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Journal of the Royal College of... 1998
Topics: Diabetes Insipidus; Humans; Polyuria; Terminology as Topic
PubMed: 9670165
DOI: No ID Found -
Swiss Medical Weekly May 2020Polyuria-polydipsia syndrome consists of the three main entities: central or nephrogenic diabetes insipidus and primary polydipsia. Reliable distinction between these...
Polyuria-polydipsia syndrome consists of the three main entities: central or nephrogenic diabetes insipidus and primary polydipsia. Reliable distinction between these diagnoses is essential as treatment differs substantially, with the wrong treatment potentially leading to serious complications. Past diagnostic measures using the classical water deprivation test had several pitfalls and clinicians were often left with uncertainity concerning the diagnosis. With the establishment of copeptin, a stable and reliable surrogate marker for arginine vasopressin, diagnosis of the polyuria-polydipsia syndrome has been newly evaluated. Whereas unstimulated basal copeptin measurement reliably diagnoses nephrogenic diabetes insipidus, two new tests using stimulated copeptin cutoff levels showed a high diagnostic accuracy in differentiating central diabetes insipidus from primary polydipsia. For the hypertonic saline infusion test, osmotic stimulation via the induction of hypernatraemia is used. This makes the test highly reliable and superior to the classical water deprivation test, but also requires close supervision and the availability of rapid sodium measurements to guarantee the safety of the test. Alternatively, arginine infusion can be used to stimulate copeptin release, opening the doors for an even shorter and safer diagnostic test. The test protocols of the two tests are provided and a new copeptin-based diagnostic algorithm is proposed to reliably differentiate between the different entities. Furthermore, the role of copeptin as a predictive marker for the development of diabetes insipidus following surgical procedures in the sellar region is described.
Topics: Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Diagnostic Tests, Routine; Glycopeptides; Humans; Polyuria
PubMed: 32374887
DOI: 10.4414/smw.2020.20237 -
Canadian Family Physician Medecin de... Feb 2015To educate primary health care professionals about the diagnosis and treatment of postobstructive diuresis (POD), a rare but potentially lethal complication associated... (Review)
Review
OBJECTIVE
To educate primary health care professionals about the diagnosis and treatment of postobstructive diuresis (POD), a rare but potentially lethal complication associated with the relief of urinary obstructions.
SOURCES OF INFORMATION
The main concepts and clinical evidence reviewed in this article were derived from a literature search of PubMed and Google Scholar. Expert opinion was used to supplement recommendations in areas with little evidence.
MAIN MESSAGE
Urinary retention is a frequently encountered presentation seen by all physicians. Most family physicians are comfortable treating these patients, initiating investigations, and organizing appropriate follow-up. This article reviews a rare but potentially lethal complication known as POD. Postobstructive diuresis is a polyuric response initiated by the kidneys after the relief of a substantial bladder outlet obstruction. In severe cases this condition can become pathologic, resulting in dehydration, electrolyte imbalances, and death if not adequately treated. Primary care physicians should be familiar with this potential clinical entity, especially as they are generally the first to encounter and treat these patients.
CONCLUSION
Physicians aware of POD will be able to identify patients at risk and arrange the appropriate monitoring after relieving a urinary obstruction. Early diagnosis and treatment of pathologic POD will prevent mortality.
Topics: Dehydration; Diuresis; Family Practice; Humans; Kidney; Physicians, Primary Care; Polyuria; Urinary Retention; Water-Electrolyte Balance
PubMed: 25821871
DOI: No ID Found -
Clinical and Experimental Nephrology Dec 2013Water excretion is regulated in large part through the regulation of osmotic water permeability of the renal collecting duct epithelium. Water permeability is controlled... (Review)
Review
Water excretion is regulated in large part through the regulation of osmotic water permeability of the renal collecting duct epithelium. Water permeability is controlled by vasopressin through regulation of the water channel, aquaporin-2 (AQP2). Two processes contribute: (1) regulation of AQP2 trafficking to the apical plasma membrane; and (2) regulation of the total amount of the AQP2 protein in the cells. Regulation of AQP2 abundance is defective in several water-balance disorders, including many polyuric disorders and the syndrome of inappropriate antidiuresis. Here we review vasopressin signaling in the renal collecting duct that is relevant to the two modes of water permeability regulation.
Topics: Animals; Aquaporin 2; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Heart Failure; Humans; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Liver Cirrhosis; Mice; Myosin-Light-Chain Kinase; Nephrotic Syndrome; Permeability; Phosphoproteins; Phosphorylation; Polyuria; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-jun; Rats; Signal Transduction; Transcription Factor AP-1; Transcription Factors; Vasopressins; beta Catenin
PubMed: 23584881
DOI: 10.1007/s10157-013-0789-5 -
Journal of Neurosciences in Rural... 2023Polyuria is urine output exceeding 3 L/d in adults, primarily due to solute and water diuresis. In a hospital setting, mannitol and diuretics commonly lead to polyuria....
