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Nephrogenic Diabetes Insipidus

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161. Polyuria in a Patient with Aspergillus Infection (PubMed)

-9041 0 Antifungal Agents 7XU7A7DROE Amphotericin B IM Aged Amphotericin B adverse effects Antifungal Agents adverse effects Aspergillosis diagnosis drug therapy microbiology Aspergillus fumigatus drug effects isolation & purification Diabetes Insipidus, Nephrogenic chemically induced diagnosis physiopathology urine Humans Kidney Concentrating Ability drug effects Kidney Tubules drug effects physiopathology Male Osmolar Concentration Polyuria chemically induced diagnosis physiopathology urine Urine (...) chemistry Surveys and Questionnaires amphotericin diabetes insipidus electrolytes hypokalemia nephrology polyuria 2017 3 16 6 0 2018 6 19 6 0 2017 3 15 6 0 ppublish 28289066 CJN.12791216 10.2215/CJN.12791216 PMC5544519 Sci Rep. 2015 Dec 17;5:18311 26674602 Am J Physiol Renal Physiol. 2000 Oct;279(4):F655-63 10997915 J Clin Invest. 1961 Dec;40:2215-24 14494941 Lancet. 1957 Dec 14;273(7007):1212-8 13492612 Prostaglandins. 1993 Jan;45(1):47-56 8424133 Drugs. 2013 Jun;73(9):919-34 23729001 J Lab Clin Med

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2017 Clinical Journal of the American Society of Nephrology : CJASN

162. A Case of Kidney Involvement in Primary Sjögren’s Syndrome (PubMed)

. However, it is atypical to see more than 1 of these manifestations in a single patient. CASE REPORT We present the case of a 24-year-old woman with polyuria and polydipsia, who was initially diagnosed with nephrogenic diabetes insipidus. She also had chronic hypokalemia and nephrolithiasis. Based on clinical presentation and work up, she was diagnosed with pSS and treated accordingly. CONCLUSIONS This was a pSS patient with tubulointerstitial nephritis, diabetes insipidus, renal tubular acidosis (...) A Case of Kidney Involvement in Primary Sjögren’s Syndrome 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

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2017 The American journal of case reports

163. Hypokalemic Paralysis due to Primary Sjögren Syndrome: Case Report and Review of the Literature (PubMed)

Hypokalemic Paralysis due to Primary Sjögren Syndrome: Case Report and Review of the Literature Tubulointerstitial nephritis (TIN) is the main renal involvement associated with primary Sjögren syndrome (pSS). TIN can manifest as distal renal tubular acidosis (RTA), nephrogenic diabetes insipidus, proximal tubular dysfunction, and others. We present a 31-year-old female with hypokalemic paralysis due to distal RTA (dRTA). She received symptomatic treatment and hydroxychloroquine with a good

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2017 Case reports in rheumatology

164. Tacrolimus Aggravated Tube Feeding Syndrome with Acute Renal Failure in a Pediatric Liver Transplant Recipient (PubMed)

nephrogenic diabetes insipidus. The diet with high renal solute load consequently resulted in an acute polyuric renal failure with severe hypernatremic dehydration. In conclusion, a hypercaloric diet in children with potentially impaired renal function due to therapy with CNIs requires precise calculation of the potential renal solute load and the associated fluid requirements.

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2017 Case reports in transplantation

165. Roflumilast and aquaporin‐2 regulation in rat renal inner medullary collecting duct (PubMed)

Roflumilast and aquaporin‐2 regulation in rat renal inner medullary collecting duct 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

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2017 Physiological reports

166. 2012 KDIGO Clinical Practice Guideline for the Evaluation and Management of CKD

, hyperglycemia, dyslipidemia, smoking, obesity, history of cardiovascular disease, ongoing exposure to nephrotoxic agents, and others. (Not Graded) Chapter 3: Management of progression and complications of CKD 3.1: PREVENTION OF CKD PROGRESSION BP and RAAS interruption 3.1.1: IndividualizeBPtargetsandagentsaccordingtoage,coexistentcardiovasculardiseaseandothercomorbidities, risk of progression of CKD, presence or absence of retinopathy (in CKD patients with diabetes), and tolerance of treatment as described (...) hypotension and drug side effects. (Not Graded) 3.1.4: We recommend that in both diabetic and non-diabetic adults with CKD and urine albumin excretiono30mg/ 24 hours (or equivalent*) whose of?ce BP is consistently4140mm Hg systolic or490mm Hg diastolic be treated with BP-lowering drugs to maintain a BP that is consistentlyr140mm Hg systolic andr90mm Hg diastolic. (1B) 3.1.5: We suggest that in both diabetic and non-diabetic adults with CKD and with urine albumin excretion of Z30mg/24 hours (or equivalent

