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Nephrogenic Diabetes Insipidus

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21. Diabetes insipidus

of both types. Both types of DI may be associated with hypernatraemia, and this may present as a medical emergency. Treatment goals are correction of any pre-existing water deficits and reduction in ongoing excessive urinary water losses. In central DI, desmopressin (DDAVP) is the treatment of choice. Nephrogenic DI is treated with an adequate fluid intake; salt restriction and diuretics may help reduce polyuria. Definition Diabetes insipidus (DI) is a metabolic disorder characterised by defective (...) . In: Kronenberg H, Melmed S, Polonsky K, et al., eds. Williams Textbook of endocrinology. 11th ed. Philadelphia, PA: Saunders Elsevier; 2008:263-287. Sands JM, Bichet DG; American College of Physicians; American Physiological Society. Nephrogenic diabetes insipidus. Ann Intern Med. 2006;144:186-194. http://www.ncbi.nlm.nih.gov/pubmed/16461963?tool=bestpractice.com History and exam presence of risk factors polyuria increased thirst/polydipsia nocturia non-specific CNS symptoms of hypernatraemia signs of volume

2017 BMJ Best Practice

22. Hypercalcemia induces targeted autophagic degradation of aquaporin-2 at the onset of nephrogenic diabetes insipidus. Full Text available with Trip Pro

Hypercalcemia induces targeted autophagic degradation of aquaporin-2 at the onset of nephrogenic diabetes insipidus. Hypercalcemia can cause renal dysfunction such as nephrogenic diabetes insipidus (NDI), but the mechanisms underlying hypercalcemia-induced NDI are not well understood. To elucidate the early molecular changes responsible for this disorder, we employed mass spectrometry-based proteomic analysis of inner medullary collecting ducts (IMCD) isolated from parathyroid hormone-treated

2017 Kidney International

23. Nephrogenic diabetes insipidus. Full Text available with Trip Pro

Nephrogenic diabetes insipidus. In nephrogenic diabetes insipidus (NDI), the kidney is unable to concentrate urine despite elevated concentrations of the antidiuretic hormone arginine-vasopressin. In congenital NDI, polyuria and polydipsia are present from birth and should be immediately recognized to avoid severe episodes of dehydration. Unfortunately, NDI is still often recognized late after a 'diagnostic odyssey' involving false leads and dangerous treatments.Once diagnosed, appropriate

2017 Current Opinion in Pediatrics

24. Prasugrel suppresses development of lithium-induced nephrogenic diabetes insipidus in mice Full Text available with Trip Pro

Prasugrel suppresses development of lithium-induced nephrogenic diabetes insipidus in mice Previously, we localized ADP-activated P2Y12 receptor (R) in rodent kidney and showed that its blockade by clopidogrel bisulfate (CLPD) attenuates lithium (Li)-induced nephrogenic diabetes insipidus (NDI). Here, we evaluated the effect of prasugrel (PRSG) administration on Li-induced NDI in mice. Both CLPD and PRSG belong to the thienopyridine class of ADP receptor antagonists. Groups of age-matched adult

2017 Purinergic signalling

25. Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus Full Text available with Trip Pro

Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus NF-E2-related factor-2 (Nrf2) regulates cellular responses to oxidative and electrophilic stress. Loss of Keap1 increases Nrf2 protein levels, and Keap1-null mice die of oesophageal hyperkeratosis because of Nrf2 hyperactivation. Here we show that deletion of oesophageal Nrf2 in Keap1-null mice allows survival until adulthood, but the animals develop polyuria with low osmolality and bilateral (...) hydronephrosis. This phenotype is caused by defects in water reabsorption that are the result of reduced aquaporin 2 levels in the kidney. Renal tubular deletion of Keap1 promotes nephrogenic diabetes insipidus features, confirming that Nrf2 activation in developing tubular cells causes a water reabsorption defect. These findings suggest that Nrf2 activity should be tightly controlled during development in order to maintain renal homeostasis. In addition, tissue-specific ablation of Nrf2 in Keap1-null mice

2017 Nature communications

26. Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus Full Text available with Trip Pro

Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus Psychiatric patients treated with lithium (Li+) may develop nephrogenic diabetes insipidus (NDI). Although the etiology of Li+-induced NDI (Li-NDI) is poorly understood, it occurs partially due to reduced aquaporin-2 (AQP2) expression in the kidney collecting ducts. A mechanism postulated for this is that Li+ inhibits adenylyl cyclase (AC) activity, leading to decreased cAMP, reduced AQP2 abundance

2017 JCI insight

27. Functional characterization of AVPR2 mutants found in Turkish patients with nephrogenic diabetes insipidus Full Text available with Trip Pro

