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The Journal of Clinical Endocrinology... Sep 2022Central diabetes insipidus (CDI) is a clinical syndrome which results from loss or impaired function of vasopressinergic neurons in the hypothalamus/posterior pituitary,... (Review)
Review
Central diabetes insipidus (CDI) is a clinical syndrome which results from loss or impaired function of vasopressinergic neurons in the hypothalamus/posterior pituitary, resulting in impaired synthesis and/or secretion of arginine vasopressin (AVP). AVP deficiency leads to the inability to concentrate urine and excessive renal water losses, resulting in a clinical syndrome of hypotonic polyuria with compensatory thirst. CDI is caused by diverse etiologies, although it typically develops due to neoplastic, traumatic, or autoimmune destruction of AVP-synthesizing/secreting neurons. This review focuses on the diagnosis and management of CDI, providing insights into the physiological disturbances underpinning the syndrome. Recent developments in diagnostic techniques, particularly the development of the copeptin assay, have improved accuracy and acceptability of the diagnostic approach to the hypotonic polyuria syndrome. We discuss the management of CDI with particular emphasis on management of fluid intake and pharmacological replacement of AVP. Specific clinical syndromes such as adipsic diabetes insipidus and diabetes insipidus in pregnancy as well as management of the perioperative patient with diabetes insipidus are also discussed.
Topics: Adult; Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Polyuria; Syndrome
PubMed: 35771962
DOI: 10.1210/clinem/dgac381 -
Presse Medicale (Paris, France : 1983) Dec 2021Diabetes insipidus (DI) is a disorder characterized by a high hypotonic urinary output of more than 50ml per kg body weight per 24 hours, with associated polydipsia of... (Review)
Review
Diabetes insipidus (DI) is a disorder characterized by a high hypotonic urinary output of more than 50ml per kg body weight per 24 hours, with associated polydipsia of more than 3 liters a day [1,2]. Central DI results from inadequate secretion and usually deficient synthesis of Arginine vasopressin (AVP) in the hypothalamus or pituitary gland. Besides central DI further underlying etiologies of DI can be due to other primary forms (renal origin) or secondary forms of polyuria (resulting from primary polydipsia). All these forms belong to the Polyuria Polydipsia Syndrom (PPS). In most cases central and nephrogenic DI are acquired, but there are also congenital forms caused by genetic mutations of the AVP gene (central DI) [3] or by mutations in the gene for the AVP V2R or the AQP2 water channel (nephrogenic DI) [4]. Primary polydipsia (PP) as secondary form of polyuria includes an excessive intake of large amounts of fluid leading to polyuria in the presence of intact AVP secretion and appropriate antidiuretic renal response. Differentiation between the three mentioned entities is difficult [5], especially in patients with Primary polydipsia or partial, mild forms of DI [1,6], but different tests for differential diagnosis, most recently based on measurement of copeptin, and a thorough medical history mostly lead to the correct diagnosis. This is important since treatment strategies vary and application of the wrong treatment can be dangerous [7]. Treatment of central DI consists of fluid management and drug therapy with the synthetic AVP analogue Desmopressin (DDAVP), that is used as nasal or oral preparation in most cases. Main side effect can be dilutional hyponatremia [8]. In this review we will focus on central diabetes insipidus and describe the prevalence, the clinical manifestations, the etiology as well as the differential diagnosis and management of central diabetes insipidus in the out- and inpatient setting.
Topics: Adult; Antidiuretic Agents; Aquaporin 2; Child; Deamino Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Glycopeptides; Humans; Mutation; Neurophysins; Pituitary Gland; Polydipsia; Polyuria; Protein Precursors; Vasopressins
PubMed: 34718110
DOI: 10.1016/j.lpm.2021.104093 -
Deutsches Arzteblatt International Mar 2018The incidence of type 1 diabetes mellitus in childhood and adolescence is steadily rising and now stands at 22.9 new cases per year per 100 000 persons up to age 15. (Review)
Review
BACKGROUND
The incidence of type 1 diabetes mellitus in childhood and adolescence is steadily rising and now stands at 22.9 new cases per year per 100 000 persons up to age 15.
METHODS
This review is based on pertinent publications retrieved by a selective literature search, with special attention to the current German S3 guideline on diabetes in childhood and adolescence.
RESULTS
Polydipsia, polyuria, and weight loss are the characteristic presenting symptoms of diabetes mellitus. The acutely presenting patient needs immediate stabilization because of the danger of rapid metabolic decompensation (risk of keto - acidosis, 21.1%). Long-term insulin therapy can be delivered either by subcutaneous injection or by an insulin pump. The goals of treatment are the near-normalization of glucose metabolism (HbA1c <7.5%), the avoidance of acute complications (hypoglycemia and ketoacidosis), the reduction of diabetes-specific sequelae (retinopathy, nephropathy, neuropathy, hypertension, and hyperlipidemia), unrestricted participation in age-appropriate everyday activities, and normal physical and psychosocial development. Children and adolescents with diabetes need individualized treatment with frequent adjustments and holistic overall care so that these goals can be effectively met.
