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Endocrinology and Metabolism Clinics of... Sep 2020The differential diagnosis of diabetes insipidus involves the distinction between central or nephrogenic diabetes insipidus and primary polydipsia. Differentiation is... (Review)
Review
The differential diagnosis of diabetes insipidus involves the distinction between central or nephrogenic diabetes insipidus and primary polydipsia. Differentiation is important because treatment strategies vary; the wrong treatment can be dangerous. Reliable differentiation is difficult especially in patients with primary polydipsia or partial forms of diabetes insipidus. New diagnostic algorithms are based on the measurement of copeptin after osmotic stimulation by hypertonic saline infusion or after nonosmotic stimulation by arginine and have a higher diagnostic accuracy than the water deprivation test. Treatment involves correcting preexisting water deficits, but is different for central diabetes insipidus, nephrogenic diabetes insipidus, and primary polydipsia.
Topics: Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Mellitus; Diagnosis, Differential; Diagnostic Techniques, Endocrine; Humans; Syndrome
PubMed: 32741486
DOI: 10.1016/j.ecl.2020.05.012 -
Annals of Internal Medicine Mar 2022Type 1 diabetes mellitus (T1DM) is an endocrine disorder in which pancreatic β cells stop producing insulin, typically due to autoimmune destruction. This results in... (Review)
Review
Type 1 diabetes mellitus (T1DM) is an endocrine disorder in which pancreatic β cells stop producing insulin, typically due to autoimmune destruction. This results in hyperglycemia and ketosis; thus, insulin replacement is vital to management. Incidence peaks in puberty and early adulthood, but onset can occur at any age. However, prevalence is highest among adults because persons with T1DM live for many years. Symptoms include polyuria, polydipsia, and weight loss. Acute complications include diabetic ketoacidosis, which requires urgent management. Long-term complications include microvascular and macrovascular disease. Patients with T1DM are at higher risk for other autoimmune diseases and psychosocial issues. Management should focus on optimizing glucose control to reduce acute and long-term complications.
Topics: Adult; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Hyperglycemia; Insulin; Ketosis
PubMed: 35254878
DOI: 10.7326/AITC202203150 -
Nature Reviews. Disease Primers Aug 2019Diabetes insipidus (DI) is a disorder characterized by excretion of large amounts of hypotonic urine. Central DI results from a deficiency of the hormone arginine... (Review)
Review
Diabetes insipidus (DI) is a disorder characterized by excretion of large amounts of hypotonic urine. Central DI results from a deficiency of the hormone arginine vasopressin (AVP) in the pituitary gland or the hypothalamus, whereas nephrogenic DI results from resistance to AVP in the kidneys. Central and nephrogenic DI are usually acquired, but genetic causes must be evaluated, especially if symptoms occur in early childhood. Central or nephrogenic DI must be differentiated from primary polydipsia, which involves excessive intake of large amounts of water despite normal AVP secretion and action. Primary polydipsia is most common in psychiatric patients and health enthusiasts but the polydipsia in a small subgroup of patients seems to be due to an abnormally low thirst threshold, a condition termed dipsogenic DI. Distinguishing between the different types of DI can be challenging and is done either by a water deprivation test or by hypertonic saline stimulation together with copeptin (or AVP) measurement. Furthermore, a detailed medical history, physical examination and imaging studies are needed to ensure an accurate DI diagnosis. Treatment of DI or primary polydipsia depends on the underlying aetiology and differs in central DI, nephrogenic DI and primary polydipsia.
Topics: Diabetes Insipidus; Humans; Neurophysins; Pituitary Gland, Posterior; Protein Precursors; Vasopressins
PubMed: 31395885
DOI: 10.1038/s41572-019-0103-2 -
Journal of Internal Medicine Jul 2021Diabetes insipidus is a disorder characterized by excretion of large amounts of hypotonic urine. Four entities have to be differentiated: central diabetes insipidus... (Review)
Review
Diabetes insipidus is a disorder characterized by excretion of large amounts of hypotonic urine. Four entities have to be differentiated: central diabetes insipidus resulting from a deficiency of the hormone arginine vasopressin (AVP) in the pituitary gland or the hypothalamus, nephrogenic diabetes insipidus resulting from resistance to AVP in the kidneys, gestational diabetes insipidus resulting from an increase in placental vasopressinase and finally primary polydipsia, which involves excessive intake of large amounts of water despite normal AVP secretion and action. Distinguishing between the different types of diabetes insipidus can be challenging. A detailed medical history, physical examination and imaging studies are needed to detect the aetiology of diabetes insipidus. Differentiation between the various forms of hypotonic polyuria is then done by the classical water deprivation test or the more recently developed hypertonic saline or arginine stimulation together with copeptin (or AVP) measurement. In patients with idiopathic central DI, a close follow-up is needed since central DI can be the first sign of an underlying pathology. Treatment of diabetes insipidus or primary polydipsia depends on the underlying aetiology and differs in central diabetes insipidus, nephrogenic diabetes insipidus and primary polydipsia. This review will discuss issues and newest developments in diagnosis, differential diagnosis and treatment, with a focus on central diabetes insipidus.
