How to Trip Rapid Review

Step 1: Select articles relevant to your search (remember the system is only optimised for single intervention studies)

Step 2: press

Step 3: review the result, and maybe amend the or if you know better! If we're unsure of the overall sentiment of the trial we will display the conclusion under the article title. We then require you to tell us what the correct sentiment is.

438 results for

Nephrogenic Diabetes Insipidus

by
...
Latest & greatest
Alerts

Export results

Use check boxes to select individual results below

SmartSearch available

Trip's SmartSearch engine has discovered connected searches & results. Click to show

121. Hsp90 inhibitor partially corrects nephrogenic diabetes insipidus in a conditional knock-in mouse model of aquaporin-2 mutation (PubMed)

Hsp90 inhibitor partially corrects nephrogenic diabetes insipidus in a conditional knock-in mouse model of aquaporin-2 mutation Mutations in aquaporin-2 (AQP2) that interfere with its cellular processing can produce autosomal recessive nephrogenic diabetes insipidus (NDI). Prior gene knock-in of the human NDI-causing AQP2 mutation T126M produced mutant mice that died by age 7 days. Here, we used a novel "conditional gene knock-in" strategy to generate adult, AQP2-T126M mutant mice. Mice

Full Text available with Trip Pro

2009 The FASEB Journal

122. Nephrogenic Diabetes Insipidus (NDI): Clinical, Laboratory and Genetic Characterization of Five Brazilian Patients (PubMed)

Nephrogenic Diabetes Insipidus (NDI): Clinical, Laboratory and Genetic Characterization of Five Brazilian Patients Nephrogenic diabetes insipidus is characterized by a lack of response in the distal nephron to the antidiuretic hormone arginine vasopressin. Manifestations include polyuria, polydipsia, hyposthenuria, recurrent episodes of dehydration and fever and growth failure. Most cases are caused by mutations in the AVPR2 gene. The mutant receptors are trapped intracellularly.We studied five (...) was significantly reduced.This study reports the clinical and laboratory characterization of Nephrogenic diabetes insipidus and reiterates the importance of the genetic basis that underlies the disease diagnosis and genetic counseling.

Full Text available with Trip Pro

2009 Clinics (Sao Paulo, Brazil)

123. Amiloride blocks lithium entry through the sodium channel thereby attenuating the resultant nephrogenic diabetes insipidus. (PubMed)

Amiloride blocks lithium entry through the sodium channel thereby attenuating the resultant nephrogenic diabetes insipidus. Lithium therapy frequently induces nephrogenic diabetes insipidus; amiloride appears to prevent its occurrence in some clinical cases. Amiloride blocks the epithelial sodium channel (ENaC) located in the apical membrane of principal cells; hence one possibility is that ENaC is the main entry site for lithium and the beneficial effect of amiloride may be through inhibiting (...) kinase 3beta. Treatment of rats with lithium downregulated AQP2 expression, reduced the principal-to-intercalated cell ratio, and caused polyuria, while simultaneous administration of amiloride attenuated all these changes. These results show that ENaC is the major entry site for lithium in principal cells both in vitro and in vivo. Blocking lithium entry with amiloride attenuates lithium-induced diabetes insipidus, thus providing a rationale for its use in treating this disorder.

Full Text available with Trip Pro

2009 Kidney International

124. Potential Role of Purinergic Signaling in Lithium-induced Nephrogenic Diabetes Insipidus. (PubMed)

Potential Role of Purinergic Signaling in Lithium-induced Nephrogenic Diabetes Insipidus. Lithium (Li)-induced nephrogenic diabetes insipidus (NDI) has been attributed to the increased production of renal prostaglandin (PG)E(2). Previously we reported that extracellular nucleotides (ATP/UTP), acting through P(2y2) receptor in rat medullary collecting duct (mCD), produce and release PGE(2). Hence we hypothesized that increased production of PGE(2) in Li-induced NDI may be mediated by enhanced

Full Text available with Trip Pro

2009 American Journal of Physiology. Renal physiology

125. Assessment of hypernatraemia

is diagnosed in males and females in equal numbers. Differentials Central diabetes insipidus Hyperosmolar hyperglycaemic state (HHS) Nephrogenic diabetes insipidus Severe diarrhoea Vomiting Limited access to water Primary hypodipsia Cushing's syndrome Primary aldosteronism Post-obstructive diuresis Laxative and bowel cleansing agent use Enteric fistulae Diuretics Heat exposure Exercise Fever Severe burns Inadequate breastfeeding of infants Salt ingestion High-protein diet Use of intravenous sodium chloride

