UNIPROT:P01185 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nocturia may be attributable to nocturnal polyuria (nocturnal urine overproduction), a diminished nocturnal bladder capacity or a combination of the two conditions.A disorder of the vasopressin (antidiuretic hormone) system with very low or undetectable levels of vasopressin at night, affecting some elderly people, may cause an increase in the nocturnal urine output, which in the most extreme cases accounts for 85% of the 24-hour diuresis. The increased urine output can be treated with desmopressin orally at bedtime, generally using low doses. Self-imposed fluid restrictions before bedtime are not effective in reducing the nocturnal urine output in this condition. Nocturia is also more prevalent in association with a reduced bladder capacity. Antimuscarinic drugs are used in attempts to depress involuntary bladder contractions. Decreased nocturnal voided volumes in men and consequent increased nocturia may suggest difficulty in emptying the bladder or detrusor overactivity. alpha(1)-Adrenoceptor antagonists and 5alpha-reductase inhibitors are often used in men with symptoms indicative of benign prostatic hyperplasia, and one of their effects is reduction of nocturia. In women, estrogen deficiency, a common consequence of the menopausal transition, causes atrophic changes within the urogenital tract. Consequently, such women are more disposed to having urogenital symptoms, among them nocturia. This review emphasises the importance of correctly diagnosing and treating nocturia in elderly patients. This will improve patients' sleep and, in turn, reduce their risk of fall injuries and the associated detrimental consequences, thereby improving patients' health and quality of life.
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PMID:Pharmacotherapy for nocturia in the elderly patient. 1743 26

The urine-concentrating mechanism performs one of the most essential functions in water and electrolyte metabolism and serves primarily to maintain extracellular osmolality within a very narrow range. The history of anti-diuresis dates back more than 100 years and includes the discovery of antidiuretic hormone (AVP), the renal AVP receptor, and most recently the water channel (aquaporin) proteins. Today, the mechanisms of antidiuresis are understood on a highly detailed molecular level including both short term and long-term regulation of AQP2 function. Furthermore, the background behind many acquired and inherited disturbances of water balance has now been revealed and has enabled a precise differential diagnosis. These include different forms of diabetes insipidus, nocturnal enuresis and nocturia in the elderly. Diabetes insipidus represents a dramatic but rare disturbance of water balance caused by deficient AVP secretion (neurogenic), reduced renal sensitivity to AVP (nephrogenic), an abnormally high fluid intake (primary polydipsia), or in rare cases by placental enzymatic degradation of AVP (gestational). Nocturnal enuresis and nocturia in the elderly represents much more common disturbances and share common pathogenic features including an abnormally high nocturnal urine production. This seems at least in part to be caused by abnormally low levels of plasma AVP during night. The increased understanding of such water balance disturbances have changed dramatically prior treatment practice by introducing antidiuresis as a treatment modality. The ongoing progress in our understanding of antidiuresis may provide the basis for the development of new antidiuretic compounds.
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PMID:Basis and therapeutical rationale of the urinary concentrating mechanism. 1772 73

Nocturia is common in the elderly population and, aside from being a nuisance, it is associated with morbidity and mortality. Nocturia results from the complex interactions of several factors: changes in the urinary system and renal function with aging, the effects of sleep on renal function, changes in sleeping patterns associated with aging, and the presence of concurrent diseases and medications. Nocturia in the elderly can be caused by many conditions; a common cause is the syndrome of nocturnal polyuria. Although the pathophysiology of nocturnal polyuria remains obscure, some investigators believe that low night-time levels of antidiuretic hormone are involved. Proper management of nocturia requires identification of the specific underlying causes. This Review provides an overview of the mechanisms, evaluation and treatment of nocturia for the practicing nephrologist.
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PMID:An overview of nocturia and the syndrome of nocturnal polyuria in the elderly. 1857 9

