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nephrogenic diabetes insipidus

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https://www.readbyqxmd.com/read/28645353/actualit%C3%A3-s-autour-de-la-prise-en-charge-des-diab%C3%A3-tes-insipides-centraux-management-of-central-diabetes-insipidus-in-2016
#1
H Lasolle, F Borson-Chazot
Diabetes insipidus is a syndrome that associates both hypotonic polyuria and polydipsia, due to insufficient or ineffective arginine vasopressin (AVP) synthesis, or to AVP resistance. The diagnosis between central/renal origin, or an abnormal thirst regulation (primary polydipsia) is required to organize an adapted management. Because water deprivation tests are not reliable, it's often based on medical history, response to treatment and MRI. Copeptin is an AVP precursor which could be very helpful for the diagnosis...
October 2016: Annales D'endocrinologie
https://www.readbyqxmd.com/read/28615247/lithium-induced-ndi-acetazolamide-reduces-polyuria-but-does-not-improve-urine-concentrating-ability
#2
Theun de Groot, Joan Doornebal, Birgitte M Christensen, Simone C Cockx, Anne P Sinke, Ruben Baumgarten, Jennifer J Bedford, Robert J Walker, Jack F Wetzels, Peter M T Deen
Lithium is the mainstay treatment for patients with bipolar disorder, but generally causes nephrogenic diabetes insipidus (NDI), a disorder in which the renal urine concentrating ability has become vasopressin-insensitive. Li-NDI is caused by lithium uptake by collecting duct principal cells and downregulation of AQP2 water channels, which are essential for water uptake from pro-urine. Recently, we found that the prophylactic administration of acetazolamide to mice effectively attenuated Li-NDI. To evaluate whether acetazolamide might benefit lithium-treated patients, we administered acetazolamide to mice with established Li-NDI and six patients with a lithium-induced urinary concentrating defect...
June 14, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28577072/regulation-of-renal-na-k-cl-cotransporters-by-vasopressin
#3
REVIEW
Sebastian Bachmann, Kerim Mutig
Vasopressin (AVP) induces antidiuresis, thus playing an essential role in body water and electrolyte homeostasis. Its antidiuretic effects are mediated chiefly by V2 vasopressin receptors (V2R) expressed along the distal nephron and collecting duct epithelia. NaCl reabsorption in the distal nephron, which includes the thick ascending limb (TAL) and distal convoluted tubule (DCT), largely depends on the activity of two structurally related Na-(K)-Cl cotransporters, NKCC2 in TAL and NCC in DCT. AVP-induced activation of these transporters contributes to urine concentration and renal electrolyte reabsorption...
June 2, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28577018/a-case-of-kidney-involvement-in-primary-sj%C3%A3-gren-s-syndrome
#4
Farid Arman, Hania Shakeri, Niloofar Nobakht, Anjay Rastogi, Mohammad Kamgar
BACKGROUND Sjögren's syndrome is an autoimmune disorder caused by the infiltration of monocytes in epithelial glandular and extra-glandular tissues. Hallmark presentations include mouth and eye dryness. Although renal involvement is uncommon in primary Sjögren's syndrome (pSS), patients may experience renal tubular acidosis type I (RTA I), tubulointerstitial nephritis, diabetes insipidus (DI), nephrolithiasis, and Fanconi syndrome. However, it is atypical to see more than 1 of these manifestations in a single patient...
June 3, 2017: American Journal of Case Reports
https://www.readbyqxmd.com/read/28504419/congenital-nephrogenic-diabetes-insipidus-complicated-with-hinman-syndrome
#5
Jiro Kino, Junji Takaya, Sachiyo Tanaka, Takahide Nakano, Kazunari Kaneko
No abstract text is available yet for this article.
May 15, 2017: Pediatrics International: Official Journal of the Japan Pediatric Society
https://www.readbyqxmd.com/read/28476225/genetics-of-diabetes-insipidus
#6
REVIEW
Marie Helene Schernthaner-Reiter, Constantine A Stratakis, Anton Luger
Diabetes insipidus is a disease characterized by polyuria and polydipsia due to inadequate release of arginine vasopressin from the posterior pituitary gland (neurohypophyseal diabetes insipidus) or due to arginine vasopressin insensitivity by the renal distal tubule, leading to a deficiency in tubular water reabsorption (nephrogenic diabetes insipidus). This article reviews the genetics of diabetes insipidus in the context of its diagnosis, clinical presentation, and therapy.
