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nephrogenic diabetes insipidus

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https://www.readbyqxmd.com/read/28285303/bartter-syndrome-with-nephrogenic-diabetes-insipidus-and-vitamin-d-resistant-rickets
#1
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
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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...
January 14, 2017: Bone
https://www.readbyqxmd.com/read/28052875/liver-x-receptor-%C3%AE-lxr%C3%AE-increases-aqp2-protein-level-via-a-post-transcriptional-mechanism-in-renal-collecting-ducts
#9
Wen Su, Shi-Zheng Huang, Min Gao, Xiao-Mu Kong, Jan-Ake 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 dDAVP stimulation, suggesting that the diabetes insipidus phenotype is of both central and nephrogenic origin...
January 4, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27959610/acetazolamide-in-lithium-induced-nephrogenic-diabetes-insipidus
#10
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
#11
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)...
November 30, 2016: Current Opinion in Pediatrics
https://www.readbyqxmd.com/read/27892464/wnt5a-induces-renal-aqp2-expression-by-activating-calcineurin-signalling-pathway
#12
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
https://www.readbyqxmd.com/read/27793629/microsecond-simulation-of-human-aquaporin-2-reveals-structural-determinants-of-water-permeability-and-selectivity
#13
Siladitya Padhi, U Deva Priyakumar
Human aquaporin 2 (AQP2) from the family of aquaporins assumes great physiological importance, owing to its association with nephrogenic diabetes insipidus (NDI). The present study provides detailed insights into the transport properties of AQP2 with the use of microsecond-scale molecular dynamics simulations, and explains how these channels conduct water molecules while at the same time excluding other molecules. Water transport is seen to be diffusion-limited, with a barrier of only 1.6kcalmol(-1), and the channel is more water-permeable than other known aquaporins...
January 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27780577/bendamustine-induced-nephrogenic-diabetes-insipidus-in%C3%A2-a%C3%A2-patient-with-al-amyloidosis
#14
Nsabimana A Uwumugambi, Vaishali Sanchorawala, Anthony C Shelton, Lauren Stern, Craig E Gordon
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...
October 22, 2016: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
https://www.readbyqxmd.com/read/27742514/transient-diabetes-insipidus-after-discontinuation-of-vasopressin-in-neurological-intensive-care-unit-patients-case-series-and-literature-review
#15
Michael A Bohl, James Forseth, Peter Nakaji
BACKGROUND: Arginine vasopressin (AVP) is a common second-line or third-line vasopressor used in critically ill neurosurgical patients. Neurosurgical indications include hyperdynamic therapy for vasospasm, maintenance of cerebral perfusion pressure in patients with intracranial hypertension, and prevention of hypotension in patients with sepsis. CASE DESCRIPTION: A series of 6 neurosurgical patients receiving AVP infusions developed severe but transient diabetes insipidus (tDI) after cessation of AVP...
January 2017: World Neurosurgery
https://www.readbyqxmd.com/read/27719738/bendamustine-induced-nephrogenic-diabetes-insipidus%C3%A2
#16
Benjamin A Derman, Milli Jain, Elizabeth A McAninch, Casey Gashti
A 59-year-old man presented with polyuria and polydipsia immediately following his sixth cycle of rituximab and bendamustine for chronic lymphocytic leukemia. He initially compensated by increasing his oral fluid intake at home, but later developed septic shock and was admitted with orders to be kept nil per os (NPO). This prompted an episode of acute hypernatremia during which he exhibited continued polyuria with inappropriately dilute urine. Desmopressin challenge yielded no response in the urine osmolality, indicating a nephrogenic source of his diabetes insipidus (DI)...
January 2017: Clinical Nephrology
https://www.readbyqxmd.com/read/27694161/egf-receptor-inhibition-by-erlotinib-increases-aquaporin-2-mediated-renal-water-reabsorption
#17
Pui W Cheung, Naohiro Nomura, Anil V Nair, Nutthapoom Pathomthongtaweechai, Lars Ueberdiek, Hua A Jenny Lu, Dennis Brown, Richard Bouley
Nephrogenic diabetes insipidus (NDI) is caused by impairment of vasopressin (VP) receptor type 2 signaling. Because potential therapies for NDI that target the canonical VP/cAMP/protein kinase A pathway have so far proven ineffective, alternative strategies for modulating aquaporin 2 (AQP2) trafficking have been sought. Successful identification of compounds by our high-throughput chemical screening assay prompted us to determine whether EGF receptor (EGFR) inhibitors stimulate AQP2 trafficking and reduce urine output...
October 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27682266/amiloride-modifies-the-progression-of-lithium-induced-renal-interstitial-fibrosis
#18
Priyakshi Kalita-DE Croft, Jennifer J Bedford, John P Leader, Robert J Walker
AIM: Long-term administration of lithium has been associated with the development of a chronic interstitial fibrosis in addition to nephrogenic diabetes insipidus (NDI). Earlier studies have demonstrated that amiloride, by blocking the epithelial sodium channel ENaC and thus preventing lithium uptake into the principal cells of the collecting ducts, can partially reverse lithium-induced NDI. However, there are no long-term studies examining whether or not amiloride also modifies the progressive chronic interstitial fibrosis and tubular atrophy often evident with long term lithium exposure...
September 28, 2016: Nephrology
https://www.readbyqxmd.com/read/27649563/signaling-modification-by-gpcr-heteromer-and-its-implication-on-x-linked-nephrogenic-diabetes-insipidus
#19
Hans K H Ng, Kaleeckal G Harikumar, Laurence J Miller, Billy K C Chow
The involvement of secretin (SCT) and secretin receptor (SCTR) in regulating body water homeostasis is well established. Identified as one of the vasopressin (Vp)-independent mechanisms in fluid balance, SCT regulates aquaporin 2 (AQP2) in the kidney distal collecting duct cells through activating intracellular cAMP production. This ability to bypass Vp-mediated water reabsorption in kidney implicates SCT's potential to treat nephrogenic diabetes insipidus (NDI). Research on NDI in the past has largely been focused on the searching for mutations in vasopressin receptor 2 (AVPR2), while the functional relationship between SCTR, AVPR2 and NDI remains unclear...
2016: PloS One
https://www.readbyqxmd.com/read/27641679/functional-recovery-of-aqp2-recessive-mutations-through-hetero-oligomerization-with-wild-type-counterpart
#20
Abdulah El Tarazi, Yoann Lussier, Sandra Da Cal, Pierre Bissonnette, Daniel G Bichet
Aquaporin-2 (AQP2) is a homotetrameric water channel responsible for the final water reuptake in the kidney. Mutations in the protein induce nephrogenic diabetes insipidus (NDI), which challenges the water balance by producing large urinary volumes. Although recessive AQP2 mutations are believed to generate non-functional and monomeric proteins, the literature identifies several mild mutations which suggest the existence of mixed wt/mut tetramers likely to carry function in heterozygotes. Using Xenopus oocytes, we tested this hypothesis and found that mild mutants (V24A, D150E) can associate with wt-AQP2 in mixed heteromers, providing clear functional gain in the process (62 ± 17% and 63 ± 17% increases, respectively), conversely to the strong monomeric R187C mutant which fails to associate with wt-AQP2...
2016: Scientific Reports
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