Desmopressin acetate is the synthetic analogue of the antidiuretic hormone arginine vasopressin. It has been employed clinically for >30 years in a range of formulations: intranasal solution (since 1972), injectable solution (since 1981), tablets (since 1987), and most recently, an oral lyophilisate (since 2005). The antidiuretic properties of desmopressin have led to its use in polyuric conditions including primary nocturnal enuresis, nocturia, and diabetes insipidus. While a large body of clinical data is available for desmopressin, and despite its widespread use, comprehensive reviews of the safety of desmopressin are lacking (although some case series have attempted to correlate patient and/or dosing characteristics with the occurrence of adverse reactions). The purpose of this paper is to review the safety of desmopressin, based on analyses of both published data (MedLine) and of adverse reactions reported to Ferring Pharmaceuticals, the major manufacturer of desmopressin. Based on the findings, suggested strategies to reduce the risk of adverse reactions are proposed. Treatment with intranasal and oral formulations of desmopressin is generally well tolerated, and side effects are usually minor. The risk of hyponatraemia, although small, can be reduced by adhering to the indications, dosing recommendations and precautions when prescribing desmopressin.
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PMID:Desmopressin 30 years in clinical use: a safety review. 1869 Sep 73

1. The kidneys are the key organs to maintain the balance of the different electrolytes in the body and the acid-base balance. Progressive loss of kidney function results in a number of adaptive and compensatory renal and extrarenal changes that allow homeostasis to be maintained with glomerular filtration rates in the range of 10-25 ml/min. With glomerular filtration rates below 10 ml/min, there are almost always abnormalites in the body's internal environment with clinical repercussions. 2. Water Balance Disorders: In advanced chronic kidney disease (CKD), the range of urine osmolality progressively approaches plasma osmolality and becomes isostenuric. This manifests clinically as symptoms of nocturia and polyuria, especially in tubulointerstitial kidney diseases. Water overload will result in hyponatremia and a decrease in water intake will lead to hypernatremia. Routine analyses of serum Na levels should be performed in all patients with advanced CKD (Strength of Recommendation C). Except in edematous states, a daily fluid intake of 1.5-2 liters should be recommended (Strength of Recommendation C). Hyponatremia does not usually occur with glomerular filtration rates above 10 ml/min (Strength of Recommendation B). If it occurs, an excessive intake of free water should be considered or nonosmotic release of vasopressin by stimuli such as pain, anesthetics, hypoxemia or hypovolemia, or the use of diuretics. Hypernatremia is less frequent than hyponatremia in CKD. It can occur because of the provision of hypertonic parenteral solutions, or more frequently as a consequence of osmotic diuresis due to inadequate water intake during intercurrent disease, or in some circumstance that limits access to water (obtundation, immobility). 3. Sodium Balance Disorders: In CKD, fractional excretion of sodium increases so that absolute sodium excretion is not modified until glomerular filtration rates below 15 ml/min (Strength of Recommendation B). Total body content of sodium is the main determinant of extracellular volume and therefore disturbances in sodium balance will lead to clinical situations of volume depletion or overload: Volume depletion due to renal sodium loss occurs in abrupt restrictions of salt intake in advanced CKD. It occurs more frequently in certain tubulointerstitial kidney diseases (salt losing nephropathies). Volume overload due to sodium retention can occur with glomerular filtration rates below 25 ml/min and leads to edema, arterial hypertension and heart failure. The use of diuretics in volume overload in CKD is useful to force natriuresis (Strength of Recommendation B). Thiazides have little effect in advanced CKD. Loop diuretics are effective and should be used in higher than normal doses (Strength of Recommendation B). The combination of thiazides and loop diuretics can be useful in refractory cases (Strength of Recommendation B). Weight and volume should be monitored regularly in the hospitalized patient with CKD (Strength of Recommendation C). 4. Potassium Balance Disorders: In CKD, the ability of the kidneys to excrete potassium decreases proportionally to the loss of glomerular filtration. Stimulation of aldosterone and the increase in intestinal excretion of potassium are the main adaptive mechanisms to maintain potassium homeostasis until glomerular filtration rates of 10 ml/min. The main causes of hyperkalemia in CKD are the following: Use of drugs that alter the ability of the kidneys to excrete potassium: ACEIs, ARBs, NSAIDs, aldosterone antagonists, nonselective beta-blockers, heparin, trimetoprim, calcineurin inhibitors. Determination of serum potassium two weeks after the initiation of treatment with ACEIs/ARBs is recommended (Strength of Recommendation C). Routine use of aldosterone antagonists in advanced CKD is not recommended (Strength of Recommendation C). Abrupt reduction in glomerular filtration rate: Constipation. Prolonged fasting. Metabolic acidosis. A low-potassium diet is recommended with GFR less than 20 ml/min, or GFR less than 50 ml/min if drugs that raise serum potassium are taken (Strength of Recommendation C). In the absence of symptoms or electrocardiographic abnormalities, review of medications, restriction of dietary potassium and use of oral ion exchange resins are usually sufficient therapeutic measures (Strength of Recommendation C). If symptoms and/or electrocardiographic abnormalities are present, the usual parenteral pharmacological measures should be used (10% calcium gluconate, insulin and glucose, salbutamol, resins, diuretics) (Strength of Recommendation A). Parenteral bicarbonate and ion exchange resins in enemas are not recommended as first-line treatment (Strength of Recommendation C). Hemodialysis should be considered in patients with glomerular filtration rates below 10 ml/min (Strength of Recommendation C). 5. Acid-Base Disorders in CKD: Moderate metabolic acidosis (Bic 16-20) mEq/L is common with glomerular filtration rates below 20 ml/min, and favors bone demineralization due to the release of calcium and phosphate from the bone, chronic hyperventilation, and muscular weakness and atrophy. Its treatment consists of administration of sodium bicarbonate, usually orally (0.5-1 mEq/kg/day), with the goal of achieving a serum bicarbonate level of 22-24 mmol/L (Strength of Recommendation C). Limitation of daily protein intake to less than 1 g/kg/day is also useful (Strength of Recommendation C). Use of sevelamer as a phosphate binder aggravates metabolic acidosis since it favors endogenous acid production and therefore acidosis should be monitored and corrected if it occurs (Strength of Recommendation C). Hypocalcemia should always be corrected before metabolic acidosis in CKD (Strength of Recommendation B). Metabolic acidosis is an infrequent disorder and requires exogenous alkali administration (bicarbonate, phosphate binders) or vomiting.
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PMID:[Electrolyte and acid-base balance disorders in advanced chronic kidney disease]. 1901 44