2018 BMJ Best Practice

126. Assessment of hypercalcaemia

renal function may be severely damaged. Taniegra ED. Hyperparathyroidism. Am Fam Physician. 2004;69:333-339. http://www.aafp.org/afp/2004/0115/p333.html http://www.ncbi.nlm.nih.gov/pubmed/14765772?tool=bestpractice.com Hypercalcaemia also causes dehydration by inducing renal resistance to vasopressin, leading to nephrogenic diabetes insipidus. Dehydration, in turn, leads to a corresponding further increase in serum calcium concentration. Pathophysiology Phosphate solubility is closely related

2018 BMJ Best Practice

127. Assessment of hypercalcaemia

renal function may be severely damaged. Taniegra ED. Hyperparathyroidism. Am Fam Physician. 2004;69:333-339. http://www.aafp.org/afp/2004/0115/p333.html http://www.ncbi.nlm.nih.gov/pubmed/14765772?tool=bestpractice.com Hypercalcaemia also causes dehydration by inducing renal resistance to vasopressin, leading to nephrogenic diabetes insipidus. Dehydration, in turn, leads to a corresponding further increase in serum calcium concentration. Pathophysiology Phosphate solubility is closely related

2018 BMJ Best Practice

128. Clinical Practice Guideline: Maintenance Intravenous Fluids in Children

to evaluate the fluid type, rate, and risk of renal injury and hyponatremia for this population. The committee did not specifically review literature for those with the following care needs: patients with significant renal concentrating defects, such as nephrogenic diabetes insipidus, and patients with voluminous diarrhea or severe burns who may have significant ongoing free-water losses. Complications Hyponatremia The reviewed studies revealed the relative risk of developing mild and moderate (...) maintenance IVFs are required does not mean that there are no indications for administering hypotonic fluids or that isotonic fluids will be safe in all patients. Patients with significant renal concentrating defects, such as nephrogenic diabetes insipidus, could develop hypernatremia if they are administered isotonic fluids. Patients with voluminous diarrhea or severe burns may require a hypotonic fluid to keep up with ongoing free-water losses. Hypotonic fluids may also be required to correct

2019 American Academy of Pediatrics

129. CRACKCast E160 – Lithium

, NSAIDS, ACE/ARB drugs Dementia Increased age SILENT: cerebellar findings with pseudodementia [4] List 4 factors which impair renal filtration of Li thium Volume depletion Kidney injury Nephrogenic DI Diuretic use [5] List 2 disease states caused by Li thium Here’s a bunch: nephrogenic diabetes insipidus Hypothyroidism (and hyperthyroidism) Both of these conditions are reversible with discontinuation of the medication and respond well to conventional management. Hypercalcemia and hyperparathyroidism (...) Somnolence Extrapyramidal symptoms Coma Seizures Cardiac Sinus node dysfunction AV blockade Brugada pattern on ECG Ischemic changes on ECG QTc prolongation AV, Atrioventricular; ECG, electrocardiogram. Mnemonic time: Leukostasis Insipidus Tremor / teratogen Hypothyroidism Increased weight Vomiting ? nausea Myocardium = ecg changes Serotonin syndrome / nms like effect [3] List risk factors for toxicity in the setting of chronic lithium use. Nephrogenic DI Renal impairment Acute illness Diuretic use

2018 CandiEM

130. Routine investigation and monitoring of adult HIV-1-positive individuals (2019 interim update)

in everyone aged >50 years, post-menopausal women, or other high-risk patients every 3 years 1 MSM + frequent partner change /IDU/chaotic lifestyle/adolescent/CSW/other drug use/chemsex/other risk. 3.3 Monitoring of patients who are now starting ART who did not start soon after the baseline visit History • Patient’s ideas about HIV and its treatment; screening for depression Examination • Only if new symptoms Assessments • Assessment of the common complications of treatment such as diabetes, heart disease (...) . Sex Transm Dis 2015; 42: 171–179. BHIVA guidelines on the routine investigation and monitoring of HIV-1-positive adults 25 4.4.4 Other assessments Recommendations • We recommend that the following assessments be made annually (2C): ? QRISK2 only if smoker or diabetic and/or BMI>30 and age >40 years (unnecessary if there is already established vascular disease); ? Hepatitis A/B vaccine course completed, any boosters required; ? Vaccines Flu annual; ? Check annual cervical smear (if resources permit

