Inappropriate ADH Syndrome
Deamino Arginine Vasopressin
Kidney Concentrating Ability
Diabetes Insipidus, Nephrogenic
Clinical review: Vasopressin and terlipressin in septic shock patients. (1/79)Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of septic shock. Terlipressin (tricyl-lysine-vasopressin) is the synthetic, long-acting analogue of vasopressin, and has comparable pharmacodynamic but different pharmacokinetic properties. Vasopressin mediates vasoconstriction via V1 receptor activation on vascular smooth muscle. Septic shock first causes a transient early increase in blood vasopressin concentrations; these concentrations subsequently decrease to very low levels as compared with those observed with other causes of hypotension. Infusions of 0.01-0.04 U/min vasopressin in septic shock patients increase plasma vasopressin concentrations. This increase is associated with reduced need for other vasopressors. Vasopressin has been shown to result in greater blood flow diversion from nonvital to vital organ beds compared with adrenaline (epinephrine). Of concern is a constant decrease in cardiac output and oxygen delivery, the consequences of which in terms of development of multiple organ failure are not yet known. Terlipressin (one or two boluses of 1 mg) has similar effects, but this drug has been used in far fewer patients. Large randomized clinical trials should be conducted to establish the utility of these drugs as therapeutic agents in patients with septic shock. (+info)
Vasopressin, not octreotide, may be beneficial in the treatment of hepatorenal syndrome: a retrospective study. (2/79)BACKGROUND: Hepatorenal syndrome (HRS) is a severe complication of cirrhosis and is associated with high mortality. Ornipressin and terlipressin are effective in treatment of HRS, but are not available in the USA. The efficacy of vasopressin (AVP) and octreotide (OCT) infusions, commonly utilized in the USA, in the treatment of HRS is unknown. This study aims to evaluate the effects of AVP and OCT on renal function, systemic haemodynamics and clinical outcomes in HRS. METHODS: This observational study evaluated patients receiving AVP or OCT therapy for HRS from January 2000 to December 2003. Recovery from HRS was defined as a decrease in the serum creatinine (SCr) to a value < or =1.5 mg/dl. RESULTS: Forty-three patients were identified: eight received AVP, 16 received OCT and 19 received both AVP and OCT. Patients who received AVP alone or in combination with OCT had significantly greater recovery rates than those receiving OCT monotherapy (42 vs 38 vs 0%, respectively, P = 0.01). The average time to response in serum creatinine (SCr) was 7+/- 2 days. The mean AVP doses were 0.23+/-0.19 U/min in patients demonstrating clinical response. Therapy with AVP was an independent predictor of recovery (odds ratio 6.4, 95% confidence interval 1.3-31.8). Patients who responded to therapy had significantly lower mortality (23 vs 67%, P = 0.008) and higher rates of liver transplantation (23 vs 0%, P = 0.005). No adverse effects related to AVP therapy were observed. CONCLUSION: When compared with OCT, HRS patients treated with AVP had significantly higher recovery rates, improved survival and were more likely to receive a liver transplant. (+info)
Acute and fatal hyponatraemia after resection of a craniopharyngioma: a preventable tragedy. (3/79)Central diabetes insipidus developed for the first time in a 14-year-old female during the resection of a craniopharyngioma. The water diuresis persisted until a vasopressin analogue (dDAVP) was given. Professor McCance was asked to explain why hypernatraemia developed, to anticipate dangers that might develop in the salt and water area with therapy, and to provide insights into why this patient died, due to the subsequent development of hyponatraemia that caused a lethal rise in intracranial pressure. The team specifically wanted Professor McCance's opinions as to why a PNa of 124 mmol/l was uniquely dangerous for this patient, and this was a particularly challenging conundrum. Nevertheless, with the aid of a mini-experiment, a careful chart review, and creative thinking, he was able to offer a novel solution, and to suggest ways to prevent its occurrence in other patients. (+info)