Nocturia is a prevalent symptom that can adversely affect quality of sleep and overall quality of life leading to morbidity and even mortality. Nocturia can be due to a range of urological conditions and non-urological diseases. Nocturia can be due to an insufficient bladder capacity and/or (nocturnal) polyuria. Some of the possibly underlying non-urological diseases can be life-threatening, implying treatment priorities. Urological treatment options include alpha-adrenoceptor antagonists, muscarinic receptor antagonists and vasopressin receptor agonists. The former two have shown beneficial but small and inconsistent effects in patients assumed to have benign prostatic hyperplasia or overactive bladder, respectively. In contrast, the vasopressin analog desmopressin has consistently shown nocturia improvement in patients with proven polyuria. While supported by lower levels of evidence, lifestyle modifications are generally considered important for nocturia treatment. We conclude that nocturia is a urinary storage symptom with a major impact on patients' lives and a complex pathophysiology.
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PMID:Nocturia: a non-specific but important symptom of urological disease. 1922 59

Nocturia is a bothersome and highly prevalent urological condition characterised by the need to wake to void at night. Contrary to popular misconception, nocturia is equally common in men and women, and although its prevalence increases with age, a significant proportion of younger people are also affected. Nocturia leads to repeated fragmentation of sleep and consequently to a serious decline in daytime functioning and in overall quality of life and health. As such, its impact should not be underestimated by clinicians. Traditionally, nocturia has been regarded as a symptom of benign prostatic enlargement and/or overactive bladder syndrome, with treatment therefore directed towards increasing the capacity of the bladder to hold urine. Such treatments have proven largely ineffective in many patients, likely because nocturnal polyuria (NP), a condition that results in overproduction of urine at night, has been found to be present in the majority of nocturia patients. As such, the traditional belief that nocturia is attributable to some other underlying pathological factors, is now being replaced by the acknowledgment that it can be a distinct clinical entity with specific pathogenesis. Frequency-volume charts are an invaluable tool, recommended for routine use in clinical practice, to determine whether nocturia is a result of excessive urine production at night, or of small voided volumes (indicating bladder storage problems), or indeed a combination of these factors. Given the specific antidiuretic action of desmopressin, a synthetic analogue of the body's own antidiuretic hormone, it should be considered as first-line therapy for patients with nocturia where NP is present.
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PMID:Thinking beyond the bladder: antidiuretic treatment of nocturia. 2052 66