2019 British HIV Association

131. CRACKCast E125 – Electrolyte Disorders

ingestion Saline infusions Saline enemas IV sodium bicarbonate Poorly diluted interval feedings Primary hyperaldosteronism Hemodialysis Cushing’s syndrome Conn’s syndrome [8] List four central and four nephrogenic causes of diabetes insipidus. Box 117.4 Central Idiopathic Familial disease Cancer Hypoxic encephalopathy Infiltrative disorders Post supraventricular tachycardia Anorexia nervosa Nephrogenic Chronic renal insufficiency Polycystic kidney disease Lithium toxicity Hypercalcemia Hypokalemia (...) : Heatstroke Increased insensible losses: Burns, sweating Gastrointestinal loss: Diarrhea, protracted vomiting, continuous gastrointestinal suction Osmotic diuresis: Glucose, mannitol, enteral feeding [2] Loss of body water: Diabetes insipidus Neurogenic Elderly with “reset” osmostat Hypothalamic dysfunction Suprasellar or infrasellar tumors Renal disease Drugs (amphotericin, phenytoin, lithium, aminoglycosides,methoxyflurane) Sickle cell disease [3] Increased sodium: Salt tablet ingestion Salt water

2017 CandiEM

132. LUTS in men

during the night (more than 35% of the 24-hour urine production). Nocturnal polyuria can be caused by: Medical conditions (such as diabetes mellitus, diabetes insipidus, adrenal insufficiency, hypercalcaemia, liver failure, polyuric renal failure, chronic heart failure, pyelonephritis, and chronic venous stasis). Drugs (such as calcium channel blockers, diuretics, and selective serotonin reuptake inhibitor [SSRI] antidepressants). [ ] Stress urinary incontinence What are the causes of stress urinary (...) men have at least one LUTS; however, symptoms are often mild or not very bothersome. Benign prostatic enlargement is a common cause of LUTs. Other causes include neurological conditions (such as dementia and diabetic neuropathy), infection, injury to the urethral area, drugs (such as diuretics and antimuscarinics), and cancer. LUTS can be grouped into storage, voiding, and post-micturition symptoms. To establish what type (or combination of types) of LUTS the man has, questions should be asked

2019 NICE Clinical Knowledge Summaries

133. Hypercalcaemia

motor neurone deficits, hypotonia, hyporeflexia, and ataxia). Gastrointestinal Nausea, vomiting, anorexia, weight loss. Constipation, abdominal pain. See the CKS topic on for more information. Peptic ulcer, pancreatitis (both rare). See the CKS topics on and for more information. Renal Renal colic due to renal stones (nephrolithiasis). See the CKS topic on for more information. Thirst, polyuria, polydipsia, nocturia, and dehydration (due to nephrogenic diabetes insipidus). Renal impairment (due (...) fractures, renal stones, or malignancy. Any past history of radiotherapy to the head and neck. Any family history of hypercalaemia (for example due to genetic forms of primary hyperparathyroidism, or familial hypocalciuric hypercalcaemia). Any , supplements, or over-the-counter preparations that may be causative or contributory. Examine the person: Assess hydration status — people with hypercalcaemia are often dehydrated due to nephrogenic diabetes insipidus due to reduced oral intake resulting from

2019 NICE Clinical Knowledge Summaries

134. Bipolar disorder

for local implementation have been added to this topic. March 2012 — minor update. The 2012/2013 QOF indicators have been added to this topic. Issued in April 2012. February 2012 — minor update. New information about the rare association of quetiapine with diabetic ketoacidosis has been added. Issued in February 2012. January 2012 — minor update. Relevant information from the Medicines and Healthcare products Regulatory Agency (MHRA) about a risk of extra-pyramidal effects or withdrawal symptoms (...) die from cardiovascular disease; around twice the expected mortality rate for the general population. Type 2 diabetes, dyslipidaemia, metabolic syndrome, obesity — between 19% and 49% of people with bipolar disorder have comorbid obesity. Chronic kidney disease. Respiratory disease (such as chronic obstructive pulmonary disease). [ ; ; ; ; ; ; ; ] Prognosis What is the prognosis? Bipolar disorder requires lifelong treatment and management. The natural history of bipolar disorder usually includes

2019 NICE Clinical Knowledge Summaries

135. Adenine acts in the kidney as a signaling factor and causes salt- and water-losing nephropathy: Early mechanism of adenine-induced renal injury. (PubMed)

depletion as indicated by a significant body weight loss, increased blood urea nitrogen (BUN), hematocrit and hemoglobin levels, all of which were significantly corrected with salt replacement. Adenine-induced urinary concentrating defect was not corrected by exogenous vasopressin (AVP), and correlated with reduced cAMP production in vivo and in vitro. In conclusion, adenine acts on renal tubules as a signaling molecule and causes nephrogenic diabetes insipidus with salt wasting, at least, by directly

2019 American Journal of Physiology. Renal physiology

136. Fluconazole Increases Osmotic Water Transport in Renal Collecting Duct through Effects on Aquaporin-2 Trafficking. (PubMed)

