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BMJ (Clinical Research Ed.) Feb 2019
Topics: Antidiuretic Agents; Deamino Arginine Vasopressin; Diabetes Insipidus; Endocrinology; Humans; Male; Osmolar Concentration; Polydipsia; Polyuria; United Kingdom; Young Adult
PubMed: 30819684
DOI: 10.1136/bmj.l321 -
The Journal of Clinical Endocrinology... Dec 2022Recent data show that patients with a diagnosis of diabetes insipidus (DI) are coming to harm. Here we give the rationale for a name change to arginine vasopressin...
Recent data show that patients with a diagnosis of diabetes insipidus (DI) are coming to harm. Here we give the rationale for a name change to arginine vasopressin deficiency and resistance for central and nephrogenic DI, respectively.
Topics: Humans; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diabetes Mellitus
PubMed: 36355385
DOI: 10.1210/clinem/dgac547 -
Experientia Supplementum (2012) 2019Body fluid homeostasis is essential for normal life. In the maintenance of water balance, the most important factor and regulated process is the excretory function of... (Review)
Review
Body fluid homeostasis is essential for normal life. In the maintenance of water balance, the most important factor and regulated process is the excretory function of the kidneys. The kidneys are capable to compensate not only the daily fluctuations of water intake but also the consequences of fluid loss (respiration, perspiration, sweating, hemorrhage). The final volume and osmolality of the excreted urine is set in the collecting duct via hormonal regulation. The hormone of water conservation is the vasopressin (AVP), and a large volume of urine is produced and excreted in the absence of AVP secretion or if AVP is ineffective in the kidneys. The aquaporin-2 water channel (AQP2) is expressed in the principal cells, and it plays an essential role in the reabsorption of water in the collecting ducts via type 2 vasopressin receptor (V2R)-mediated mechanism. If neural or hormonal regulation fails to operate the normal function of AVP-V2R-AQP2 system, it can result in various diseases such as diabetes insipidus (DI) or nephrogenic syndrome of inappropriate diuresis (NSIAD). The DI is characterized by excessive production of hyposmotic urine ("insipidus" means tasteless) due to the inability of the kidneys to concentrate urine. In this chapter, we focus and discuss the pathophysiology of nephrogenic DI (NDI) and the potential therapeutic interventions in the light of the current experimental data.
Topics: Aquaporin 2; Diabetes Insipidus, Nephrogenic; Humans; Receptors, Vasopressin; Water-Electrolyte Balance
PubMed: 31588538
DOI: 10.1007/978-3-030-25905-1_15 -
The American Journal of Case Reports Dec 2021BACKGROUND Diabetes insipidus (DI) is a clinical syndrome characterized by polyuria and polydipsia that result from a deficiency of antidiuretic hormone (ADH), central...
BACKGROUND Diabetes insipidus (DI) is a clinical syndrome characterized by polyuria and polydipsia that result from a deficiency of antidiuretic hormone (ADH), central DI, or resistance to ADH, nephrogenic DI. In otherwise healthy patients with DI, normal thirst mechanism, and free access to water, the thirst system can maintain plasma osmolality in the near-normal range. However, in cases where DI presents with adipsia, cognitive impairment, or restricted access to water, true hypernatremia may occur, leading to severe morbidity and mortality. CASE REPORT We report a case of a 2-year-old boy who had global developmental delay and post-brain debulking surgery involving the hypothalamic region, which resulted in central DI and thirst center dysfunction. We describe the clinical presentation, the current understanding of adipsic DI, and a new practical approach for management. The main guidelines of treatment include (1) fixed desmopressin dosing that allows minimal urinary breakthroughs in-between the doses; (2) timely diaper weight-based replacement of water; (3) bodyweight-based fluid correction 2 times a day, and (4) providing the nutritional and water requirements in a way similar to any healthy child but at fixed time intervals. CONCLUSIONS This plan of management showed good effectiveness in controlling plasma sodium level and volume status of a child with adipsic DI without interfering with his average growth. This home treatment method is practical and readily available, provided that the family remains very adherent.
Topics: Child; Child, Preschool; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hypernatremia; Male; Thirst
PubMed: 34898594
DOI: 10.12659/AJCR.934193 -
European Journal of Endocrinology May 2022The differential diagnosis of diabetes insipidus is challenging. The most reliable approaches are copeptin measurements after hypertonic saline infusion or arginine,... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
The differential diagnosis of diabetes insipidus is challenging. The most reliable approaches are copeptin measurements after hypertonic saline infusion or arginine, which is a known growth hormone secretagogue but has recently also been shown to stimulate the neurohypophysis. Similar to arginine, glucagon stimulates growth hormone release, but its effect on the neurohypophysis is poorly studied.