2012 National Kidney Foundation

167. Nocturia. A guide to assessment and management

Effect Medication Increased urine output Diuretics SSRIs Calcium channel blockers Lithium (nephrogenic diabetes insipidus in 40% of users) Tetracylines Precipitate insomnia and other central nervous system effects Stimulants Centrally active antihypertensives (α-blockers, β-blockers, methyldopa) Decongestants Psychotropic medications Parkinsonian medications Phenytoin Precipitate LUTS Ketamine Cyclophosphamide Management Management should be directed to correctly identifying the underlying aetiology (...) ) Pathophysiology Global polyuria Global polyuria is continuously raised urine output defined as >40 mL/kg/24 hours. 1 The most common cause is primary polydipsia. Polydipsia can also be a compensatory mechanism for fluid loss, such as the osmotic diuresis of uncontrolled diabetes mellitus. Global polyuria can also result from diabetes insipidus. 13 Nocturnal polyuria Nocturnal polyuria (NP) is increased urine production at night. Nocturnal polyuria exists when the nocturnal urine volume represents >20

2012 Clinical Practice Guidelines Portal

168. Functional Recovery of AQP2 Recessive Mutations Through Hetero-Oligomerization with Wild-Type Counterpart (PubMed)

Functional Recovery of AQP2 Recessive Mutations Through Hetero-Oligomerization with Wild-Type Counterpart 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

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2016 Scientific reports

169. Prorenin Receptor, a Necessary Component in Urine Concentration Mechanism (PubMed)

. Gov't Comment 2016 04 20 United States J Am Soc Nephrol 9013836 1046-6673 0 Aquaporin 2 0 Receptors, Cell Surface 0 Receptors, Vasopressin 0 prorenin receptor IM J Am Soc Nephrol. 2016 Oct;27(10):3022-3034 27000064 Aquaporin 2 Diabetes Insipidus, Nephrogenic Humans Receptors, Cell Surface Receptors, Vasopressin aquaporin diabetes insipidus prorenin prostaglandin vasopressin 2016 4 22 6 0 2018 8 21 6 0 2016 4 22 6 0 ppublish 27098238 ASN.2016030344 10.1681/ASN.2016030344 PMC5042682 Hypertension. 2009

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2016 Journal of the American Society of Nephrology : JASN

170. Trial of Desmopressin Orally Disintegrating Tablets (ODT) for Nocturia Due to Nocturnal Polyuria in Japanese Female Subjects

of >2.8 L based on the voiding diary at Visit 2 Central or nephrogenic diabetes insipidus at Visit 1 Syndrome of inappropriate antidiuretic hormone secretion at Visit 1 Suspicion or evidence of cardiac failure at Visit 1 Uncontrolled hypertension at Visit 1 Uncontrolled diabetes mellitus at Visit 1 Hyponatraemia (serum sodium level <135 mmol/L) at Visit 1 Renal insufficiency at Visit 1 Hepatic and/or biliary diseases at Visit 1 Known or suspected hypersensitivity to desmopressin ODTs or previous

2016 Clinical Trials

171. Trial of Desmopressin Orally Disintegrating Tablets (ODT) for Nocturia Due to Nocturnal Polyuria in Japanese Male Subjects

, or neoplasia at Visit 1 History of any neurological disease affecting bladder function or muscle strength at Visit 1 Habitual or psychogenic polydipsia based on medical history at Visit 1 or 24 hour urine output of >2.8 L based on the voiding diary at Visit 2 Central or nephrogenic diabetes insipidus at Visit 1 Syndrome of inappropriate antidiuretic hormone secretion at Visit 1 Suspicion or evidence of cardiac failure at Visit 1 Uncontrolled hypertension at Visit 1 Uncontrolled diabetes mellitus at Visit 1

2016 Clinical Trials

172. Bartter's and Gitelman's syndrome. (PubMed)

syndrome best fits in the group with the loop and DCT combination.Besides secondary hyperaldosteronism, loop disorders present a whole spectrum of (secondary) pathophysiologic characteristics with significant diagnostic and therapeutic impact, such as polyhydramnios, hyperprostaglandinuria, nephrogenic diabetes insipidus, and nephrocalcinosis. Recent reports indicate that neonatal hyperparathyroidism has also to be added to the clinical presentation of isolated loop disorders.As long as gene therapy

2016 Current Opinion in Pediatrics

173. EGF Receptor Inhibition by Erlotinib Increases Aquaporin 2-Mediated Renal Water Reabsorption. (PubMed)

EGF Receptor Inhibition by Erlotinib Increases Aquaporin 2-Mediated Renal Water Reabsorption. 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

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2016 Journal of the American Society of Nephrology

174. What we need to know about the effect of lithium on the kidney. (PubMed)

What we need to know about the effect of lithium on the kidney. Lithium has been a valuable treatment for bipolar affective disorders for decades. Clinical use of lithium, however, has been problematic due to its narrow therapeutic index and concerns for its toxicity in various organ systems. Renal side effects associated with lithium include polyuria, nephrogenic diabetes insipidus, proteinuria, distal renal tubular acidosis, and reduction in glomerular filtration rate. Histologically, chronic

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2016 American Journal of Physiology. Renal physiology