, a VR2 blocker that causes a nephrogenic diabetes insipidus-like excessive loss of hypotonic urine.Fluconazole increased plasma membrane localization of AQP2 in principal cells independent of AVP. It also led to an increased AQP2 abundance associated with alterations in phosphorylation status and ubiquitination as well as inhibition of RhoA. In isolated mouse collecting ducts, fluconazole increased transepithelial water reabsorption. In mice, fluconazole increased collecting duct AQP2 plasma membrane (...) localization and reduced urinary output. Fluconazole also reduced urinary output in tolvaptan-treated mice.Fluconazole promotes collecting duct AQP2 plasma membrane localization in the absence of AVP. Therefore, it might have utility in treating forms of diabetes insipidus (e.g., X-linked nephrogenic diabetes insipidus) in which the kidney responds inappropriately to AVP.Copyright © 2019 by the American Society of Nephrology.

2019 Journal of the American Society of Nephrology

137. Impact of Long-Term Lithium Treatment on Renal Function in Patients With Bipolar Disorder Based on Novel Biomarkers. (PubMed)

Impact of Long-Term Lithium Treatment on Renal Function in Patients With Bipolar Disorder Based on Novel Biomarkers. Lithium in the form of lithium carbonate (Li2CO3) has become one of the most effective and widely prescribed drugs for mood stabilization. However, lithium has adverse effects on renal tubular functions, such as decreased concentrating function of the kidneys, and even occasional symptoms of nephrogenous diabetes insipidus occur with additional evidence of glomerular disruption

2019 Journal of Clinical Psychopharmacology

138. EJE Prize 2019 - New diagnostic approaches for patients with polyuria-polydipsia syndrome. (PubMed)

EJE Prize 2019 - New diagnostic approaches for patients with polyuria-polydipsia syndrome. Diabetes insipidus (DI), be it from central or nephrogenic origin, must be differentiated from secondary forms of hypotonic polyuria such as primary polydipsia. Differentiation is crucial since wrong treatment can have deleterious consequences. Since decades, the gold standard for differentiation has been the water deprivation test, which has limitations leading to an overall unsatisfying diagnostic (...) . A high correlation between copeptin and AVP has been shown. Accordingly, copeptin mirrors the amount of AVP in the circulation and has led to a "revival" of the direct test in the differential diagnosis of DI. We have shown that a baseline copeptin, without prior thirsting, unequivocally identifies patients with nephrogenic DI. In contrast, for the differentiation between central DI and primary polydipsia, a stimulated copeptin level of 4.9 pmol/L upon hypertonic saline infusion differentiates

2019 European Journal of Endocrinology

139. An uncommon case of arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome and review of the renal involvement: Questions. (PubMed)

-consanguineous parents, diagnosed with an incomplete phenotype of arthrogryposis, renal dysfunction, and cholestasis syndrome with arthrogryposis and renal tubular dysfunction but without cholestasis. At 11 years of age, she was found to have impaired renal function, nephrotic-range proteinuria, Fanconi syndrome, and distal renal tubular acidosis. She also had hypercalciuria, nephrogenic diabetes insipidus, and small kidneys by renal ultrasound. Genetic analysis using whole exome sequencing showed a mutation

2019 Pediatric Nephrology

140. Renal concentrating ability and glomerular filtration rate in lithium-treated patients. (PubMed)

. Demographic and clinical characteristics and blood and urine samples were collected. Additionally, a dDAVP-test was performed to determine maximal RCA.A dDAVP-test was performed in 98 patients (37 males, 61 females). Mean age was 51 years (SD: 12), median duration of lithium therapy 7 years (IQR: 4-15), mean maximal urine osmolality (Uosmol) 725 mOsmol/kg (SD: 153), and median eGFR 84 ml/min/1.73 m2 (IQR: 68-95). Fifty patients (51%) had an impaired RCA and 17 patients (17%) had nephrogenic diabetes (...) insipidus (Uosmol 600-800 and < 600 mOsmol/kg, respectively). Notably, clinical symptoms did not predict an impaired RCA. Nineteen patients (19%) had an eGFR ≤ 60 ml/min/ 1.73 m2. Multivariable regression analysis showed a significant association between the duration of lithium treatment and maximal Uosmol (B = -6.1, 95%-CI: -9.4, -2.9, p < 0.001) and eGFR (B = -0.6, 95%-CI: 0.2, -3.3; p < 0.01).RCA is impaired in the majority of lithium-treated patients. Both RCA and eGFR are inversely associated

2019 Netherlands Journal of Medicine

To help you find the content you need quickly, you can filter your results via the categories on the right-hand side >>>>