DESIGN
Double-blind, randomized, placebo-controlled trial including 22 healthy participants, 10 patients with central diabetes insipidus, and 10 patients with primary polydipsia at the University Hospital Basel, Switzerland.
METHODS
Each participant underwent the glucagon test (s.c. injection of 1 mg glucagon) and placebo test. The primary objective was to determine whether glucagon stimulates copeptin and to explore whether the copeptin response differentiates between diabetes insipidus and primary polydipsia. Copeptin levels were measured at baseline, 30, 60, 90, 120, 150, and 180 min after injection.
RESULTS
In healthy participants, glucagon stimulated copeptin with a median increase of 7.56 (2.38; 28.03) pmol/L, while placebo had no effect (0.10 pmol/L (-0.70; 0.68); P < 0.001). In patients with diabetes insipidus, copeptin showed no relevant increase upon glucagon, with an increase of 0.55 (0.21; 1.65) pmol/L, whereas copeptin was stimulated in patients with primary polydipsia with an increase of 15.70 (5.99; 24.39) pmol/L. Using a copeptin cut-off level of 4.6pmol/L had a sensitivity of 100% (95% CI: 100-100) and a specificity of 90% (95% CI: 70-100) to discriminate between diabetes insipidus and primary polydipsia.
CONCLUSION
Glucagon stimulates the neurohypophysis, and glucagon-stimulated copeptin has the potential for a safe, novel, and precise test in the differential diagnosis of diabetes insipidus.
Topics: Arginine; Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Glucagon; Glycopeptides; Growth Hormone; Humans; Polydipsia, Psychogenic
PubMed: 35521789
DOI: 10.1530/EJE-22-0033 -
La Revue Du Praticien Apr 2022"Central diabetes insipidus Diabetes insipidus may remain undetected for a long time, the ionogram remaining normal as long as polydipsia compensates for diuresis. In...
"Central diabetes insipidus Diabetes insipidus may remain undetected for a long time, the ionogram remaining normal as long as polydipsia compensates for diuresis. In the first place, and by argument of frequency, polyuria should rule out diabetes. Diabetes insipidus is evoked in the presence of an incapacitating polyuro polydipsic syndrome, especially at night. Pituitary MRI eliminate a tumoral or infiltrative cause and confirm a central cause by the disappearance of the physiological t1 hypersignal in the post-pituitary gland. A water restriction test should only be performed in a hospital setting under close supervision. Lifetime hormone replacement therapy is appropriate in situations of pregnancy, risk of dehydration, and signs of overdose must be known by the patient, who must be educated about his or her disease."
Topics: Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Female; Hospitals; Humans; Magnetic Resonance Imaging; Male; Pregnancy; Syndrome
PubMed: 35638996
DOI: No ID Found -
Annales D'endocrinologie Jun 2016Diabetes insipidus (DI) is a rare complication of pregnancy. It is usually transient, being due to increased placental production of vasopressinase that inactivates... (Review)
Review
Diabetes insipidus (DI) is a rare complication of pregnancy. It is usually transient, being due to increased placental production of vasopressinase that inactivates circulating vasopressin. Gestational, transient DI occurs late in pregnancy and disappears few days after delivery. Acquired central DI can also occur during pregnancy, for example in a patient with hypophysitis or neuroinfundibulitis during late pregnancy or postpartum. Finally, pre-existing central or nephrogenic DI may occasionally be unmasked by pregnancy. Treatment with dDAVP (desmopressin, Minirin(®)) is very effective on transient DI of pregnancy and also on pre-existing or acquired central DI. Contrary to vasopressin, dDAVP is not degraded by vasopressinase. Nephrogenic DI is insensitive to dDAVP and is therefore more difficult to treat during pregnancy if fluid intake needs to be restricted.