Polyuria is urine output exceeding 3 L/d in adults, primarily due to solute and water diuresis. In a hospital setting, mannitol and diuretics commonly lead to polyuria. We have found an interesting association of polyuria with glycopyrrolate; to the best of our knowledge, no case is reported in the literature. Here, we are describing a case of Guillain-Barre Syndrome, which developed polyuria during the hospital stay, which was secondary to glycopyrrolate.
PubMed: 37692823
DOI: 10.25259/JNRP_73_2023 -
Minerva Urology and Nephrology Feb 2022
Topics: COVID-19; Humans; Polyuria; SARS-CoV-2
PubMed: 33887897
DOI: 10.23736/S2724-6051.21.04396-2 -
Veterinary Clinical Pathology Dec 2012Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals,... (Review)
Review
Aquaporin-2 (AQP2), the vasopressin-regulated water channel of the renal collecting duct, is dysregulated in numerous disorders of water balance in people and animals, including those associated with polyuria (urinary tract obstruction, hypokalemia, inflammation, and lithium toxicity) and with dilutional hyponatremia (syndrome of inappropriate antidiuresis, congestive heart failure, cirrhosis). Normal regulation of AQP2 by vasopressin involves 2 independent regulatory mechanisms: (1) short-term regulation of AQP2 trafficking to and from the apical plasma membrane, and (2) long-term regulation of the total abundance of the AQP2 protein in the cells. Most disorders of water balance are the result of dysregulation of processes that regulate the total abundance of AQP2 in collecting duct cells. In general, the level of AQP2 in a collecting duct cell is determined by a balance between production via translation of AQP2 mRNA and removal via degradation or secretion into the urine in exosomes. AQP2 abundance increases in response to vasopressin chiefly due to increased translation subsequent to increases in AQP2 mRNA. Vasopressin-mediated regulation of AQP2 gene transcription is poorly understood, although several transcription factor-binding elements in the 5' flanking region of the AQP2 gene have been identified, and candidate transcription factors corresponding to these elements have been discovered in proteomics studies. Here, we review progress in this area and discuss elements of vasopressin signaling in the collecting duct that may impinge on regulation of AQP2 in health and in the context of examples of polyuric diseases.
Topics: Animals; Aquaporin 2; Humans; Kidney Tubules, Collecting; Polyuria; Signal Transduction; Vasopressins; Water-Electrolyte Imbalance
PubMed: 23130944
DOI: 10.1111/j.1939-165x.2012.00488.x -
JAMA Network Open Dec 2022Despite access to routine laboratory evaluation, primary hyperparathyroidism (PHP) remains underdiagnosed and undertreated.
IMPORTANCE
Despite access to routine laboratory evaluation, primary hyperparathyroidism (PHP) remains underdiagnosed and undertreated.
OBJECTIVE
To determine the consequences associated with missed diagnoses and prolonged time to diagnosis and treatment of PHP.
DESIGN, SETTING, AND PARTICIPANTS
This is a retrospective cohort study of patients older than 40 years with 2 instances of hypercalcemia during 2010 to 2020 and 3 years of follow-up. Patients were recruited from 63 health care organizations in the TriNetX Research Network. Data analysis was performed from January 2010 to September 2020.
EXPOSURES
Elevated serum calcium.
MAIN OUTCOMES AND MEASURES
Existing symptoms and diagnoses associated with PHP (osteoporosis, fractures, urolithiasis, major depressive disorder, anxiety, hypertension, gastroesophageal reflux disease, malaise or fatigue, joint pain or myalgias, constipation, insomnia, polyuria, weakness, abdominal pain, headache, nausea, amnesia, and gallstones) compared in patients deemed high-risk and without a diagnosis and matched controls, and those who experienced times from documented hypercalcemia to diagnosis and diagnosis to treatment within or beyond 1 year.
RESULTS
There were 135 034 patients analyzed (96 554 women [72%]; 28 892 Black patients [21%] and 88 010 White patients [65%]; 3608 Hispanic patients [3%] and 98 279 non-Hispanic patients [73%]; mean [SD] age, 63 [10] years). Two groups without a documented diagnosis of PHP were identified as high risk: 20 176 patients (14.9%) with parathyroid hormone greater than or equal to 50 pg/mL and 24 905 patients (18.4%) with no parathyroid hormone level obtained or recorded explanation for hypercalcemia. High-risk patients experienced significantly increased rates of all associated symptoms and diagnoses compared with matched controls. Just 9.7% of those with hypercalcemia (13 136 patients) had a diagnosis of PHP. Compared with individuals who received a diagnosis within 1 year of hypercalcemia, those whose workup exceeded 1 year had significantly increased rates of major depressive disorder, anxiety, hypertension, gastroesophageal reflux disease, malaise or fatigue, joint pain or myalgias, polyuria, weakness, abdominal pain, and headache at 3 years. The rate of osteoporosis increased from 17.1% (628 patients) to 25.4% (935 patients) over the study period in the group with delayed diagnosis. Among those with a diagnosis, 5280 patients (40.2%) underwent parathyroidectomy. Surgery beyond 1 year of diagnosis was associated with significantly increased rates of osteoporosis and hypertension at 3 years after diagnosis compared with those treated within 1 year.
