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Nephrogenic Diabetes Insipidus

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181. Does lower urine-specific gravity predict decline in renal function and hypernatremia in older adults exposed to psychotropic medications? An exploratory analysis Full Text available with Trip Pro

Does lower urine-specific gravity predict decline in renal function and hypernatremia in older adults exposed to psychotropic medications? An exploratory analysis Exposure to psychotropic agents, including lithium, antipsychotics and antidepressants, has been associated with nephrogenic diabetes insipidus (NDI). This is especially concerning in older adults already at risk of developing chronic kidney disease (CKD) and hypernatremia with advanced aging. This study investigates whether commonly

2015 Clinical kidney journal

182. Pilot Study of Mirabegron in Pediatric Patients With Overactive Bladder

a reliable form of birth control for the duration of the study and for at least one month after ending study treatment. Patients without symptom improvement or with partial response under medical therapy (at least 2 different antimuscarinic agents) or with significantly bothersome S/E on antimuscarinics. Exclusion Criteria: Subject has a diagnostic of dysfunctional voiding Post-voiding residue > 20 cc Polyuria (> 75 ml/kg/b.w./24 hours) Nephrogenic of central diabetes insipidus Constipation at screening

2015 Clinical Trials

183. Add-on Mirabegron in Pediatric Patients With Refractory Overactive Bladder

has a diagnostic of dysfunctional voiding Post-voiding residue > 20 cc Polyuria (> 75 ml/kg/b.w./24 hours) Nephrogenic of central diabetes insipidus Constipation at screening (if the patient is treated and the treatment is successful, the patient will be eligible to the study) Urinary tract infection at visit 2-3-4. If UTI is present at the screening visit, the UTI must be treated and the success of the treatment must be documented with a negative urinalysis at visit 2. QTc interval greater than

2015 Clinical Trials

184. Extension Study of Fesoterodine for Overactive Bladder Syndrome in Children.

. Sexually active male subjects agree to use a condom for the duration of the study and for at least one month after ending study treatment and the female partner to use a reliable form of birth control for the duration of the study and for at least one month after ending study treatment. Exclusion Criteria: Subject has a diagnostic of dysfunctional voiding Post-voiding residue > 20 cc Polyuria (> 75 ml/kg/b.w./24 hours) Nephrogenic of central diabetes insipidus Constipation at screening (if the patient

2015 Clinical Trials

185. Effect of Statin Treatment on Urinary AQP2 (uAQP2/01)

farnesylpyrophosphate (FPP) and geranylgeranylpyrophosphate (GGPP). Water balance disorders are often associated with defects of AQP2 trafficking. Nephrogenic Diabetes Insipidus (NDI) is characterized by the inability of the kidney to respond to AVP stimulation and is caused by either mutations in AQP2 or vasopressin type-2 receptor (AVPR2) genes. Mutations in the AVPR2 gene lead to X-linked NDI (X-NDI). This cause of 90% of all diagnosed congenital NDI cases. Conventional treatment of X-NDI patients consists (...) University of Bari Investigators Layout table for investigator information Principal Investigator: Piero Portincasa University of Bari Medical School More Information Go to Publications of Results: Procino G. Fluvastatin Increases AQP2 Urine Excretion in a Dyslipidemic Patient with Nephrogenic Diabetes Insipidus: An In Vivo and In Vitro Study. Journal of Diabetes & Metabolism 2014; 5(7); 1000408 Other Publications: Layout table for additonal information Responsible Party: piero portincasa, Professor

2015 Clinical Trials

187. Diagnostic accuracy of copeptin in the differential diagnosis of the polyuria-polydipsia syndrome: A prospective multicenter study. Full Text available with Trip Pro

Diagnostic accuracy of copeptin in the differential diagnosis of the polyuria-polydipsia syndrome: A prospective multicenter study. The polyuria-polydipsia syndrome comprises primary polydipsia (PP) and central and nephrogenic diabetes insipidus (DI). Correctly discriminating these entities is mandatory, given that inadequate treatment causes serious complications. The diagnostic "gold standard" is the water deprivation test with assessment of arginine vasopressin (AVP) activity. However, test (...) sodium exceeded 147 mmol/L. Circulating copeptin and AVP levels were measured regularly throughout the test. Final diagnosis was based on the water deprivation/saline infusion test results, clinical information, and the treatment response.Fifty-five patients were enrolled (11 with complete central DI, 16 with partial central DI, 18 with PP, and 10 with nephrogenic DI). Without prior thirsting, a single baseline copeptin level >21.4 pmol/L differentiated nephrogenic DI from other etiologies with a 100

2015 Journal of Clinical Endocrinology and Metabolism

188. Cyclophosphamide-induced vasopressin-independent activation of aquaporin-2 in the rat kidney. Full Text available with Trip Pro