Functional characterization of AVPR2 mutants found in Turkish patients with nephrogenic diabetes insipidus Diabetes insipidus is a rare disorder characterized by an impairment in water balance because of the inability to concentrate urine. While central diabetes insipidus is caused by mutations in the AVP, the reason for genetically determined nephrogenic diabetes insipidus can be mutations in AQP2 or AVPR2 After release of AVP from posterior pituitary into blood stream, it binds to AVPR2 (...) , which is one of the receptors for AVP and is mainly expressed in principal cells of collecting ducts of kidney. Receptor activation increases cAMP levels in principal cells, resulting in the incorporation of AQP2 into the membrane, finally increasing water reabsorption. This pathway can be altered by mutations in AVPR2 causing nephrogenic diabetes insipidus. In this study, we functionally characterize four mutations (R68W, ΔR67-G69/G107W, V162A and T273M) in AVPR2, which were found in Turkish

2017 Endocrine connections

28. Hereditary Nephrogenic Diabetes Insipidus: Pathophysiology and Possible Treatment. An Update Full Text available with Trip Pro

Hereditary Nephrogenic Diabetes Insipidus: Pathophysiology and Possible Treatment. An Update Under physiological conditions, excessive loss of water through the urine is prevented by the release of the antidiuretic hormone arginine-vasopressin (AVP) from the posterior pituitary. In the kidney, AVP elicits a number of cellular responses, which converge on increasing the osmotic reabsorption of water in the collecting duct. One of the key events triggered by the binding of AVP to its type-2 (...) receptor (AVPR2) is the exocytosis of the water channel aquaporin 2 (AQP2) at the apical membrane the principal cells of the collecting duct. Mutations of either AVPR2 or AQP2 result in a genetic disease known as nephrogenic diabetes insipidus, which is characterized by the lack of responsiveness of the collecting duct to the antidiuretic action of AVP. The affected subject, being incapable of concentrating the urine, presents marked polyuria and compensatory polydipsia and is constantly at risk

2017 International journal of molecular sciences

29. Novel de novo AVPR2 Variant in a Patient with Congenital Nephrogenic Diabetes Insipidus Full Text available with Trip Pro

Novel de novo AVPR2 Variant in a Patient with Congenital Nephrogenic Diabetes Insipidus Early diagnosis and treatment of congenital nephrogenic diabetes insipidus (CNDI) are essential due to the risk of intellectual disability caused by repeated episodes of dehydration and rapid rehydration. Timely genetic testing for disease-causing variants in the arginine vasopressin receptor 2 (AVPR2) gene is possible in at-risk newborns with a known family history of X-linked CNDI. In this study, a Swedish

2017 Case Reports in Nephrology and Dialysis

30. Aliskiren Increases Aquaporin-2 Expression and Attenuates Lithium-induced Nephrogenic Diabetes Insipidus. Full Text available with Trip Pro

Aliskiren Increases Aquaporin-2 Expression and Attenuates Lithium-induced Nephrogenic Diabetes Insipidus. The direct renin inhibitor aliskiren has been shown to be retained and persist in medullary collecting ducts even after treatment is discontinued, suggesting a new mechanism of action for this drug. The purpose of the present study was to investigate whether aliskiren regulates renal aquaporin expression in the collecting ducts and improves urinary concentrating defect induced by lithium (...) protein expression in inner medullary collecting duct principal cells and prevents lithium-induced nephrogenic diabetes insipidus likely via cAMP-PKA pathways.Copyright © 2017 the American Physiological Society.

2017 American Journal of Physiology. Renal physiology

31. A novel SLC12A1 gene mutation associated with hyperparathyroidism, hypercalcemia, nephrogenic diabetes insipidus, and nephrocalcinosis in four patients. (Abstract)

A novel SLC12A1 gene mutation associated with hyperparathyroidism, hypercalcemia, nephrogenic diabetes insipidus, and nephrocalcinosis in four patients. Solute Carrier Family 12 member 1 (SLC12A1) gene encodes the sodium-potassium-chloride co-transporter (NKCC2) at the apical membrane of the thick ascending loop of Henle (TAL). Bartter's syndrome (BS) type I is a rare, autosomal recessive, renal tubular disorder associated with mutation of the SLC12A1 gene. Presenting features include (...) , hypercalcemia, hypokalemic metabolic alkalosis, nephrocalcinosis, and nephrogenic diabetes insipidus. The link between calcium and parathyroid hormone abnormalities in patients with SLC12A1 mutations is unclear; the cases described suggest an association between primary hyperparathyroidism and loss of function mutation of SLC12A1, which may result in an aberrant threshold of the calcium sensing receptor at the level of the kidney.Copyright © 2017 Elsevier Inc. All rights reserved.