Desmopressin, a synthetic analog of the antidiuretic hormone, is used in the treatment of enuresis nocturna in children and increasingly also in adults. Nocturia in the elderly causes sleeping disorders and is associated with a higher risk of falling and increased mortality. Desmopressin leads to a significant decrement of nocturia and consequently, a better sleep quality and is for this reason increasingly prescribed in the old. Desmopressin causes borderline hyponatremia (130-135 mmol/l) in 15% and severe hyponatremia in 5% of all adult users. Factors that predispose to hyponatremia are a higher dose, age > 65 years, a low-normal serum sodium, a high 24-hour urine volume and co-medication (thiazide diuretics, tricyclic antidepressants, serotonin-reuptake-inhibitors, chlorpromazine, carbamazipine, loperamide, Non-Steroidal-Anti-Inflammatory-Drugs). Hyponatremia is associated with headache, nausea, vomiting, dizziness, and can cause somnolence, loss of consciousness and death. We present two cases where initiation of desmopressin led to hyponatremia, requiring hospitalization. In view of the high risk of desmopressin-associated hyponatremia in the older population, alternative treatment strategies for nocturia must be considered first. If desmopressin is prescribed, strict follow-up of serum sodium levels is necessary.
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PMID:[Desmopressin for nocturia in the old: an inappropriate treatment due to the high risk of side-effects?]. 2122 78

In this mini-review, current evidence for how the vasopressin/V2-type receptor/aquaporin axis developed co-evolutionary as a crucial part of the urine-concentrating mechanism will be presented. The present-day human kidney, allowing the concentration of urine up to a maximal osmolality around 1200 mosmol kg(-1)-or urine to plasma osmolality ratio around 4-with essentially no sodium secreted is the result of up to 3 billion years evolution. Moving from aquatic to terrestrial habitats required profound changes in kidney morphology, most notable the loops of Henle modifying the kidneys from basically a water excretory system to a water conserving system. Vasopressin-like molecules has during the evolution played a significant role in body fluid homeostasis, more specifically, the osmolality of body liquids by controlling the elimination/reabsorption of fluid trough stimulating V2-type receptors to mobilize aquaporin water channels in the renal collector tubules. Recent evidence supports that all components of the vasopressin/V2-type receptor/aquaporin axis can be traced back to early precursors in evolutionary history. The potential clinical and pharmacological implications of a better phylogenetic understanding of these biological systems so essential for body fluid homeostasis relates to any pathological aspects of the urine-concentrating mechanism, in particular deficiencies of any part of the vasopressin-V2R-AQP2 axis causing central or nephrogenic diabetes insipidus-and for broader patient populations also in preventing and treating disturbances in human circadian regulation of urine volume and osmolality that may lead to enuresis and nocturia.
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PMID:The evolutionary origin of the vasopressin/V2-type receptor/aquaporin axis and the urine-concentrating mechanism. 2237 25

Approximately 20% of patients with common variable immunodeficiency (CVID) have any autoimmune disease, as concurrent as prior to diagnosis, even during follow-up. In recent years, cases of CVID associated to endocrine autoimmune diseases have been reported. To our knowledge, no cases of CVID with diabetes insipidus has been reported previously. The authors present the case of a 37-year-old male, diagnosed of CVID, who had thirst, polyuria and nocturia for several years. After a water deprivation test and a complete resolution of patient's symptoms with vasopressin (DDAVP) treatment, diagnosis of partial central diabetes insipidus was finally made. Patients diagnosed of CVID could develop water misbalance due to posterior hypophysis autoimmune disorder. A high index of clinical suspicion, an early diagnosis and treatment of these disease could avoid future complications and improve the quality of life of these patients.
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PMID:Partial central diabetes insipidus in patient with common variable immunodeficiency. 2276 Dec 33

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