Cyclophosphamide-induced vasopressin-independent activation of aquaporin-2 in the rat kidney. Because cyclophosphamide-induced hyponatremia was reported to occur without changes in plasma vasopressin in a patient with central diabetes insipidus, we hypothesized that cyclophosphamide or its active metabolite, 4-hydroperoxycyclophosphamide (4-HC), may directly dysregulate the expression of water channels or sodium transporters in the kidney. To investigate whether intrarenal mechanisms (...) and cAMP accumulation in response to 4-HC were significantly reduced by tolvaptan cotreatment in primary cultured IMCD cells and IMCD suspensions, respectively. We demonstrated that, in the rat kidney, cyclophosphamide may activate V2R and induce upregulation of AQP2 in the absence of vasopressin stimulation, suggesting the possibility of drug-induced nephrogenic syndrome of inappropriate antidiuresis (NSIAD). Copyright © 2015 the American Physiological Society.

2015 American Journal of Physiology. Renal physiology

189. Lithium nephrotoxicity Full Text available with Trip Pro

Lithium nephrotoxicity Reports of toxic effects on the kidney of lithium treatment emerged very soon after lithium therapy was introduced. Lithium-induced nephrogenic diabetes insipidus is usually self-limiting or not clinically dangerous. Some reports of irreversible chronic kidney disease and renal failure were difficult to attribute to lithium treatment since chronic kidney disease and renal failure exist in the population at large. In recent years, large-scale epidemiological studies have

2015 International journal of bipolar disorders

190. Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report Full Text available with Trip Pro

Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report A man with past lithium use for more than 15 years, but off lithium for two years and not carrying the diagnosis of diabetes mellitus or nephrogenic diabetes insipidus (NDI), presented with coma and hyperglycemic hyperosmolar state (HHS). Following correction of HHS, he developed persistent hypernatremia accompanied by large volumes of urine with low osmolality and no response to desmopressin (...) injections. Urine osmolality remained < 300 mOsm/kg after injection of vasopressin. Improvement in serum sodium concentration followed the intake of large volumes of water plus administration of amiloride and hydrochlorothiazide. Severe hyperglycemia may trigger symptomatic lithium-induced NDI years after cessation of lithium therapy. Patients with new-onset diabetes mellitus who had been on prolonged lithium therapy in the past require monitoring of their serum sodium concentration after hyperglycemic

2015 World journal of nephrology

191. Pharmacological treatment of bipolar disorder in primary care Full Text available with Trip Pro

(incidence < 1%) † Dose range and serum levels Dosing considerations Lithium GIT: nausea, vomiting, epigastric discomfort, dry mouth, metallic taste, diarrhoea, weight gain CNS: fatigue, headache, difficulty concentrating, vertigo, fine tremor Skin: dry skin, exacerbation of psoriasis or acne, rash Metabolic: hypermagnesaemia, hypercalcaemia, hypothyroidism Other: benign electrocardiogram changes, leukocytosis Nephrogenic diabetes insipidus, hyperparathyroidism, memory impairment, hair loss, arrhythmias

2010 Clinical Practice Guidelines Portal

192. Clinical profile and outcome of renal tubular disorders in children: A single center experience Full Text available with Trip Pro

tubular disorders attending a tertiary care pediatric nephrology center from 2005 to 2010. Growth and renal outcomes were assessed by Z scores and estimated glomerular filtration rate at diagnosis and. The common disorders encountered were distal renal tubular acidosis (d-RTA) (44%), Bartter-like (Bartter's and Gitelman) syndromes (22%) followed by hereditary Fanconi syndrome (cystinosis and idiopathic Fanconi syndrome) (13%) and few cases of nephrogenic diabetes insipidus, hypophosphatemic rickets

2014 Indian Journal of Nephrology

193. Fesoterodine and Oxybutynin XL for Overactive Bladder Syndrome in Children

control for the duration of the study and for at least one month after ending study treatment. Exclusion Criteria: Subject has a diagnostic of dysfunctional voiding Post-voiding residue > 20 cc Polyuria (> 75 ml/kg/b.w./24 hours) Nephrogenic of central diabetes insipidus Constipation at screening (if the patient is treated and the treatment is successful, the patient will be eligible to the study) Urinary tract infection at visit 2-3-4. If UTI is present at the screening visit, the UTI must be treated

2014 Clinical Trials

194. Lithium Causes G2 Arrest of Renal Principal Cells. Full Text available with Trip Pro

Lithium Causes G2 Arrest of Renal Principal Cells. Vasopressin-regulated expression and insertion of aquaporin-2 channels in the luminal membrane of renal principal cells is essential for urine concentration. Lithium affects urine concentrating ability, and approximately 20% of patients treated with lithium develop nephrogenic diabetes insipidus (NDI), a disorder characterized by polyuria and polydipsia. Lithium-induced NDI is caused by aquaporin-2 downregulation and a reduced ratio