High-throughput identification of IMCD proteins using LC-MS/MS. (4/79)The inner medullary collecting duct (IMCD) is an important site of vasopressin-regulated water and urea transport. Here we have used protein mass spectrometry to investigate the proteome of the IMCD cell and how it is altered in response to long-term vasopressin administration in rats. IMCDs were isolated from inner medullas of rats, and IMCD proteins were identified by liquid chromatography/tandem mass spectrometry (LC-MS/MS). We present a WWW-based "IMCD Proteome Database" containing all IMCD proteins identified in this study (n = 704) and prior MS-based identification studies (n = 301). We used the isotope-coded affinity tag (ICAT) technique to identify IMCD proteins that change in abundance in response to vasopressin. Vasopressin analog (dDAVP) or vehicle was infused subcutaneously in Brattleboro rats for 3 days, and IMCDs were isolated for proteomic analysis. dDAVP and control samples were labeled with different cleavable ICAT reagents (mass difference 9 amu) and mixed. This was followed by one-dimensional SDS-PAGE separation, in-gel trypsin digestion, biotin-avidin affinity purification, and LC-MS/MS identification and quantification. Responses to vasopressin for a total of 165 proteins were quantified. Quantification, based on semiquantitative immunoblotting of 16 proteins for which antibodies were available, showed a high degree of correlation with ICAT results. In addition to aquaporin-2 and gamma-epithelial Na channel (gamma-ENaC), five of the immunoblotted proteins were substantially altered in abundance in response to dDAVP, viz., syntaxin-7, Rap1, GAPDH, heat shock protein (HSP)70, and cathepsin D. A 28-protein vasopressin signaling network was constructed using literature-based network analysis software focusing on the newly identified proteins, providing several new hypotheses for future studies. (+info)
Distribution, activity and evidence for the release of an anti-diuretic peptide in the kissing bug Rhodnius prolixus. (5/79)In the haematophagous insect Rhodnius prolixus, diuresis is accomplished through the combined actions of peptidergic diuretic hormones and 5-HT released from neurohaemal sites on the abdominal nerves. Preliminary work on anti-diuresis in this blood-feeder, previously believed to occur through a decrease in the levels of the diuretic factors, indicates that an anti-diuretic hormone, with properties similar to CAP2b (pELYAFPRVamide; recently renamed Mas-CAPA-1), might also be present in R. prolixus. Here, we present evidence from immunohistochemical analysis that suggests a PRXamide-like neuropeptide may be released from the abdominal neurohaemal sites beginning 3-4 h following feeding; a time that coincides with the cessation of diuresis. We also show evidence for an endogenous factor, isolated from the central nervous system using reversed-phase high performance liquid chromatography, which mimics the effects of Mas-CAPA-1. Specifically, this endogenous anti-diuretic factor inhibits rates of 5-HT-stimulated secretion in a dose-dependent manner and elevates intracellular cGMP levels of Malpighian tubules stimulated with 5-HT. (+info)
Nocturnal polyuria in monosymptomatic nocturnal enuresis refractory to desmopressin treatment. (6/79)The transition from day to night is associated with a pronounced decline in diuresis with reductions in the amount of excreted water, electrolytes, and other end products of our metabolism. Failure to do so leads to a large urine output at night, a condition known as nocturnal polyuria, encountered in a large proportion of children with nocturnal enuresis. The aim of this study was to clarify the mechanisms responsible for the nocturnal polyuria seen in enuretics with inadequate response to desmopressin (dDAVP). Forty-six enuretics (7-14 yr of age) and fifteen age-matched controls were admitted for a 24-h protocol with standardized fluid and sodium intake, comprising urine collections, blood sampling, and blood pressure monitoring. We included patients with severe enuresis (5 +/- 1 wet nights/wk) showing <50% reduction in wet nights on dDAVP. We characterized the patients on the basis of their nocturnal urine production. The children with nocturnal polyuria excreted larger amounts of sodium and urea at night than nonpolyurics and controls. Solute-free water reabsorption as well as urinary arginine vasopressin and aquaporin-2 excretion were normal in polyurics, and no differences were found in atrial natriuretic peptide, angiotensin II, aldosterone, and renin levels. Urinary prostaglandin E2 (PGE2) excretion was significantly higher in polyurics. The nocturnal polyuria in children with dDAVP-resistant nocturnal enuresis seems to be the result of augmented sodium and urea excretion. The high urinary PGE2 levels found in these children point toward a role for increased prostaglandin synthesis in the pathogenesis of enuresis-related polyuria. (+info)