June 2017: Endocrinology and Metabolism Clinics of North America
https://www.readbyqxmd.com/read/28409346/development-and-diseases-of-the-collecting-duct-system
#7
Lihe Chen, Paul J Higgins, Wenzheng Zhang
The collecting duct of the mammalian kidney is important for the regulation of extracellular volume, osmolarity, and pH. There are two major structurally and functionally distinct cell types: principal cells and intercalated cells. The former regulates Na(+) and water homeostasis, while the latter participates in acid-base homeostasis. In vivo lineage tracing using Cre recombinase or its derivatives such as CreGFP and CreER(T2) is a powerful new technique to identify stem/progenitor cells in their native environment and to decipher the origins of the tissue that they give rise to...
2017: Results and Problems in Cell Differentiation
https://www.readbyqxmd.com/read/28405619/role-of-adenylyl-cyclase-6-in-the-development-of-lithium-induced-nephrogenic-diabetes-insipidus
#8
Søren Brandt Poulsen, Tina Bøgelund Kristensen, Heddwen L Brooks, Donald E Kohan, Timo Rieg, Robert A Fenton
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, and less membrane targeting. We hypothesized that Li-NDI would not develop in mice lacking AC6. Whole-body AC6 knockout (AC6(-/-)) mice and potentially novel connecting tubule/principal cell-specific AC6 knockout (AC6(loxloxCre)) mice had approximately 50% lower urine osmolality and doubled water intake under baseline conditions compared with controls...
April 6, 2017: JCI Insight
https://www.readbyqxmd.com/read/28285303/bartter-syndrome-with-nephrogenic-diabetes-insipidus-and-vitamin-d-resistant-rickets
#9
Sriram Krishnamurthy, Anbazhagan Jagadeesh
No abstract text is available yet for this article.
February 15, 2017: Indian Pediatrics
https://www.readbyqxmd.com/read/28276300/value-of-renal-biopsy-in-diagnosing-infantile-nephropathic-cystinosis-associated-with-secondary-nephrogenic-diabetes-insipidus
#10
Emily Joyce, Jacqueline Ho, Areeg El-Gharbawy, Cláudia M Salgado, Sarangarajan Ranganathan, Miguel Reyes-Múgica
Cystinosis is the most common cause of inherited renal Fanconi syndrome in young children, and typically presents with laboratory findings of a proximal tubulopathy and corneal crystals by one year of age. We describe here renal biopsy findings in a 20-month-old patient with an atypical presentation of distal renal tubular acidosis, diabetes insipidus, and the absence of corneal crystals. Although renal biopsy is usually not necessary to establish the diagnosis of cystinosis, when the patient presents with atypical signs and symptoms, a renal biopsy may be extremely valuable...
January 2017: Pediatric and Developmental Pathology
https://www.readbyqxmd.com/read/28258576/diabetes-insipidus
#11
H A Jenny Lu
Disruption of water and electrolyte balance is frequently encountered in clinical medicine. Regulating water metabolism is critically important. Diabetes insipidus (DI) presented with excessive water loss from the kidney is a major disorder of water metabolism. To understand the molecular and cellular mechanisms and pathophysiology of DI and rationales of clinical management of DI is important for both research and clinical practice. This chapter will first review various forms of DI focusing on central diabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI ) ...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28228402/aliskiren-increases-aquaporin-2-expression-and-attenuates-lithium-induced-nephrogenic-diabetes-insipidus
#12
Yu Lin, Tiezheng Zhang, Pinning Feng, Miaojuan Qiu, Qiaojuan Liu, Suchun Li, Peili Zheng, Yonglun Kong, Moshe Levi, Chunling Li, Weidong Wang
The direct renin inhibitor aliskiren has been shown to retain and persist in medullary collecting ducts even after treatment was 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 in mice. The mice were either fed with normal chow or LiCl diet (40mM/kg dry food/day for 4 days and 20mM/kg dry food/day for last 3 days) for seven days...
February 22, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28139295/hypercalcemia-induces-targeted-autophagic-degradation-of-aquaporin-2-at-the-onset-of-nephrogenic-diabetes-insipidus
#13
Sookkasem Khositseth, Komgrid Charngkaew, Chatikorn Boonkrai, Poorichaya Somparn, Panapat Uawithya, Nusara Chomanee, D Michael Payne, Robert A Fenton, Trairak Pisitkun
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 rats at onset of hypercalcemia-induced NDI. Forty-one proteins, including the water channel aquaporin-2, exhibited significant changes in abundance, most of which were decreased...
January 27, 2017: Kidney International
https://www.readbyqxmd.com/read/28134709/nephrogenic-diabetes-insipidus
#14
D Bockenhauer, Daniel G Bichet
PURPOSE OF REVIEW: 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 treatment can be started...