2014 Journal of the American Society of Nephrology

195. Early targets of lithium in rat kidney inner medullary collecting duct include p38 and ERK1/2. Full Text available with Trip Pro

Early targets of lithium in rat kidney inner medullary collecting duct include p38 and ERK1/2. Almost half of patients receiving lithium salts have nephrogenic diabetes insipidus. Chronic lithium exposure induces AQP2 downregulation and changes in the cellular composition of the collecting duct. In order to understand these pathophysiological events, we determined the earliest lithium targets in rat inner medullary collecting duct (IMCD) by examining changes in the IMCD phosphoproteome after

2014 Kidney International

196. Urinary concentration: different ways to open and close the tap. Full Text available with Trip Pro

Urinary concentration: different ways to open and close the tap. Nephrogenic diabetes insipidus (NDI) provides an excellent model for the benefits and insights that can be gained from studying rare diseases. The discovery of underlying genes identified key molecules involved in urinary concentration, including the type 2 vasopressin receptor AVPR2 and the water channel AQP2, which constitute obvious pharmacologic targets. Subsequently developed drugs targeting AVPR2 not only provide potential

2014 Pediatric Nephrology

197. Common α2A and α2C adrenergic receptor polymorphisms do not affect plasma membrane trafficking Full Text available with Trip Pro

Common α2A and α2C adrenergic receptor polymorphisms do not affect plasma membrane trafficking Various naturally occurring polymorphic forms of human G protein-coupled receptors (GPCRs) have been identified and linked to diverse pathological diseases, including receptors for vasopressin type 2 (nephrogenic diabetes insipidus) and gonadotropin releasing hormone (hypogonadotropic hypogonadism). In most cases, polymorphic amino acid mutations disrupt protein folding, altering receptor function

2014 Naunyn-Schmiedeberg's archives of pharmacology

198. Hypercalcemia and Spinal Cord Injury (Diagnosis)

levels that may occur in hypercalcemia of malignancy. Acute hypercalcemia induces natriuresis (nephrogenic diabetes insipidus) and polyuria, possibly resulting in extracellular fluid contraction and dehydration. Chronic hypercalcemia can reduce renal concentrating ability, further exacerbating polyuria and polydipsia. The disorder also causes urinary stones, nephrocalcinosis, and chronic renal failure. As bone resorption diminishes after spinal cord injury, hypercalcemia resolves. Eventually

2014 eMedicine.com

199. Light Chain-Associated Renal Disorders (Diagnosis)

function; depending on the site of action, this may result in the following: Fanconi syndrome (proximal tubular dysfunction) Distal renal tubular acidosis Nephrogenic diabetes insipidus Light chain deposition disease Light chain deposition disease (LCDD) is a systemic disease caused by the overproduction and extracellular deposition of monoclonal light chains. [ , ] Deposition does not mean pathogenicity. Deposition of light-chains similar to LCDD by IF but with no or only scanty granular electron (...) by the kidney, and only a minute amount of light-chain protein normally appears in the urine. Light-chain proteins appear in urine in high concentration either when the production of light-chain proteins is markedly increased or when the ability of the proximal tubules to reabsorb all the filtered protein is diminished. The most characteristic histologic lesion of light chain deposition disease (LCDD) is nodular glomerulosclerosis, which must be distinguished from diabetic glomerulosclerosis by using

2014 eMedicine.com

200. Lithium Nephropathy (Diagnosis)

, Hoegberg LCG, Gosselin S, Roberts DM. Lithium Poisoning. J Intensive Care Med . 2017 May. 32 (4):249-263. . Nielsen J, Kwon TH, Christensen BM, et al. Dysregulation of renal aquaporins and epithelial sodium channel in lithium-induced nephrogenic diabetes insipidus. Semin Nephrol . 2008 May. 28(3):227-44. . Mu J, Johansson M, Hansson GC, et al. Lithium evokes a more pronounced natriuresis when administered orally than when given intravenously to salt-depleted rats. Pflugers Arch . 1999 Jul. 438(2):159 (...) ways. Acutely and chronically, lithium salts produce a natriuresis that is associated with an impaired regulation of the expression of the epithelial sodium channel in the cortical collecting tubule. [ , ] Specifically, lithium use partially inhibits the ability of aldosterone to increase apical membrane ENaC expression, resulting in inappropriate sodium losses. [ ] The most common complication of long-term lithium therapy is nephrogenic diabetes insipidus. [ , , ] At the cellular level

2014 eMedicine.com

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