-
Journal of Avian Medicine and Surgery Apr 2024Diabetes mellitus (DM) is an uncommon, poorly documented metabolic disorder of birds. Extrapolating knowledge from DM in mammals is challenging because of marked... (Review)
Review
Diabetes mellitus (DM) is an uncommon, poorly documented metabolic disorder of birds. Extrapolating knowledge from DM in mammals is challenging because of marked differences in avian physiology and metabolism. A literature review from December 1991 to January 2022 identified 14 publications covering 16 diabetic birds, 63% (10/16) of which belonged to the order Psittaciformes with as the predominant genus. No sex predilection was noted, but males generally presented at a younger age. Commonly reported clinical signs included polyuria 94% (15/16), polydipsia 88% (14/16), weight loss 75% (12/16), lethargy 63% (10/16), and polyphagia 38% (6/16). Diagnosis of DM was based on the presence of clinical signs and persistent hyperglycemia 100% (16/16), often with glucosuria 93% (13/14), response to insulin therapy 80% (8/10), and pancreatic pathology 90% (9/10). Specific treatment for DM was initiated in 14 patients, but blood glucose regulation for 6 months or longer was only achieved in 6 birds. Five of the regulated birds were managed with injectable long-acting insulin and 1 with oral glipizide combined with dietary modifications. However, glipizide yielded poor results in other cases, likely attributable to a lack of functional beta cells. Three diabetic birds progressed to remission. Treatment proved unsuccessful for 7 patients with a mean survival time of 36 days from diagnosis. One patient was lost to follow-up, and 2 were euthanized immediately following diagnosis. Histological examination of the pancreas frequently (90%, 9/10) revealed abnormalities including atrophy, fibrosis, and vacuolization of the endocrine islets with or without lymphoplasmacytic pancreatitis. Comorbidities, including hemosiderosis and infection, were common. This review suggests that birds diagnosed with DM are primarily affected by a type I diabetes as observed in dogs and humans. In contrast to mammalian species, avian DM is often associated with underlying disease and a complete clinical workup is essential to diagnose and address secondary disease conditions prior to initiating long-term insulin therapy.
Topics: Animals; Bird Diseases; Birds; Diabetes Mellitus
PubMed: 38686885
DOI: 10.1029/AVIANMS-D-22-00057 -
Urology Nov 2019Nocturnal polyuria (NP), the most common etiology of nocturia, can be caused by various medical conditions, including cardiovascular disease, obstructive sleep apnea,... (Review)
Review
Nocturnal polyuria (NP), the most common etiology of nocturia, can be caused by various medical conditions, including cardiovascular disease, obstructive sleep apnea, renal tubular dysfunction, as well as medications (eg, diuretics) and/or behavioral patterns. NP in the absence of underlying medical conditions has been described as NP syndrome and is thought be the result of impaired circadian release of endogenous arginine vasopressin. Desmopressin, a synthetic arginine vasopressin analog, has been shown to be an effective replacement therapy in adults with nocturia due to NP. Further studies on the subset of patients with NP syndrome are warranted to maximize benefit from antidiuretic treatment. In addition, a connection between the pathophysiological mechanisms underlying NP and essential hypertension has been suggested, and hypertension has been shown to be a significant risk factor for nocturia, while an association between NP and brain natriuretic peptide levels has also been reported in patients with nocturia. Hypertension is now viewed as a disorder of blood vessels and treatment is directed at the vasculature rather than the blood pressure, with the latter currently serving as a biomarker for arterial injury. Nocturia is thought to be associated with the beginning of this cardiovascular continuum as studies have reported a link between coronary heart disease and nocturia. Therefore, there is an increasing need to elucidate the complex mechanisms implicated in the association between nocturia and hypertension to promote the development of more individualized therapies for the treatment of nocturia.
Topics: Forecasting; Humans; Hypertension; Natriuretic Peptide, Brain; Nocturia; Polyuria; Prevalence; Vascular Diseases; Vascular Stiffness
PubMed: 31233816
DOI: 10.1016/j.urology.2019.06.014 -
Journal of the American Society of... Nov 2022Ureteral obstruction is marked by disappearance of the vasopressin-dependent water channel aquaporin-2 (AQP2) in the renal collecting duct and polyuria upon reversal....
BACKGROUND
Ureteral obstruction is marked by disappearance of the vasopressin-dependent water channel aquaporin-2 (AQP2) in the renal collecting duct and polyuria upon reversal. Most studies of unilateral ureteral obstruction (UUO) models have examined late time points, obscuring the early signals that trigger loss of AQP2.
METHODS
We performed RNA-Seq on microdissected rat cortical collecting ducts (CCDs) to identify early signaling pathways after establishment of UUO.