175. Plasma Apelin concentrations in Patients with Polyuria-Polydipsia Syndrome. (PubMed)

analysis of a prospective study performed in tertiary care hospitals in Switzerland and Germany and 113 healthy volunteers as a control group.Plasma apelin and copeptin levels were measured in 15 patients with complete central diabetes insipidus (DI), seven patients with complete nephrogenic DI, 19 patients with primary polydipsia (PP), and 113 healthy volunteers.Plasma apelin levels were highest in patients with complete nephrogenic DI (413 pmol/L; interquartile range, 332-504 pmol/L; P = .01 (...) ) and lower in patients with PP (190 [172-215] pmol/L; P < .001) or complete central DI (209 [174-241] pmol/L; P = .02) as compared to healthy volunteers (254 [225-311] pmol/L). Plasma apelin to copeptin ratio in patients with PP (53 [38-92] pmol/pmol; P > .9) was similar to healthy volunteers (57 [37-102] pmol/pmol). In contrast, the apelin to copeptin ratio was higher in patients with complete central DI (89 [73-135] pmol/pmol; P = .02) and lower in patients with complete nephrogenic DI (7 [6-10] pmol

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2016 Journal of Clinical Endocrinology and Metabolism

176. Metformin, an AMPK activator, stimulates the phosphorylation of Aquaporin 2 and Urea Transporter A1 in Inner Medullary Collecting Ducts. (PubMed)

Metformin, an AMPK activator, stimulates the phosphorylation of Aquaporin 2 and Urea Transporter A1 in Inner Medullary Collecting Ducts. Nephrogenic diabetes insipidus (NDI) is characterized by production of very large quantities of dilute urine due to an inability of the kidney to respond to vasopressin. Congenital NDI results from mutations in the type 2 vasopressin receptor (V2R) in ∼90% of families. These patients do not have mutations in aquaporin-2 (AQP2) or urea transporter UT-A1 (UT-A1

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2016 American Journal of Physiology. Renal physiology

177. Demonstration of the functional impact of vasopressin signalling in thick ascending limb by a targeted transgenic rat approach. (PubMed)

diabetes insipidus (NDI), which has chiefly been related with impaired aquaporin 2-mediated water reabsorption in the collecting ducts. Previous work also suggested the AVP-V2R-mediated activation of Na(+)-K(+)-2Cl(-)-cotransporters (NKCC2) along the thick ascending limb (TAL) in the context of urine concentration, but its individual contribution to NDI or, more generally, to overall renal function was unclear. We hypothesized that V2R-mediated effects in TAL essentially determine its reabsorptive (...) Demonstration of the functional impact of vasopressin signalling in thick ascending limb by a targeted transgenic rat approach. The antidiuretic hormone vasopressin (AVP) regulates renal salt and water reabsorption along the distal nephron and collecting duct system. These effects are mediated by vasopressin 2 receptors (V2R) and release of intracellular Gs-mediated cAMP to activate epithelial transport proteins. Inactivating mutations in the V2R gene lead to the X-linked form of nephrogenic

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2016 American Journal of Physiology. Renal physiology

178. Lithium toxicity after Roux-en-Y bariatric surgery (PubMed)

Lithium toxicity after Roux-en-Y bariatric surgery A 61-year-old woman with medical history significant for morbid obesity, type II diabetes mellitus, nephrogenic diabetes insipidus and bipolar disorder, had been stable on lithium carbonate therapy for several years. She had undergone a Roux-en-Y bypass surgery and, at the time of her surgery, her lithium level was found to be 0.61 mEq/L on a maintenance dose of 600 mg orally twice per day. She was discharged 8 days postoperatively on the same

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2016 BMJ case reports

179. Effects of GLP-1 Analogues on Fluid Intake in Patients With Primary Polydipsia (The GOLD-Study)

or probable central or nephrogenic Diabetes insipidus, expected from patient's history Polyuria secondary to diabetes mellitus, hypokalemia, hypercalcemia Pregnancy Previous treatment with GLP-1 agonists within the last 3 month History of pancreatitis Severe renal insufficiency (eGFR (CKD EPI) <30 ml/min/1,73 m2) Cancer Contacts and Locations Go to Information from the National Library of Medicine To learn more about this study, you or your doctor may contact the study research staff using the contact (...) : Layout table for MeSH terms Polydipsia Polydipsia, Psychogenic Diabetes Insipidus Pathologic Processes Signs and Symptoms Behavioral Symptoms Neurobehavioral Manifestations Kidney Diseases Urologic Diseases Pituitary Diseases Endocrine System Diseases Dulaglutide Hypoglycemic Agents Physiological Effects of Drugs

2016 Clinical Trials

180. Copeptin in the diagnosis of vasopressin-dependent disorders of fluid homeostasis. (PubMed)

pmol/l identify patients with nephrogenic diabetes insipidus. Conversely, copeptin levels measured upon osmotic stimulation differentiate primary polydipsia from partial central diabetes insipidus. In patients with hyponatraemia, low levels of copeptin together with low urine osmolality identify patients with primary polydipsia, and the ratio of copeptin to urinary sodium can distinguish the syndrome of inappropriate antidiuretic hormone secretion from other AVP-dependent forms of hyponatraemia.

2016 Nature reviews. Endocrinology

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