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Nephrogenic Diabetes Insipidus

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141. Safety and Efficacy of Hydrochlorothiazide in the Treatment of Hypernatremia in Critically Ill Patients

to hydrochlorothiazide or other thiazides. Nephrogenic Diabetes Insipidus. Renal impairment KDIGO 3 Indication of renal replacement therapy. Acute neurological insult. Heart failure American Heart Association classification (AHA), class D. Liver cirrhosis Child-Pugh C. Pregnant women Exclusive palliative care Dying, with expected survival less than 48 hours 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

2018 Clinical Trials

142. Lithium and nephrotoxicity: a literature review of approaches to clinical management and risk stratification. (Full text)

Lithium and nephrotoxicity: a literature review of approaches to clinical management and risk stratification. Despite lithium being the most efficacious treatment for bipolar disorder, its use has been decreasing at least in part due to concerns about its potential to cause significant nephrotoxicity. Whilst the ability of lithium to cause nephrogenic diabetes insipidus is well established, its ability to cause chronic kidney disease is a much more vexing issue, with various studies suggesting (...) both positive and negative causality. Despite these differences, the weight of evidence suggests that lithium has the potential to cause end stage kidney disease, albeit over a prolonged period.A search strategy for this review was developed to identify appropriate studies, sourced from the electronic databases EMBASE, PubMed (NLM) and MEDLINE. Search terms included lithium with the AND operator to combine with nephrotoxicity or nephropathy or chronic kidney disease or nephrogenic diabetes

2018 BMC Nephrology PubMed abstract

143. Copeptin levels and commonly used laboratory parameters in hospitalised patients with severe hypernatraemia - the “Co-MED study” (Full text)

%]), followed by salt overload (SO) (n = 20 [22%]), central diabetes insipidus (CDI) (n = 5 [5%]) and nephrogenic diabetes insipidus (NDI) (n = 2 [2%]). Low urine osmolality was indicative for patients with CDI and NDI (P < 0.01). Patients with CDI had lower copeptin levels than patients with DH or SO (both P < 0.01) or those with NDI. Copeptin identified CDI with an AUC of 0.99 (95% CI 0.97-1.00), and a cut-off value ≤ 4.4pmol/L showed a sensitivity of 100% and a specificity of 99% to predict CDI

2018 Critical Care PubMed abstract

144. Effects of sildenafil, metformin, and simvastatin on ADH‐independent urine concentration in healthy volunteers (Full text)

Effects of sildenafil, metformin, and simvastatin on ADH‐independent urine concentration in healthy volunteers Nephrogenic diabetes insipidus (NDI) is a rare disorder characterized by resistance of the kidney to the action of antidiuretic hormone (ADH), resulting in a decrease in the capacity of the kidney to concentrate the urine. NDI can be inherited or acquired due to, for example, chronic lithium therapy. Current treatment options are limited to attempts to lower urine output by a low

2018 Physiological reports PubMed abstract

145. The Emerging Role of microRNAs in Aquaporin Regulation (Full text)

The Emerging Role of microRNAs in Aquaporin Regulation Aquaporins (AQPs) are membrane channels widely distributed in human tissues. AQPs are essential for water and energy homeostasis being involved in a broad range of pathophysiological processes such as edema, brain injury, glaucoma, nephrogenic diabetes insipidus, salivary and lacrimal gland dysfunction, cancer, obesity and related metabolic complications. Compelling evidence indicates that AQPs are targets for therapeutic intervention

2018 Frontiers in chemistry PubMed abstract

146. 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

147. 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

148. Prostaglandin E2 in the Regulation of Water Transport in Renal Collecting Ducts (Full text)

mechanisms. Each EP receptor plays a unique role in regulating water reabsorption in renal collecting ducts. This brief review highlights the role of PGE₂ in the regulation of water reabsorption and discusses the involvement of each EP receptor subtype in renal collecting duct. A better understanding of the role of PGE₂ in renal water transport process may improve disease management strategies for water balance disorders, including nephrogenic diabetes insipidus.