RESULTS
Vasopressin V2 receptor (AVPR2) mRNA was decreased 3 hours after UUO, identifying one cause of AQP2 loss. Collecting duct principal cell differentiation markers were lost, including many not regulated by vasopressin. Immediate early genes in CCDs were widely induced 3 hours after UUO, including , , and (confirmed at the protein level). Simultaneously, expression of NF-κB signaling response genes known to repress increased. RNA-Seq for CCDs at an even earlier time point (30 minutes) showed widespread mRNA loss, indicating a "stunned" profile. Immunocytochemical labeling of markers of mRNA-degrading P-bodies DDX6 and 4E-T indicated an increase in P-body formation within 30 minutes.
CONCLUSIONS
Immediately after establishment of UUO, collecting ducts manifest a stunned state with broad disappearance of mRNAs. Within 3 hours, there is upregulation of immediate early and inflammatory genes and disappearance of the V2 vasopressin receptor, resulting in loss of AQP2 (confirmed by lipopolysaccharide administration). The inflammatory response seen rapidly after UUO establishment may be relevant to both UUO-induced polyuria and long-term development of fibrosis in UUO kidneys.
Topics: Rats; Animals; Aquaporin 2; Ureteral Obstruction; Polyuria; Kidney; Vasopressins; RNA, Messenger; Kidney Tubules, Collecting
PubMed: 35918145
DOI: 10.1681/ASN.2022050601 -
European Urology Focus May 2020We review the role of the heart, kidneys, and bladder in the pathophysiology of nocturia and nocturnal polyuria. Lower urinary tract symptoms such as nocturia have often... (Review)
Review
We review the role of the heart, kidneys, and bladder in the pathophysiology of nocturia and nocturnal polyuria. Lower urinary tract symptoms such as nocturia have often been associated with lower urinary tract dysfunction. It is known that the bladder contributes to nocturia in the case of low functional capacity, urgency, and detrusor overactivity. Heart diseases, especially arterial hypertension and congestive heart failure, are closely related to nocturnal polyuria. The main mechanisms include renal hyperfiltration and elevated atrial natriuretic peptide. A number of drugs frequently used in cardiovascular disorders are implicated in nocturia; diuretics, calcium channel blockers, and β-blockers induce nocturnal polyuria and thus nocturia, whereas alpha-blockers improve nocturia. Among the different forms of hypertension, nondipping arterial hypertension has been associated with a higher risk of nocturnal polyuria. Besides the role of the kidneys in nocturia linked to arterial hypertension, chronic kidney disease is an independent predictor of nocturia through an osmotic diuresis mechanism. Some evidence suggests a close relationship between the heart (nondipping arterial hypertension), kidneys (chronic kidney disease), and nocturia/nocturnal polyuria. These complex interactions between the heart, kidneys, and bladder warrant a multidisciplinary approach in patients with nocturia. PATIENT SUMMARY: We review the different mechanisms that lead to nocturia and nocturnal polyuria. The complex interactions between the heart, the kidneys, and the bladder warrant a multidisciplinary approach in patients with nocturia. Careful investigation of the cause of nocturia can improve its management.
Topics: Heart; Heart Diseases; Humans; Kidney; Kidney Diseases; Nocturia; Urinary Bladder; Urinary Bladder Diseases
PubMed: 31395515
DOI: 10.1016/j.euf.2019.07.007 -
International Urology and Nephrology Oct 2020A recent update in International Continence Society (ICS) terminology now recognizes nocturnal polyuria (NP) and diurnal polyuria (DP) as related subcategories of...
PURPOSE
A recent update in International Continence Society (ICS) terminology now recognizes nocturnal polyuria (NP) and diurnal polyuria (DP) as related subcategories of "Polyuria (global symptom)". This study determines the real-world clinical overlap between NP, DP, and 24-h polyuria (24hP) among men with nocturia.
METHODS
Analysis of frequency-volume charts from men ≥ 18 years with ≥ 1 nocturnal void(s). Three separate analyses were performed using different rate criteria for NP, DP, and 24hP: (1) urine production > 90 mL/h (extrapolated from a proposed definition for NP); (2) > 125 mL/h (extrapolated from a proposed definition for 24hP [3000 mL/24 h]); and (3) > 1.67 mL/kg/h (extrapolated from the current ICS definition for 24hP [> 40 mL/kg/24 h]). Subjects were categorized as having one of five mathematically permissible phenotypic combinations: (1) isolated NP, (2) isolated DP, (3) NP + 24hP, (4) DP + 24hP, and (5) NP + DP + 24hP.