2017 Bone

32. 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

2018 FP Notebook

34. A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus. Full Text available with Trip Pro

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

35. Bendamustine-Induced Nephrogenic Diabetes Insipidus in a Patient With AL Amyloidosis. (Abstract)

Bendamustine-Induced Nephrogenic Diabetes Insipidus in a Patient With AL Amyloidosis. Nephrogenic diabetes insipidus is a condition characterized by polyuria with dilute urine due to the inability of the principal cells of the renal collecting ducts to respond to antidiuretic hormone and concentrate urine. Nephrogenic diabetes insipidus can be drug induced, and several chemotherapeutic agents have been reported to cause it. Bendamustine is a traditional chemotherapeutic agent being studied (...) for treatment for relapsed systemic AL amyloidosis. We report a case of a 59-year-old man with AL amyloidosis who developed partial nephrogenic diabetes insipidus after receiving bendamustine for treatment of AL amyloidosis. The nephrogenic diabetes insipidus responded well to sodium restriction, hydrochlorothiazide, and desmopressin treatment, allowing the patient to receive subsequent bendamustine cycles without polyuria. Nephrogenic diabetes insipidus resolved shortly after completion of bendamustine

2016 American Journal of Kidney Diseases

36. Congenital Nephrogenic Diabetes Insipidus Presented With Bilateral Hydronephrosis and Urinary Infection: A Case Report. Full Text available with Trip Pro

Congenital Nephrogenic Diabetes Insipidus Presented With Bilateral Hydronephrosis and Urinary Infection: A Case Report. Nephrogenic diabetes insipidus (NDI) is a condition resulting from the kidney's impaired response to circulating antidiuretic hormone (ADH), leading to polydipsia and polyuria. Urinary tract dilatation caused by NDI is a rare situation. Here, we report a case of congenital NDI presented with bilateral hydronephrosis.A 15-year-old boy complaining a history of intermittent fever (...) was admitted to Peking Union Medical College Hospital. He voided 10 to 15 L of urine daily. Radiographic examination revealed severe dilatation of bilateral renal pelvis, ureter, and bladder. Urinalysis shows hyposthenuria.He was diagnosed NDI since born. Transient insertion of a urethral catheter helped to relieve fever. Medical therapy of hydrochlorothiazide and amiloride was prescribed and effective.Dilatation of urinary tract caused by diabetes insipidus is rare, but may be present in severe condition

2016 Medicine

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

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

38. 4-PBA Improves Lithium-induced Nephrogenic Diabetes Insipidus by Attenuating ER Stress. Full Text available with Trip Pro

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

39. Analysis of the V2 Vasopressin Receptor (V2R) Mutations Causing Partial Nephrogenic Diabetes Insipidus Highlights a Sustainable Signaling by a Non-peptide V2R Agonist Full Text available with Trip Pro

Analysis of the V2 Vasopressin Receptor (V2R) Mutations Causing Partial Nephrogenic Diabetes Insipidus Highlights a Sustainable Signaling by a Non-peptide V2R Agonist Disease-causing mutations in G protein-coupled receptor (GPCR) genes, including the V2 vasopressin receptor (V2R) gene, often cause misfolded receptors, leading to a defect in plasma membrane trafficking. A novel V2R mutation, T273M, identified in a boy with partial nephrogenic diabetes insipidus (NDI), shows intracellular

2016 The Journal of biological chemistry

40. A novel mutation affecting the arginine‐137 residue of AVPR2 in dizygous twins leads to nephrogenic diabetes insipidus and attenuated urine exosome aquaporin‐2 Full Text available with Trip Pro

A novel mutation affecting the arginine‐137 residue of AVPR2 in dizygous twins leads to nephrogenic diabetes insipidus and attenuated urine exosome aquaporin‐2 Mutations in the vasopressin V2 receptor gene AVPR2 may cause X-linked nephrogenic diabetes insipidus by defective apical insertion of aquaporin-2 in the renal collecting duct principal cell. Substitution mutations with exchange of arginine at codon 137 can cause nephrogenic syndrome of inappropriate antidiuresis or congenital X (...) -linked nephrogenic diabetes insipidus. We present a novel mutation in codon 137 within AVPR2 with substitution of glycine for arginine in male dizygotic twins. Nephrogenic diabetes insipidus was demonstrated by water deprivation test and resistance to vasopressin administration. While a similar urine exosome release rate was shown between probands and controls by western blotting for the marker ALIX, there was a selective decrease in exosome aquaporin-2 versus aquaporin-1 protein in probands compared

2016 Physiological reports

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