 2018 11 13 0002-9297 22 2 1970 Mar American journal of human genetics Am. J. Hum. Genet. Nephrogenic diabetes insipidus: absence of close linkage with Xg. 221-7 Bode H H HH Miettinen O S OS eng Journal Article United States Am J Hum Genet 0370475 0002-9297 0 Isoantigens 11000-17-2 Vasopressins AIM IM Chromosome Mapping Color Vision Defects Diabetes Insipidus genetics Genotype Humans Isoantigens Kidney Tubules

1970 American Journal of Human Genetics

77. Failure to detect the carrier in congenital nephrogenic diabetes insipidus. Full Text available with Trip Pro

Failure to detect the carrier in congenital nephrogenic diabetes insipidus. 5018633 1972 06 22 2018 11 13 1468-2044 47 251 1972 Feb Archives of disease in childhood Arch. Dis. Child. Failure to detect the carrier in congenital nephrogenic diabetes insipidus. 137-9 Uttley W S WS Thistlethwaite D D eng Journal Article England Arch Dis Child 0372434 0003-9888 IM Adult Diabetes Insipidus congenital genetics urine Female Genotype Humans Infant, Newborn Male Middle Aged Osmolar Concentration Pedigree

1972 Archives of Disease in Childhood

78. Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies Full Text available with Trip Pro

Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies The physiological basis for the polyuria and polydipsia occurring in some manic-depressive patients treated with lithium salts was studied in vivo and in vitro. Three lithium-treated polyuric patients, in whom other causes of a concentrating defect were excluded, had abnormal urinary concentrating abilities after a standard water depreviation test. Two of these patients failed to respond to exogenous vasopressin (ADH (...) for the diabetes insipidus syndrome manifested by these three patients. The defect in water transport was further characterized in toad urinary bladders in vitro. Short-circuit current (I) and water flow (W) were studied under basal, ADH-stimulated, and cyclic adenosine 3',5'-monophosphate (c-AMP)-stimulated conditions. Increasing mucosal [Li(+)] progressively inhibited basal I, and both I and W induced by ADH. Significant inhibition of basal and ADH-induced I was observed at mucosal [Li(+)] < 1.1 mEq/liter

1972 Journal of Clinical Investigation

79. Nephrogenic Diabetes Insipidus: Effects of 3,5, Cyclic-adenosine Monophosphate Full Text available with Trip Pro

Nephrogenic Diabetes Insipidus: Effects of 3,5, Cyclic-adenosine Monophosphate 4343784 1973 01 18 2018 11 13 1468-2044 47 255 1972 Oct Archives of disease in childhood Arch. Dis. Child. Nephrogenic diabetes insipidus. Effects of 3,5, cyclic-adenosine monophosphate. 794-7 Jones N F NF Barraclough M A MA Barnes N N Cottom D G DG eng Journal Article England Arch Dis Child 0372434 0003-9888 11000-17-2 Vasopressins 8W8T17847W Urea 9NEZ333N27 Sodium AYI8EX34EU Creatinine E0399OZS9N Cyclic AMP IM (...) Adolescent Blood Pressure drug effects Child Creatinine urine Cyclic AMP administration & dosage therapeutic use Diabetes Insipidus drug therapy Glomerular Filtration Rate Humans Infant Injections, Intravenous Kidney Tubules abnormalities Osmolar Concentration Sodium urine Urea urine Urine Vasopressins therapeutic use 1972 10 1 1972 10 1 0 1 1972 10 1 0 0 ppublish 4343784 PMC1648252 Am J Physiol. 1966 Jul;211(1):255-9 5911047 Am J Physiol. 1967 Apr;212(4):939-44 6024462 Clin Sci. 1968 Apr;34(2):253-60

1972 Archives of Disease in Childhood

80. A non-invasive test for receptor binding applied to nephrogenic diabetes insipidus. Full Text available with Trip Pro

A non-invasive test for receptor binding applied to nephrogenic diabetes insipidus. Studies in animals have determined the importance of specific receptors to the action of many hormones and drugs. In man, a non-invasive external counting technique has been used and absence of receptor function has been demonstrated in a patient with nephrogenic diabetes insipidus using radioactively labelled arginine vasopressin. This is in contrast to the findings in a patient with pituitary diabetes (...) insipidus and a normal control. These results suggest a model for the study of hormone and drug kinetics in man avoiding multiple samplings of biological fluids.

1977 Postgraduate medical journal

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