April 2017: Current Opinion in Pediatrics
https://www.readbyqxmd.com/read/28108651/roflumilast-and-aquaporin-2-regulation-in-rat-renal-inner-medullary-collecting-duct
#15
Ezigbobiara N Umejiego, Yanhua Wang, Mark A Knepper, Chung-Lin Chou
Roflumilast is a cyclic nucleotide phosphodiesterase inhibitor that is FDA-approved for treatment of chronic obstructive pulmonary disease. With a view toward possible use for treatment of patients with X-linked nephrogenic diabetes insipidus (NDI) due to hemizygous mutations in the V2 vasopressin receptor, this study sought to determine the effect of roflumilast on aquaporin-2 (AQP2) phosphorylation, AQP2 trafficking, and water permeability in the rat inner medullary collecting duct (IMCD). In the presence of the vasopressin analog dDAVP (0...
January 2017: Physiological Reports
https://www.readbyqxmd.com/read/28095294/a-novel-slc12a1-gene-mutation-associated-with-hyperparathyroidism-hypercalcemia-nephrogenic-diabetes-insipidus-and-nephrocalcinosis-in-four-patients
#16
Sariya Wongsaengsak, Alaina P Vidmar, Ananta Addala, Elaine S Kamil, Paola Sequeira, Benjamin Fass, Pisit Pitukcheewanont
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: hypokalemic metabolic alkalosis, hypercalciuria and nephrocalcinosis. The many allelic variants reported present with a spectrum of phenotypes, biochemical abnormalities and clinical severities...
April 2017: Bone
https://www.readbyqxmd.com/read/28052875/liver-x-receptor-%C3%AE-increases-aquaporin-2-protein-level-via-a-posttranscriptional-mechanism-in-renal-collecting-ducts
#17
Wen Su, Shi-Zheng Huang, Min Gao, Xiao-Mu Kong, Jan-Åke Gustafsson, Su-Juan Xu, Bing Wang, Feng Zheng, Li-Hong Chen, Nan-Ping Wang, You-Fei Guan, Xiao-Yan Zhang
Liver X receptors (LXRs) including LXRα and LXRβ are nuclear receptor transcription factors and play an important role in lipid and glucose metabolism. It has been previously reported that mice lacking LXRβ but not LXRα develop a severe urine concentrating defect, likely via a central mechanism. Here we provide evidence that LXRβ regulates water homeostasis through increasing aquaporin 2 (AQP2) protein levels in renal collecting ducts. LXRβ(-/-) mice exhibited a reduced response to desmopressin (dDAVP) stimulation, suggesting that the diabetes insipidus phenotype is of both central and nephrogenic origin...
April 1, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27959610/acetazolamide-in-lithium-induced-nephrogenic-diabetes-insipidus
#18
LETTER
Craig E Gordon, Swapna Vantzelfde, Jean M Francis
No abstract text is available yet for this article.
November 17, 2016: New England Journal of Medicine
https://www.readbyqxmd.com/read/27906863/bartter-s-and-gitelman-s-syndrome
#19
Hannsjörg W Seyberth, Stefanie Weber, Martin Kömhoff
PURPOSE OF REVIEW: The clinical presentations of Bartter's syndrome and Gitelman's syndrome will be reviewed including two most recently described hypokalemic salt-losing tubulopathies. By taking the quite heterogeneous presentations and the apparently different pathophysiologies as the basis, the applicability of the physiologic classification has been tested. RECENT FINDINGS: According to the physiologic approach, salt-losing tubulopathies can be divided into two major groups (with completely different tubular defects): first, disorders of the thick ascending limb of Henle's loop (loop disorders); second, disorders of the distal convolute tubule (DCT disorders)...
April 2017: Current Opinion in Pediatrics
https://www.readbyqxmd.com/read/27892464/wnt5a-induces-renal-aqp2-expression-by-activating-calcineurin-signalling-pathway
#20
Fumiaki Ando, Eisei Sohara, Tetsuji Morimoto, Naofumi Yui, Naohiro Nomura, Eriko Kikuchi, Daiei Takahashi, Takayasu Mori, Alain Vandewalle, Tatemitsu Rai, Sei Sasaki, Yoshiaki Kondo, Shinichi Uchida
Heritable nephrogenic diabetes insipidus (NDI) is characterized by defective urine concentration mechanisms in the kidney, which are mainly caused by loss-of-function mutations in the vasopressin type 2 receptor. For the treatment of heritable NDI, novel strategies that bypass the defective vasopressin type 2 receptor are required to activate the aquaporin-2 (AQP2) water channel. Here we show that Wnt5a regulates AQP2 protein expression, phosphorylation and trafficking, suggesting that Wnt5a is an endogenous ligand that can regulate AQP2 without the activation of the classic vasopressin/cAMP signalling pathway...
November 28, 2016: Nature Communications
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