Vasopressin increases plasma membrane accumulation of urea transporter UT-A1 in rat inner medullary collecting ducts. (7/79)Urea transport, mediated by the urea transporter A1 (UT-A1) and/or UT-A3, is important for the production of concentrated urine. Vasopressin rapidly increases urea transport in rat terminal inner medullary collecting ducts (IMCD). A previous study showed that one mechanism for rapid regulation of urea transport is a vasopressin-induced increase in UT-A1 phosphorylation. This study tests whether vasopressin or directly activating adenylyl cyclase with forskolin also increases UT-A1 accumulation in the plasma membrane of rat IMCD. Inner medullas were harvested from rats 45 min after injection with vasopressin or vehicle. UT-A1 abundance in the plasma membrane was significantly increased in the membrane fraction after differential centrifugation and in the biotinylated protein population. Vasopressin and forskolin each increased the amount of biotinylated UT-A1 in rat IMCD suspensions that were treated ex vivo. The observed changes in the plasma membrane are specific, as the amount of biotinylated UT-A1 but not the calcium-sensing receptor was increased by forskolin. Next, whether forskolin or the V(2)-selective agonist dDAVP would increase apical membrane expression of UT-A1 in MDCK cells that were stably transfected with UT-A1 (UT-A1-MDCK cells) was tested. Forskolin and dDAVP significantly increased UT-A1 abundance in the apical membrane in UT-A1-MDCK cells. It is concluded that vasopressin and forskolin increase UT-A1 accumulation in the plasma membrane in rat IMCD and in the apical plasma membrane of UT-A1-MDCK cells. These findings suggest that vasopressin regulates urea transport by increasing UT-A1 accumulation in the plasma membrane and/or UT-A1 phosphorylation. (+info)
The role of vasopressin in congestive heart failure. (8/79)Neurohormonal abnormalities contribute to the pathophysiology of congestive heart failure (CHF). Successful approaches to improving the prognosis of patients with CHF are based largely on therapeutic interruption of activated neurohormonal systems. The use of antagonists and inhibitors of the renin-angiotensin-aldosterone and sympathetic nervous systems has significantly improved clinical outcomes in CHF. Excessive secretion of arginine vasopressin (AVP) has the potential for deleterious effects on various physiologic processes in CHF Inhibition of AVP through vasopressin receptor antagonist therapy is a potentially beneficial new therapeutic approach to CHF (+info)
A more detailed explanation of Inappropriate ADH Syndrome may be as follows:
Inappropriate ADH syndrome is a rare endocrine disorder characterized by excessive antidiuretic hormone (ADH) secretion, leading to water retention and hyponatremia. Hyponatremia occurs when the body contains too much water and not enough sodium, causing an imbalance in the electrolyte levels of the blood. This condition can be caused by various factors such as a tumor or other abnormality that increases ADH production or decreases sodium levels in the body. Symptoms of Inappropriate ADH syndrome may include headaches, nausea, vomiting, seizures, and in severe cases, coma.
If left untreated, Inappropriate ADH Syndrome can lead to more serious complications such as seizures or coma. Treatment options for this condition typically involve surgery, radiation therapy, or medication to remove the tumor or other abnormality causing the excessive ADH production and restore sodium levels in the body. It is important to seek medical attention if symptoms persist or worsen over time as early diagnosis and treatment can improve the chances of a successful outcome for this condition.
In summary, Inappropriate ADH Syndrome is an uncommon endocrine disorder caused by excessive ADH secretion leading to hyponatremia due to water retention, which can cause severe symptoms such as headache, nausea, vomiting, seizures, and coma if left untreated. Treatment options involve surgery, radiation therapy, or medication to remove the tumor or other abnormality causing excessive ADH production and restore sodium levels in the body. Early diagnosis and treatment are crucial for a successful outcome.
Hyponatremia can be caused by various factors, such as excessive fluid intake, certain medications, kidney or liver disease, and hormonal imbalances. Symptoms may include headache, nausea, vomiting, fatigue, muscle weakness, and in severe cases, seizures or coma.
Treatment for hyponatremia typically involves correcting the underlying cause of the condition. This may involve discontinuing certain medications, addressing any underlying medical conditions, or limiting fluid intake. In severe cases, hospitalization may be necessary to monitor and treat the condition. In some instances, sodium supplements or diuretics may be prescribed to help correct sodium levels.
It is important to note that hyponatremia can be a serious condition, and prompt medical attention should be sought if symptoms persist or worsen over time. A healthcare professional should be consulted for proper diagnosis and treatment.