CONCLUSION
Every physician must be able to diagnose the initial presentation of diabetes and to initiate the first steps in its management. The patient should be referred as soon as possible to a diabetes team that has experience in the treatment of children and adolescents.
Topics: Adolescent; Child; Child, Preschool; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Disabled Children; Female; Germany; Humans; Hypoglycemic Agents; Infant; Insulin; Male; Polydipsia; Polyuria; Weight Loss
PubMed: 29563012
DOI: 10.3238/arztebl.2018.0146 -
Urology Nov 2019Nocturnal polyuria (NP), characterized by overproduction of urine at night (greater than 20%-33% of total 24-hour urine volume depending on age), is a major contributing... (Review)
Review
Nocturnal polyuria (NP), characterized by overproduction of urine at night (greater than 20%-33% of total 24-hour urine volume depending on age), is a major contributing factor in most nocturia cases. Nocturia can be caused by intake, urological, nephrological, hormonal, sleep, and cardiovascular factors. It is therefore important to accurately diagnose both the type of nocturia and the potentially associated medical conditions to determine appropriate treatment. Diagnostic tools, in addition to a thorough history and physical examination, include voiding/bladder diary analyses and questionnaires to diagnose nocturia type (NP, diminished nocturnal/global bladder capacity, global polyuria) and causative factors. Lifestyle modifications are the first intervention implemented for the management of nocturia and NP but, as symptoms progress, such measures may be insufficient, and pharmacotherapy may be initiated. While drugs for benign prostatic hyperplasia and overactive bladder have demonstrated statistically significant reductions in nocturnal voids, patients often fail to achieve a clinically meaningful response. Antidiuretic treatment is warranted for patients with nocturia due to NP because, in many patients, it treats the underlying cause (ie, insufficient secretion of antidiuretic hormone arginine vasopressin) that leads to overproduction of urine at night and has been shown to provide statistically significant reductions in nocturnal voids. Desmopressin, a synthetic analog of arginine vasopressin, is the only antidiuretic treatment indicated specifically for nocturia due to NP. Overall, the pathophysiology of NP is complex and differs from that of other types of nocturia. A multidisciplinary approach is necessary to effectively diagnose and manage this bothersome condition.
Topics: Diuresis; Humans; Nocturia; Polyuria; Treatment Outcome
PubMed: 31586470
DOI: 10.1016/j.urology.2019.09.022 -
Cleveland Clinic Journal of Medicine Jan 2006Diabetes insipidus, characterized by excretion of copious volumes of dilute urine, can be life-threatening if not properly diagnosed and managed. It can be caused by two... (Review)
Review
Diabetes insipidus, characterized by excretion of copious volumes of dilute urine, can be life-threatening if not properly diagnosed and managed. It can be caused by two fundamentally different defects: inadequate or impaired secretion of antidiuretic hormone (ADH) from the posterior pituitary gland (neurogenic or central diabetes insipidus) or impaired or insufficient renal response to ADH (nephrogenic diabetes insipidus). The distinction is essential for effective treatment.
Topics: Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Humans; Polyuria
PubMed: 16444918
DOI: 10.3949/ccjm.73.1.65 -
Current Urology Reports Feb 2018To assess current pharmacological principles used for treatment of nocturia/nocturnal polyuria. (Review)
Review
PURPOSE OF REVIEW
To assess current pharmacological principles used for treatment of nocturia/nocturnal polyuria.
RECENT FINDINGS
The pathophysiology of nocturia is often multifactorial, but two main mechanisms have been identified, occurring alone or in combination: low functional bladder capacity and nocturnal polyuria. The multifactorial pathophysiology not only implies several possible targets for therapeutic intervention but also means that it is unlikely that one treatment modality including drugs will be successful in all patients. Drugs approved for the treatment of male LUTS and male and female OAB are known to be far more effective for treatment of the daytime symptoms than for nocturia. Several pharmacological principles have been tested with varying success. The treatment of choice should depend upon the main underlying cause, thus aiming primarily to increase bladder capacity by counteracting detrusor overactivity and/or reducing nocturnal polyuria. Using current available agents, effective, personalized treatment should be designed taking into account gender, co-morbidities, and identified etiological factors. However, there is a medical need for new, approved drugs for treatments for patients with nocturia.
Topics: Aged; Female; Humans; Male; Nocturia; Polyuria
PubMed: 29427214
DOI: 10.1007/s11934-018-0750-y -
The New England Journal of Medicine Aug 2018The indirect water-deprivation test is the current reference standard for the diagnosis of diabetes insipidus. However, it is technically cumbersome to administer, and...
BACKGROUND
The indirect water-deprivation test is the current reference standard for the diagnosis of diabetes insipidus. However, it is technically cumbersome to administer, and the results are often inaccurate. The current study compared the indirect water-deprivation test with direct detection of plasma copeptin, a precursor-derived surrogate of arginine vasopressin.