CONCLUSIONS AND RELEVANCE
Many patients were at high risk for PHP without a documented diagnosis. Complications in these patients, as well as those who received a diagnosis after prolonged workup or time to treatment, resulted in patient harm. System-level interventions are necessary to ensure proper diagnosis and prompt treatment of PHP.
Topics: Adult; Female; Humans; Middle Aged; Calcium; Depressive Disorder, Major; Hypercalcemia; Hyperparathyroidism, Primary; Osteoporosis; Parathyroid Hormone; Polyuria; Retrospective Studies; Aged; Male
PubMed: 36574247
DOI: 10.1001/jamanetworkopen.2022.48332 -
The Turkish Journal of Pediatrics 2022Monosymptomatic nocturnal enuresis (MNE) is defined as involuntary nighttime urination of children over five years of age without any congenital or acquired defect in...
BACKGROUND
Monosymptomatic nocturnal enuresis (MNE) is defined as involuntary nighttime urination of children over five years of age without any congenital or acquired defect in the central nervous system. Many factors, mainly nocturnal polyuria, sleep disorders, decreased bladder capacity, and bladder dysfunctions play a role in the etiology of MNE.
METHODS
Eighty-three children diagnosed with MNE were included in the study. Complete blood cell count, blood biochemistry, renin, and aldosterone levels of all children were obtained. Twenty-four-hour urine samples were collected separately daytime and nighttime and urinary electrolytes were evaluated. Also, 24-hour ambulatory blood pressure monitoring (ABPM) was performed for each patient. The results were evaluated by comparing both enuretic children vs. control group and enuretic children with polyuria vs. without polyuria.
RESULTS
When we compared the enuretic children and the control group in terms of urinary electrolytes, the fractional excretion of sodium (FENa) and fractional excretion of potassium (FEK) values of the enuretic group were higher than the control. The evaluation of the 24-hour ABPM findings revealed no significant difference in terms of the mean arterial pressure (MAP) and diastolic blood pressure (DBP) during the daytime and nighttime measurements. The daytime systolic blood pressure (SBP), however, was significantly lower in the enuretic group. When enuretic children with and without polyuria and the control group were compared, the nighttime, FENa, FEK, as well as nighttime urinary excretion of calcium and protein were significantly higher in enuretic children with polyuria. No difference was detected on the MAP, SBP, or DBP values.
CONCLUSIONS
In conclusion, the nighttime urinary solute excretion of enuretic children was found to be higher and this condition may especially be associated with pathogenesis of nighttime polyuria. In enuretic children, nighttime blood pressure changes were not influential in the etiopathogenesis in all patient groups and multiple mechanisms may play a role in the pathogenesis of enuresis.
Topics: Blood Pressure; Blood Pressure Monitoring, Ambulatory; Child; Electrolytes; Humans; Nocturnal Enuresis; Polyuria
PubMed: 35611421
DOI: 10.24953/turkjped.2020.3343 -
Therapeutic Advances in Urology 2021This narrative review synthesizes current evidence on the medical management of nocturnal polyuria, including antidiuretic replacement therapy as well as other emerging... (Review)
Review
This narrative review synthesizes current evidence on the medical management of nocturnal polyuria, including antidiuretic replacement therapy as well as other emerging modalities, with particular emphasis on areas of active investigation and future research directions. Relative to earlier formulations, the pharmacological profiles of novel desmopressin acetate nasal spray and orally disintegrating tablet formulations appear favorable in optimizing the balance between efficacy and safety. Additionally, several highly selective small-molecule arginine vasopressin 2 receptor agonists are under active development, while appropriately timed short-acting diuretics, pharmacotherapy for hypertension, nonsteroidal anti-inflammatory drugs, and sex hormone replacement therapy are also a focal point of extensive ongoing nocturnal polyuria research. Emerging laboratory technologies now make feasible a sub-stratification of nocturnal polyuria patients into substrate-based phenotypes for individualized treatment. An increasingly refined understanding of the pathogenesis of nocturnal polyuria, and arginine vasopressin dysregulation in particular, has also introduced new opportunities for point-of-care testing in patients with nocturnal polyuria.
PubMed: 33796148
DOI: 10.1177/1756287220988438