There are two main types of DI: central diabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI). CDI is caused by a defect in the hypothalamus or pituitary gland, which can lead to a lack of vasopressin. NDI is caused by a problem with the kidneys, which can prevent them from responding properly to vasopressin.
Symptoms of DI include excessive thirst and urination, fatigue, headaches, and dehydration. Treatment for DI typically involves replacing vasopressin through injections or oral medications, as well as addressing any underlying causes. In some cases, DI can be managed with desmopressin, a synthetic version of vasopressin.
Overall, diabetes insipidus is a rare and complex condition that requires careful management to prevent complications such as dehydration and electrolyte imbalances.
In diabetes, polyuria is caused by high levels of glucose in the blood that cannot be properly absorbed by the body. The excess glucose spills into the urine, drawing water with it and increasing the volume of urine. This can lead to dehydration and electrolyte imbalances if left untreated.
In kidney disease, polyuria can be caused by damage to the kidneys that impairs their ability to concentrate urine. As a result, the body produces more urine than usual to compensate for the lack of concentrating ability.
Polyuria can also be a symptom of certain endocrine disorders such as diabetes insipidus, where the body produces too much antidiuretic hormone (ADH) or vasopressin, which leads to an excessive amount of urine production.
To diagnose polyuria, a healthcare provider may perform a physical examination, take a medical history, and conduct diagnostic tests such as urinalysis, blood glucose testing, and imaging studies. Treatment for polyuria depends on the underlying cause and may include medication, lifestyle changes, and in some cases, dialysis.
The symptoms of water intoxication can vary depending on the severity of the condition, but may include:
* Nausea and vomiting
* Confusion and disorientation
* Slurred speech
* Weakness or fatigue
* Increased heart rate
* Low blood pressure
In severe cases, water intoxication can cause seizures, coma, and even death.
The diagnosis of water intoxication is based on a combination of symptoms, medical history, and laboratory tests, such as blood tests to measure electrolyte levels. Treatment typically involves cessation of fluid intake, administration of electrolytes, and monitoring of vital signs. In severe cases, hospitalization may be necessary to monitor and treat the condition.
Prevention of water intoxication is key, and this can be achieved by drinking fluids in moderation and avoiding excessive intake during physical activity or in hot weather. It is also important to monitor fluid intake in individuals who are at risk, such as endurance athletes or those with certain medical conditions.
In summary, water intoxication is a serious condition that can occur when a person consumes too much water, leading to an imbalance of electrolytes in the body. It is important to be aware of the symptoms and seek medical attention if they occur, as prompt treatment can help prevent complications and death.
The exact cause of NDI is not always known, but it can be due to various factors such as genetic mutations, injury to the pituitary gland or the hypothalamus (parts of the brain that regulate hormone production), certain medications, and kidney disease. The symptoms of NDI can vary in severity and may include:
Excessive thirst and drinking (polydipsia)
Frequent urination (polyuria)
Increased urine output at night (nocturia)
Dry mouth and skin
Fatigue and weakness
To diagnose NDI, a healthcare provider will typically perform a physical exam, take a medical history, and use laboratory tests to assess the levels of vasopressin and other hormones in the body. Treatment for NDI may include medications to reduce urine production, such as desmopressin (DDAVP), and addressing any underlying causes. In some cases, a kidney transplant may be necessary. With proper treatment, people with NDI can lead active lives, but they must be careful to manage their fluid intake and output to avoid dehydration or overhydration.
Water-electrolyte imbalance can be caused by various factors such as excessive sweating, diarrhea, vomiting, burns, and certain medications. It can also be a complication of other medical conditions like kidney disease, heart failure, and liver disease.
Symptoms of water-electrolyte imbalance may include:
* Dehydration or overhydration
* Changes in blood pH (acidosis or alkalosis)
* Electrolyte abnormalities (such as low sodium, high potassium, or low bicarbonate)
* Muscle weakness or cramping
* Confusion or disorientation
* Heart arrhythmias
Treatment of water-electrolyte imbalance depends on the underlying cause and the severity of symptoms. Fluid replacement, electrolyte supplements, and medications to correct pH levels may be prescribed by a healthcare professional. In severe cases, hospitalization may be necessary to monitor and treat the condition.
It is important to seek medical attention if you experience any symptoms of water-electrolyte imbalance, as untreated imbalances can lead to serious complications such as seizures, coma, and even death.