METHODS
From 2013 to 2017, we recruited 156 patients with hypotonic polyuria at 11 medical centers to undergo both water-deprivation and hypertonic saline infusion tests. In the latter test, plasma copeptin was measured when the plasma sodium level had increased to at least 150 mmol per liter after infusion of hypertonic saline. The primary outcome was the overall diagnostic accuracy of each test as compared with the final reference diagnosis, which was determined on the basis of medical history, test results, and treatment response, with copeptin levels masked.
RESULTS
A total of 144 patients underwent both tests. The final diagnosis was primary polydipsia in 82 patients (57%), central diabetes insipidus in 59 (41%), and nephrogenic diabetes insipidus in 3 (2%). Overall, among the 141 patients included in the analysis, the indirect water-deprivation test determined the correct diagnosis in 108 patients (diagnostic accuracy, 76.6%; 95% confidence interval [CI], 68.9 to 83.2), and the hypertonic saline infusion test (with a copeptin cutoff level of >4.9 pmol per liter) determined the correct diagnosis in 136 patients (96.5%; 95% CI, 92.1 to 98.6; P<0.001). The indirect water-deprivation test correctly distinguished primary polydipsia from partial central diabetes insipidus in 77 of 105 patients (73.3%; 95% CI, 63.9 to 81.2), and the hypertonic saline infusion test distinguished between the two conditions in 99 of 104 patients (95.2%; 95% CI, 89.4 to 98.1; adjusted P<0.001). One serious adverse event (desmopressin-induced hyponatremia that resulted in hospitalization) occurred during the water-deprivation test.
CONCLUSIONS
The direct measurement of hypertonic saline-stimulated plasma copeptin had greater diagnostic accuracy than the water-deprivation test in patients with hypotonic polyuria. (Funded by the Swiss National Foundation and others; ClinicalTrials.gov number, NCT01940614 .).
Topics: Adult; Deamino Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Female; Glycopeptides; Humans; Hyponatremia; Male; Middle Aged; Osmolar Concentration; Polydipsia; Polyuria; ROC Curve; Saline Solution, Hypertonic; Sensitivity and Specificity; Urine; Water Deprivation
PubMed: 30067922
DOI: 10.1056/NEJMoa1803760 -
European Journal of Case Reports in... 2021Gemfibrozil is a lipid-regulating agent used mainly to treat patients with hypertriglyceridaemia, especially those at risk for acute pancreatitis. Like any other...
UNLABELLED
Gemfibrozil is a lipid-regulating agent used mainly to treat patients with hypertriglyceridaemia, especially those at risk for acute pancreatitis. Like any other pharmacological agent, gemfibrozil has known adverse effects, mainly gastrointestinal, such as cholelithiasis, gallstones, elevated transaminase, and other non-specific symptoms including dyspepsia, nausea and vomiting. Other reported adverse reactions are dizziness and vertigo, myopathy and rhabdomyolysis, angioedema, urticaria and rash. As far as we knew, gemfibrozil does not have urinary tract adverse reactions. In this report, we present a case of polyuria secondary to gemfibrozil with a score of 9 on the Naranjo scale, and a literature review.
LEARNING POINTS
Gemfibrozil has known, mainly gastrointestinal, adverse effects.We aim to increase awareness of the urinary side effects of gemfibrozil so unnecessary investigations can be avoided.
PubMed: 33987132
DOI: 10.12890/2021_002546 -
American Journal of Kidney Diseases :... Apr 2022
Topics: Humans; Hypercalcemia; Kidney; Polyuria
PubMed: 35331383
DOI: 10.1053/j.ajkd.2021.09.030 -
Archives of Disease in Childhood Apr 2001We describe four cases of eosinophilic cystitis in whom no specific cause could be found, and review the literature. Complaints at presentation included urgency,... (Review)
Review
We describe four cases of eosinophilic cystitis in whom no specific cause could be found, and review the literature. Complaints at presentation included urgency, frequency, abdominal pain, and haematuria. In three patients the symptoms and ultrasound pictures suggested a bladder tumour. One patient was treated with anticholinergics and corticosteroids without relief of symptoms; a localised eosinophilic tumour was excised in one patient who remained symptom free; and two patients were managed conservatively with spontaneous resolution of bladder pathology and symptoms. One case was identified by random bladder biopsy in 150 consecutive patients with unexplained irritable micturition complaints. Eosinophilic cystitis is rare in children. After biopsy, we consider a wait and see policy is justified as symptoms tend to disappear spontaneously. Routine bladder biopsies in children with unexplained bladder symptoms is not justifiable.
Topics: Adolescent; Anti-Allergic Agents; Child; Child, Preschool; Chronic Disease; Cystitis; Enuresis; Eosinophilia; Eosinophils; Female; Hematuria; Humans; Hypersensitivity; Ketotifen; Male; Polyuria; Urinary Bladder; Urinary Bladder Neoplasms
PubMed: 11259238
DOI: 10.1136/adc.84.4.344