RESULTS
167, 95, and 61 patients were included at criteria 1, 2, and 3, respectively, with 56%, 43%, and 30% of patients demonstrating overlapping phenotypes (i.e., phenotypic combinations 3-5) at cut-offs 1-3, respectively. The prevalence of NP was similar across cut-offs (81-87%), but the prevalence of NP without 24hP was highly threshold-dependent (43-73%).
CONCLUSION
Consistent with current ICS terminology, there exists a substantial overlap between NP, DP, and 24hP. As demonstrated in the current study, absolute volume-based criteria for NP/DP/24hP are indeed conducive to the diagnosis of concurrent NP + 24hP, and may be preferred over proportion-based NP criteria when both NP + 24hP are suspected.
Topics: Aged; Humans; Male; Middle Aged; Nocturia; Polyuria; Retrospective Studies; Terminology as Topic; Time Factors
PubMed: 32435976
DOI: 10.1007/s11255-020-02502-1 -
Frontiers in Endocrinology 2022Central diabetes insipidus (CDI) is a rare endocrine disease deriving from an insufficient production or secretion of anti-diuretic hormone. Recently, CDI has been... (Review)
Review
Central diabetes insipidus (CDI) is a rare endocrine disease deriving from an insufficient production or secretion of anti-diuretic hormone. Recently, CDI has been reported as a rare side effect triggered by immune checkpoint inhibitors (ICI) in cancer patients. Despite its current rarity, CDI triggered by ICI is expected to affect an increasing number of patients because of the expanding use of these effective drugs in a growing number of solid and hematologic malignancies. An appropriate assessment of the severity of adverse events induced by anticancer agents is crucial in their management, including dosing adjustment and temporary withdrawal or discontinuation treatment. However, assessment of the severity of CDI induced by ICI may be challenging, as its main signs and symptoms (polyuria, dehydration, weight loss, and hypernatremia) can be incompletely graded. Indeed, the current grading system of toxicity induced by anticancer treatments does not include polyuria. Additionally, dehydration in patients affected by diabetes insipidus, including ICI-induced CDI, is different in certain aspects from that due to other conditions seen in cancer patients, such as vomiting and diarrhea. This prompted us to reflect on the need to grade polyuria, and how to grade it, and to consider a specific grading system for dehydration associated with CDI induced by ICI. Here we propose a new grading system for polyuria and dehydration, as critical symptoms of the CDI syndrome occurring in patients on ICI treatment, to obtain better management of both the adverse event and the triggering drugs.
Topics: Dehydration; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Immune Checkpoint Inhibitors; Neoplasms; Polyuria
PubMed: 35388297
DOI: 10.3389/fendo.2022.840971 -
Central European Journal of Urology 2020Desmopressin is an effective and safe therapy for nocturia caused by nocturnal polyuria. However, many physicians are unsure about the proper diagnosis of nocturnal... (Review)
Review
INTRODUCTION
Desmopressin is an effective and safe therapy for nocturia caused by nocturnal polyuria. However, many physicians are unsure about the proper diagnosis of nocturnal polyuria and the identification of patients who may benefit from desmopressin treatment. Therefore, to support urologists in their routine clinical practice, the aim of this study was to provide a comprehensive paradigm for diagnosing nocturnal polyuria with recommendations for the use of desmopressin.
MATERIAL AND METHODS
A multidisciplinary group of experts reviewed the available literature. Findings were compiled into a practice-based approach for workup and treatment.
RESULTS
We designed the nocturia diagnostic pathway to confirm nocturnal polyuria, identify possible causes of nocturnal polyuria, and classify patients with indications and contraindications for desmopressin therapy. A bladder diary remains a basic diagnostic tool. Underlying conditions that may lead to nocturnal polyuria include mainly cardiac insufficiency, arterial hypertension, chronic kidney failure, obstructive sleep apnea, peripheral edema, and excessive fluid intake at night. Treatment for nocturia caused by nocturnal polyuria is based on conservative management and pharmacotherapy, but pharmacological treatment should not precede a prior attempt at conservative treatment. Before administration of desmopressin, patients should be assessed for serum sodium concentration and carefully educated about the symptoms of hyponatremia. Older individuals or persons with risk factors for the development of hyponatremia should be checked regularly for hyponatremia during desmopressin therapy.
CONCLUSIONS
People with nocturia due to nocturnal polyuria should be evaluated carefully before initiating desmopressin treatment. Patients treated with desmopressin should be followed for both clinical efficacy and treatment-related adverse effects.
