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Nephrogenic Diabetes Insipidus

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181. Antihypertensive therapy in patients on chronic lithium treatment for bipolar disorders. (PubMed)

Antihypertensive therapy in patients on chronic lithium treatment for bipolar disorders. Bipolar disorders are chronic conditions treated with lithium, which exerts deleterious effects on the kidney, among which nephrogenic diabetes insipidus, tubular acidosis and ultimately chronic kidney disease. Conversely, drugs that alter renal function can modify its serum levels and lead to the potentially fatal lithium intoxication. A search in the main library databases from 1975 to 2015 to identify

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2016 Journal of Hypertension

182. Molecular mechanisms in lithium-associated renal disease: a systematic review. (PubMed)

English-language original research articles published prior to November 2015 that specifically investigated lithium's effects on nephrogenic diabetes insipidus (NDI) and chronic kidney disease (CKD), using molecular markers.From a total of 3510 records, 71 pre-clinical studies and two relevant clinical studies were identified. Molecular alterations were reported in calcium signaling, inositol monophosphate, extracellular-regulated, prostaglandin, sodium/solute transport, G-protein-coupled receptors

2016 International urology and nephrology

183. Mutations of vasopressin receptor 2 including novel L312S have differential effects on trafficking. (PubMed)

L312S mutation as well as for previously described V2R gain-of-function mutants (NSIAD; R137C and R137L), loss-of-function mutants (nephrogenic diabetes insipidus; R137H, R181C, and M311V), and a putative silent V266A V2R polymorphism. In doing so, we describe differences in trafficking between unique V2R substitutions, even at the same amino acid position, therefore highlighting the value of full and thorough characterization of receptor function beyond simple signaling pathway analysis. (...) Mutations of vasopressin receptor 2 including novel L312S have differential effects on trafficking. Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is a genetic disease first described in 2 unrelated male infants with severe symptomatic hyponatremia. Despite undetectable arginine vasopressin levels, patients have inappropriately concentrated urine resulting in hyponatremia, hypoosmolality, and natriuresis. Here, we describe and functionally characterize a novel vasopressin type 2

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2016 Molecular Endocrinology

184. A 4-year-old boy presenting with persistent urinary incontinence: Questions. (PubMed)

) associated with partial nephrogenic diabetes insipidus. He was started on daily desmopressin. Within 3 days the urinary incontinence resolved as did the polyuria and faecal incontinence. His grandmother was referred to the geneticist and eventually the adult nephrologist. This case highlights the importance of being thorough when confronted with a difficult diagnosis. It also emphasizes that a test result does not necessarily equate to the presence or absence of a condition since the test with 100 (...) A 4-year-old boy presenting with persistent urinary incontinence: Questions. A 4-year-old boy was referred to the nephrologist with daytime urinary incontinence and suspicion of an overactive bladder. At the age of 17 months he had been referred to the pediatric endocrinologist because of polyuria and polydipsia in order to exclude diabetes insipidus. Repeated water deprivation tests and a magnetic resonance imaging scan of the brain were normal. Diabetes insipidus was excluded, and primary

2016 Pediatric Nephrology

185. Wnt5a induces renal AQP2 expression by activating calcineurin signalling pathway (PubMed)

Wnt5a induces renal AQP2 expression by activating calcineurin signalling pathway 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

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2016 Nature communications

186. Altered Nitric Oxide System in Cardiovascular and Renal Diseases (PubMed)

. A pressure-overload may cause severer left ventricular hypertrophy and dysfunction in eNOS null mice than in wild-type mice. iNOS-derived NO has detrimental effects on the myocardium. NO plays an important role in regulating the angiogenesis and slowing the interstitial fibrosis of the obstructed kidney. In unilateral ureteral obstruction, the expression of eNOS was decreased in the affected kidney. In triply n/i/eNOS null mice, nephrogenic diabetes insipidus developed along with reduced aquaporin-2

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2016 Chonnam medical journal

187. Receptor Antagonism/Agonism Can Be Uncoupled from Pharmacoperone Activity (PubMed)

Receptor Antagonism/Agonism Can Be Uncoupled from Pharmacoperone Activity Pharmacoperones rescue misrouted mutants of the vasopressin receptor type 2 (V2R) and enable them to traffic to the correct biological locus where they function. Previously, a library of nearly 645,000 structures was interrogated with a high throughput screen; pharmacoperones were identified for V2R mutants with a view toward correcting the underlying mutational defects in nephrogenic diabetes insipidus. In the present

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2016 Molecular and cellular endocrinology

188. Lithium and the Kidney: Old Observations & New Insights

very similar to sodium. It has a molecular weight of 7 daltons, has a moderate volume of distribution, is <10% protein bound and is therefore readily dialyzable. Lithium may cause of myriad of renal related toxicities, some of which are classic descriptions and some which are less well known. Much of this has been discussed on RFN before ( , ) but I felt a refresher with some additions was due. Nephrogenic Diabetes Insipidus (NDI) This is perhaps the best know and most common complication

2014 Renal Fellow Network

189. Pharmacological treatment of bipolar disorder in primary care

(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

190. 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

191. 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

192. 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

193. 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

194. Vasopressin regulates renal calcium excretion in humans (PubMed)

(nephrogenic or central) under acute vasopressin receptor agonist action and in 10 patients undergoing oral water load test affected or not by inappropriate antidiuretic hormone secretion (SIADH). Synthetic V2 receptor agonist (dDAVP) reduced significantly calcium fractional excretion from 1.71% to 0.58% (P < 0.05) in patients with central diabetes insipidus. In patients with nephrogenic diabetes insipidus (resistant to AVP), calcium fractional excretion did not change significantly after injection (0.48 (...) Vasopressin regulates renal calcium excretion in humans Antidiuretic hormone or arginine vasopressin (AVP) increases water reabsorption in the collecting ducts of the kidney. Three decades ago, experimental models have shown that AVP may increase calcium reabsorption in rat kidney. The objective of this study was to assess whether AVP modulates renal calcium excretion in humans. We analyzed calcium, potassium, and sodium fractional excretion in eight patients affected by insipidus diabetes

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2015 Physiological reports

195. Does lower urine-specific gravity predict decline in renal function and hypernatremia in older adults exposed to psychotropic medications? An exploratory analysis (PubMed)

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

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2015 Clinical kidney journal

196. Lithium in the Kidney: Friend and Foe? (PubMed)

Lithium in the Kidney: Friend and Foe? Trace amounts of lithium are essential for our physical and mental health, and administration of lithium has improved the quality of life of millions of patients with bipolar disorder for >60 years. However, in a substantial number of patients with bipolar disorder, long-term lithium therapy comes at the cost of severe renal side effects, including nephrogenic diabetes insipidus and rarely, ESRD. Although the mechanisms underlying the lithium-induced renal

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2015 Journal of the American Society of Nephrology

197. Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report (PubMed)

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

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2015 World journal of nephrology

198. Lithium nephrotoxicity (PubMed)

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

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2015 International journal of bipolar disorders

200. Diagnostic accuracy of copeptin in the differential diagnosis of the polyuria-polydipsia syndrome: A prospective multicenter study. (PubMed)

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

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2015 Journal of Clinical Endocrinology and Metabolism

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