Topics: Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Female; Humans; Pregnancy; Pregnancy Complications; Vasopressins
PubMed: 27172867
DOI: 10.1016/j.ando.2016.04.005 -
BMC Psychiatry Jul 2018Lithium is the gold-standard treatment for bipolar disorder, is highly effective in treating major depressive disorder, and has anti-suicidal properties. However,... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
Lithium is the gold-standard treatment for bipolar disorder, is highly effective in treating major depressive disorder, and has anti-suicidal properties. However, clinicians are increasingly avoiding lithium largely due to fears of renal toxicity. Nephrogenic Diabetes Insipidus (NDI) occurs in 15-20% of lithium users and predicts a 2-3 times increased risk of chronic kidney disease (CKD). We recently found that use of statins is associated with lower NDI risk in a cross-sectional study. In this current paper, we describe the methodology of a randomized controlled trial (RCT) to treat lithium-induced NDI using atorvastatin.
METHODS
We will conduct a 12-week, double-blind placebo-controlled RCT of atorvastatin for lithium-induced NDI at McGill University, Montreal, Canada. We will recruit 60 current lithium users, aged 18-85, who have indicators of NDI, which we defined as urine osmolality (UOsm) < 600 mOsm/kg after 10-h fluid restriction. We will randomize patients to atorvastatin (20 mg/day) or placebo for 12 weeks. We will examine whether this improves measures of NDI: UOsm and aquaporin (AQP2) excretion at 12-week follow-up, adjusted for baseline.
RESULTS
Not applicable.
CONCLUSION
The aim of this clinical trial is to provide preliminary data about the efficacy of atorvastatin in treating NDI. If successful, lithium could theoretically be used more safely in patients with a reduced subsequent risk of CKD, hypernatremia, and acute kidney injury (AKI). If future definitive trials confirm this, this could potentially allow more patients to benefit from lithium, while minimizing renal risk.
TRIAL REGISTRATION
ClinicalTrials.gov NCT02967653 . Registered in February 2017.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Atorvastatin; Bipolar Disorder; Canada; Cross-Sectional Studies; Depressive Disorder, Major; Diabetes Insipidus, Nephrogenic; Double-Blind Method; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Kidney; Lithium Compounds; Male; Middle Aged; Young Adult
PubMed: 30012135
DOI: 10.1186/s12888-018-1793-9 -
Physiological Reports Nov 2017This is a editorial focus written to highlight the findings by Yang et al in the article “The Soluble (Pro)Renin Receptor Does Not Influence Lithium‐Induced Diabetes...
This is a editorial focus written to highlight the findings by Yang et al in the article “The Soluble (Pro)Renin Receptor Does Not Influence Lithium‐Induced Diabetes Insipidus but Does Provoke Beiging of White Adipose Tissue in Mice.”
Topics: Adipose Tissue, White; Animals; Diabetes Insipidus; Lithium; Mice; Renin
PubMed: 29138355
DOI: 10.14814/phy2.13405 -
Best Practice & Research. Clinical... Sep 2020In the pregnant patient, hypotonic polyuria in the setting of elevated serum osmolality and polydipsia should narrow the differential to causes related to diabetes... (Review)
Review
In the pregnant patient, hypotonic polyuria in the setting of elevated serum osmolality and polydipsia should narrow the differential to causes related to diabetes insipidus (DI). Gestational DI, also called transient DI of pregnancy, is a distinct entity, unique from central DI or nephrogenic DI which may both become exacerbated during pregnancy. These three different processes relate to vasopressin, where increased metabolism, decreased production or altered renal sensitivity to this neuropeptide should be considered. Gestational DI involves progressively rising levels of placental vasopressinase throughout pregnancy, resulting in decreased endogenous vasopressin and resulting hypotonic polyuria worsening through the pregnancy. Gestational DI should be distinguished from central and nephrogenic DI that may be seen during pregnancy through use of clinical history, urine and serum osmolality measurements, response to desmopressin and potentially, the newer, emerging copeptin measurement. This review focuses on a brief overview of osmoregulatory and vasopressin physiology in pregnancy and how this relates to the clinical presentation, pathophysiology, diagnosis and management of gestational DI, with comparisons to the other forms of DI during pregnancy. Differentiating the subtypes of DI during pregnancy is critical in order to provide optimal management of DI in pregnancy and avoid dehydration and hypernatremia in this vulnerable population.
Topics: Dehydration; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Female; Humans; Hypernatremia; Neurophysins; Osmoregulation; Polydipsia; Polyuria; Pregnancy; Pregnancy Complications; Protein Precursors; Vasopressins; Water-Electrolyte Balance
PubMed: 32205050
DOI: 10.1016/j.beem.2020.101384