Topics: Diabetes Insipidus; Diagnosis, Differential; Humans
PubMed: 33713498
DOI: 10.1111/joim.13261 -
The Veterinary Clinics of North... Apr 2022Chronic kidney disease (CKD) is rare in horses with an overall prevalence reported to be 0.12%. There is often a continuum from Acute Kidney Injury (AKI) to CKD, and... (Review)
Review
Chronic kidney disease (CKD) is rare in horses with an overall prevalence reported to be 0.12%. There is often a continuum from Acute Kidney Injury (AKI) to CKD, and patients with CKD may be predisposed to episodes of AKI. The most common clinical signs are non-specific with weight loss, polyuria/polydipsia and ventral edema. Less common clinical signs are poor appetite and performance, dull hair coat, oral ulcerations, gastro-intestinal ulceration, gingivitis, dental tartar and diarrhea. Rarely, horses may develop forebrain signs. Creatinine increases when at least 2/3 of kidney function have been lost and a more accurate assessment of kidney function is an estimated glomerular filtration rate measuring iohexol clearance time combined with protein content in the urine. Tubulointerstitial disease and glomerulonephritis are common causes of chronic kidney disease together with pyelonephritis and nephrolithiasis. Dietary changes and avoiding nephrotoxic drugs are key in slowing down the degenerative process.
Topics: Animals; Glomerular Filtration Rate; Horse Diseases; Horses; Kidney Failure, Chronic; Prognosis; Renal Insufficiency, Chronic
PubMed: 35365250
DOI: 10.1016/j.cveq.2021.11.003 -
Journal of Pediatric Endocrinology &... Apr 2022Nephrogenic diabetes insipidus (NDI) is characterized by the inability to concentrate urine that results in polyuria and polydipsia, despite having normal or elevated... (Review)
Review
Nephrogenic diabetes insipidus (NDI) is characterized by the inability to concentrate urine that results in polyuria and polydipsia, despite having normal or elevated plasma concentrations of arginine vasopressin (AVP). In this study, we review the clinical aspects and diagnosis of NDI, the various etiologies, current treatment options and potential future developments. NDI has different clinical manifestations and approaches according to the etiology. Hereditary forms of NDI are mainly caused by mutations in the genes that encode key proteins in the AVP signaling pathway, while acquired causes are normally associated with specific drug exposure, especially lithium, and hydroelectrolytic disorders. Clinical manifestations of the disease vary according to the degree of dehydration and hyperosmolality, being worse when renal water losses cannot be properly compensated by fluid intake. Regarding the diagnosis of NDI, it is important to consider the symptoms of the patient and the diagnostic tests, including the water deprivation test and the baseline plasma copeptin measurement, a stable surrogate biomarker of AVP release. Without proper treatment, patients may developcomplications leading to high morbidity and mortality, such as severe dehydration and hypernatremia. In that sense, the treatment of NDI consists in decreasing the urine output, while allowing appropriate fluid balance, normonatremia, and ensuring an acceptable quality of life. Therefore, therapeutic options include nonpharmacological interventions, including sufficient water intake and a low-sodium diet, and pharmacological treatment. The main medications used for NDI are thiazide diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), and amiloride, used isolated or in combination.
Topics: Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Mellitus; Humans; Mutation; Polyuria; Quality of Life
PubMed: 35146976
DOI: 10.1515/jpem-2021-0566 -
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 -
American Journal of Kidney Diseases :... Feb 2020Overall body fluid concentration is regulated within a narrow range by the concerted action of the hypothalamic-pituitary axis to influence water intake through thirst... (Review)
Review
Overall body fluid concentration is regulated within a narrow range by the concerted action of the hypothalamic-pituitary axis to influence water intake through thirst and water excretion via the effect of vasopressin, or antidiuretic hormone, on renal collecting duct water permeability. Sodium is the principal extracellular cation; abnormalities in overall effective body fluid concentration, or tonicity, manifest as disturbances in serum sodium concentration. Depending on its severity and chronicity, hyponatremia can lead to significant symptoms, primarily related to central nervous system function. Failure to correct hyponatremia can lead to permanent neurologic damage, as can over rapid correction. It is thus essential to stay within specific limits for correction, particularly for chronic hyponatremia. Hypernatremia also leads to central nervous system dysfunction, although goals for its correction rate are less well established. This Core Curriculum article discusses the normal regulation of tonicity and serum sodium concentration and the diagnosis and management of hypo- and hypernatremia.
Topics: Curriculum; Disease Management; Humans; Hypernatremia; Hyponatremia; Sodium; Water-Electrolyte Imbalance
PubMed: 31606238
DOI: 10.1053/j.ajkd.2019.07.014 -
Best Practice & Research. Clinical... Sep 2020The two main differential diagnoses of central diabetes insipidus are nephrogenic diabetes insipidus and primary polydipsia. Reliable distinction between those entities... (Review)
Review
The two main differential diagnoses of central diabetes insipidus are nephrogenic diabetes insipidus and primary polydipsia. Reliable distinction between those entities is essential as treatment differs substantially with the wrong treatment potentially leading to serious complications. Past diagnostic measures using the indirect water deprivation test had several pitfalls, resulting in a low diagnostic accuracy. With the introduction of copeptin, a stable and reliable surrogate marker for arginine vasopressin, diagnosis of diabetes insipidus was new evaluated. While unstimulated basal copeptin measurement reliably diagnoses nephrogenic diabetes insipidus, a stimulation test is needed to differentiate patients with central diabetes insipidus from patients with primary polydipsia. Stimulation can either be achieved through hypertonic saline infusion or arginine infusion. While the former showed high diagnostic accuracy and superiority over the indirect water deprivation test in a recent validation study, the diagnostic accuracy for arginine-stimulated copeptin was slightly lower, but superior in test tolerance. In summary of the recent findings, a new copeptin based diagnostic algorithm is proposed for the reliable diagnosis of diabetes insipidus.
Topics: Biomarkers; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Diagnostic Techniques, Endocrine; Humans; Neurophysins; Polyuria; Protein Precursors; Vasopressins
PubMed: 32387127
DOI: 10.1016/j.beem.2020.101398