PubMed: 33552576
DOI: 10.5173/ceju.2020.0283 -
Journal of Pediatric Urology Feb 2023Nocturnal enuresis (NE) is common in children, but its pathophysiology is still not fully understood. Despite the recognition of three major pathways, nocturnal... (Review)
Review
INTRODUCTION
Nocturnal enuresis (NE) is common in children, but its pathophysiology is still not fully understood. Despite the recognition of three major pathways, nocturnal polyuria, nocturnal bladder dysfunction and sleep disorders, their inter-relations remain elusive. The autonomic nervous system (ANS) which is greatly involved in both diuresis and sleep might have an important role in NE.
METHODS
A comprehensive electronic search of Medline database was performed, to identify articles reporting on the role of the autonomic nervous system (ANS) in enuretic children regarding sleep regulation, cardiovascular function and diuresis-related hormones and neurotransmitters.
RESULTS
Of an initial total of 646 articles, 45 studies were finally selected for data extraction according to inclusion criteria, published between 1960 and 2022. Of these studies 26 reported on sleep regulation, 10 on cardiovascular functions and 12 on ANS-associated hormones and neurotransmitters. Evidence on parasympathetic or sympathetic overstimulation in enuretic individuals is suggesting that NE could be attributed to a dysregulation of ANS. Sleep studies have shown increased rapid eye movement sleep time in polyuric enuretic children pointing to sympathetic overactivity, whereas patients with overactive bladder have non-rapid eye movement related enuretic episodes, potentially associated with parasympathetic stimulation. Twenty-four-hour blood pressure monitoring demonstrated "non-dipping" phenomenon, suggesting sympathetic involvement, whereas heart-rate analysis showed parasympathetic hyperfunction. Nocturnal lower levels of arginine-vasopressin, angiotensin II and aldosterone in polyuric children with NE as compared to non-polyuric and controls and potential involvement of dopamine and serotonin in sleep and micturition suggest that ANS-associated hormones and neurotransmitters have a role in the pathogenesis of NE.
CONCLUSION
Summarizing the existing data we suggest that ANS dysregulation related either with sympathetic or parasympathetic overactivity may provide a unifying model in understanding the pathogenesis of NE in different enuretic subpopulations. This observation provides new insights in future research and new potential treatment options.
Topics: Child; Humans; Nocturnal Enuresis; Autonomic Nervous System; Primary Dysautonomias; Polyuria; Sleep
PubMed: 37310191
DOI: 10.1016/j.jpurol.2022.10.015 -
Nature Reviews. Endocrinology May 2024Polyuria-polydipsia syndrome can be caused by central diabetes insipidus, nephrogenic diabetes insipidus or primary polydipsia. To avoid confusion with diabetes... (Review)
Review
Polyuria-polydipsia syndrome can be caused by central diabetes insipidus, nephrogenic diabetes insipidus or primary polydipsia. To avoid confusion with diabetes mellitus, the name 'central diabetes insipidus' was changed in 2022 to arginine vasopressin (AVP) deficiency and 'nephrogenic diabetes insipidus' was renamed as AVP resistance. To differentiate the three entities, various osmotic and non-osmotic copeptin-based stimulation tests have been introduced in the past decade. The hypertonic saline test plus plasma copeptin measurement emerged as the test with highest diagnostic accuracy, replacing the water deprivation test as the gold standard in differential diagnosis of the polyuria-polydipsia syndrome. The mainstay of treatment for AVP deficiency is AVP replacement with desmopressin, a synthetic analogue of AVP specific for AVP receptor 2 (AVPR2), which usually leads to rapid improvements in polyuria and polydipsia. The main adverse effect of desmopressin is dilutional hyponatraemia, which can be reduced by regularly performing the so-called desmopressin escape method. Evidence from the past few years suggests an additional oxytocin deficiency in patients with AVP deficiency. This potential deficiency should be further evaluated in future studies, including feasible provocation tests for clinical practice and interventional trials with oxytocin substitution.
PubMed: 38693275
DOI: 10.1038/s41574-024-00985-x -
La Revue de Medecine Interne May 2023Post-Obstructive Diuresis (POD) is a polyuria that occurs following the release of an obstruction from the urinary tract that prevents the flow of urine. POD requires... (Review)
Review
Post-Obstructive Diuresis (POD) is a polyuria that occurs following the release of an obstruction from the urinary tract that prevents the flow of urine. POD requires prompt diagnosis to avoid complications. Although its pathophysiology is better understood, there is little scientific evidence for its treatment. Restoration of renal homeostasis requires correction of blood volume and electrolyte disturbances to prevent complications, which can be serious. In this article, we propose a synthesis of knowledge on the subject, as well as a management strategy.
Topics: Humans; Diuresis; Kidney; Polyuria; Physicians
PubMed: 36764894
DOI: 10.1016/j.revmed.2023.01.011