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Nephrogenic Diabetes Insipidus

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61. Soluble (Pro)Renin Receptor as a Potential Therapy for Diabetes Insipidus. (PubMed)

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

62. The soluble (Pro) renin receptor does not influence lithium‐induced diabetes insipidus but does provoke beiging of white adipose tissue in mice (PubMed)

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

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2017 Physiological reports

63. Hydrochorothiazide attenuates lithium-induced Nephrogenic Diabetes Insipidus independently of the sodium-chloride co-transporter. (PubMed)

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

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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. (PubMed)

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

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2013 American Journal of Physiology. Renal physiology

65. Inherited secondary nephrogenic diabetes insipidus: Concentrating on humans. (PubMed)

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

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2013 American Journal of Physiology. Renal physiology

66. Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment. (PubMed)

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

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2013 Endocrine Reviews

67. Membrane Protein Stability Analyses by Means of Protein Energy Profiles in Case of Nephrogenic Diabetes Insipidus (PubMed)

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

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2012 Computational and mathematical methods in medicine

68. Vasopressin increases S261 phosphorylation in AQP2-P262L, a mutant in recessive nephrogenic diabetes insipidus. (PubMed)

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

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2012 Transplantation

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

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

70. Congenital nephrogenic diabetes insipidus: the current state of affairs. (PubMed)

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

71. Novel compound aquaporin 2 mutations in nephrogenic diabetes insipidus (PubMed)

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

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2012 Clinics

72. 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

73. Two new large deletions of the AVPR2 gene causing nephrogenic diabetes insipidus and a review of previously published deletions. (PubMed)

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

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2012 Transplantation

74. 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 (PubMed)

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

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2011 NDT Plus

75. Functional characterization of novel loss-of-function mutations in the vasopressin type 2 receptor gene causing nephrogenic diabetes insipidus. (PubMed)

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

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2011 Transplantation

76. Studies with angiotensin in nephrogenic diabetes insipidus. (PubMed)

Studies with angiotensin in nephrogenic diabetes insipidus. 4293073 1967 12 15 2018 11 13 0008-4409 97 14 1967 Sep 30 Canadian Medical Association journal Can Med Assoc J Studies with angiotensin in nephrogenic diabetes insipidus. 841-5 Orr F R FR Filipich R L RL eng Case Reports Comparative Study Journal Article Canada Can Med Assoc J 0414110 0008-4409 11000-17-2 Vasopressins 11128-99-7 Angiotensin II 9NEZ333N27 Sodium AYI8EX34EU Creatinine RWP5GA015D Potassium AIM IM Adult Angiotensin II (...) therapeutic use Blood Pressure drug effects Creatinine Diabetes Insipidus drug therapy genetics Female Humans Kidney Failure, Chronic genetics Kidney Function Tests Male Potassium urine Sodium urine Vasopressins therapeutic use 1967 9 30 1967 9 30 0 1 1967 9 30 0 0 ppublish 4293073 PMC1923438 Lancet. 1965 Nov 13;2(7420):987-8 4159217 Can Med Assoc J. 1961 Feb 25;84:403-19 13704363 J Clin Invest. 1955 Sep;34(9):1410-6 13252088 J Clin Invest. 1965 Jul;44:1171-86 14328394 Proc R Soc Med. 1965 Dec;58(12):1005

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1967 Canadian Medical Association Journal

77. Nephrogenic diabetes insipidus induced by demethylchlortetracycline (Declomycin). (PubMed)

Nephrogenic diabetes insipidus induced by demethylchlortetracycline (Declomycin). 4966354 1968 04 27 2018 11 13 0008-1264 107 5 1967 Nov California medicine Calif Med Nephrogenic diabetes insipidus induced by demethylchlortetracycline (Declomycin). 420-2 Torin D E DE eng Case Reports Journal Article United States Calif Med 0410260 0008-1264 5R5W9ICI6O Demeclocycline IM Adult Demeclocycline adverse effects Diabetes Insipidus chemically induced Female Humans Kidney Diseases chemically induced

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1967 California Medicine

78. A non-invasive test for receptor binding applied to nephrogenic diabetes insipidus. (PubMed)

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.

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1977 Postgraduate medical journal

79. Nephrogenic diabetes insipidus and Werdnig-Hoffmann disease in a child: an unusual association. (PubMed)

Nephrogenic diabetes insipidus and Werdnig-Hoffmann disease in a child: an unusual association. The unusual association of Werdnig-Hoffmann disease and nephrogenic diabetes insipidus in a 5-month-old child is described for the first time. The association is casual, considering the different pathways of genetical transmission in these two diseases. The possibility of identifying the heterozygote is discussed and it appears to be limited to nephrogenic diabetes insipidus.

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1978 Journal of Medical Genetics

80. Congenital nephrogenic diabetes insipidus in a baby girl. (PubMed)

Congenital nephrogenic diabetes insipidus in a baby girl. A 6-week-old girl with fever, hypernatraemia, dehydration, and polyuria failed to concentrate urine in response to exogenous vasopressin administration. There was no family history of nephrogenic diabetes insipidus. When she was 15 months old, the infusion of vasopressin did not produce an increase in urinary cyclic-AMP.

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1978 Archives of Disease in Childhood

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