2017 International journal of molecular sciences PubMed abstract

149. Lithium induces aerobic glycolysis and glutaminolysis in collecting duct principal cells. (Abstract)

Lithium induces aerobic glycolysis and glutaminolysis in collecting duct principal cells. Lithium, given to bipolar disorder patients, causes nephrogenic diabetes insipidus (Li-NDI), a urinary-concentrating defect. Li-NDI occurs due to downregulation of principal cell AQP2 expression, which coincides with principal cell proliferation. The metabolic effect of lithium on principal cells, however, is unknown and investigated here. In earlier studies, we showed that the carbonic anhydrase (CA

2017 American Journal of Physiology. Renal physiology

150. A New Optical Sweat Test Method Based on a Citric Acid-derived Multi-halide Sensor

diagnosis of Cystic Fibrosis (CF) OR Healthy volunteers Exclusion Criteria: Participants under medications or with disorders known to cause a positive error in the sweat test will be excluded in the study. Common causes of positive error in sweat test are mineralocorticoid hormone therapy, adrenal insufficiency, glycogen storage diseases, hypothyroidism, hypoparathyroidism, nephrogenic diabetes insipidus, G6PD deficiency or ectodermal dysplasia OR Any other skin or soft tissue disorders that could

2017 Clinical Trials

151. Polyuria in a Patient with Aspergillus Infection (Full text)

-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

2017 Clinical Journal of the American Society of Nephrology : CJASN PubMed abstract

152. Tacrolimus Aggravated Tube Feeding Syndrome with Acute Renal Failure in a Pediatric Liver Transplant Recipient (Full text)

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.

2017 Case reports in transplantation PubMed abstract

153. A Case of Kidney Involvement in Primary Sjögren’s Syndrome (Full text)

. 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

2017 The American journal of case reports PubMed abstract

154. Hypokalemic Paralysis due to Primary Sjögren Syndrome: Case Report and Review of the Literature (Full text)

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

2017 Case reports in rheumatology PubMed abstract

155. Roflumilast and aquaporin‐2 regulation in rat renal inner medullary collecting duct (Full text)

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

2017 Physiological reports PubMed abstract

156. Trial Investigating the Long Term Safety and Tolerability of Desmopressin Orally Disintegrating Tablets (ODT) for Nocturia Due to Nocturnal Polyuria in Japanese Subjects

at Visit 1a History of any neurological disease affecting bladder function or muscle strength at Visit 1a Habitual or psychogenic polydipsia based on medical history at Visit 1a or 24-hour urine output of >2.8 L based on the voiding diary at Visit 1b Central or nephrogenic diabetes insipidus at Visit 1a Syndrome of inappropriate antidiuretic hormone secretion at Visit 1a Suspicion or evidence of cardiac failure at Visit 1a Uncontrolled hypertension at Visit 1a and Visit 1b Hyponatraemia (serum sodium

2017 Clinical Trials

157. Effects of Glucagon Like Peptide 1 (GLP-1) Analogues on Fluid Intake

Adult) Sexes Eligible for Study: All Accepts Healthy Volunteers: Yes Criteria Inclusion Criteria: - Age 18 to 65 years Exclusion Criteria: Known or probable central or nephrogenic Diabetes insipidus, based on patient's history Polyuria secondary to diabetes mellitus, hypokalemia, hypercalcemia Primary Polydipsia, defined as more than 4 liters fluid intake per day BMI <18 or >30kg/m2 Pregnancy Previous treatment with GLP-1 agonists within the last 3 month History of pancreatitis Severe renal

2017 Clinical Trials

158. A Trial to Investigate Efficacy, Safety and Tolerability of FE 201836 for Nocturia Due to Nocturnal Polyuria in Adults

, spina bifida) Habitual (fluid intake >3L per day) or psychogenic polydipsia Uncontrolled hypertension, as judged by the investigator Uncontrolled diabetes mellitus, as judged by the investigator Central or nephrogenic diabetes insipidus Known history of Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion History of gastric retention Suspicion or evidence of congestive heart failure, (New York Heart Association (NYHA) class II, III, IV) Hyponatraemia: Serum sodium level <135 mmol/L

2017 Clinical Trials

159. Liver X Receptor β (LXRβ) Increases AQP2 Protein Level via a Post-transcriptional Mechanism in Renal Collecting Ducts. (Abstract)

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. AQP2 protein abundance in the renal inner medulla was significantly reduced in LXRβ-/- mice but with little change in AQP2 mRNA levels. In vitro studies showed that AQP2 protein levels were elevated upon LXR agonist treatment in both primary cultured mouse inner medullary

2017 American Journal of Physiology. Renal physiology

160. Lithium-induced NDI: Acetazolamide reduces polyuria, but does not improve urine concentrating ability. (Full text)

Lithium-induced NDI: Acetazolamide reduces polyuria, but does not improve urine concentrating ability. Lithium is the mainstay treatment for patients with bipolar disorder, but it 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 aquaporin-2 (AQP2) water channels, which are essential for water uptake from

2017 American Journal of Physiology. Renal physiology PubMed abstract

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