Thiazide diuretics
Diuretic
A diuretic is any substance that promotes diuresis, the increased production of urine. This includes forced diuresis. There are several categories of diuretics. All diuretics increase the excretion of water from bodies, although each class does so in a distinct way. Alternatively, an antidiuretic, such as vasopressin, is an agent or drug which reduces the excretion of water in urine.
Full Answer
What is the diuretic effect of thiazide diuretics?
Thiazides have been used in patients with nephrogenic diabetes insipidus (NDI) to decrease urine volume, but the mechanism by which it produces the …
Which diuretics are used in the treatment of nephrogenic diabetes insipidus (NDI)?
Apr 23, 2018 · The diuretic effect of thiazide diuretics is useful if you have oedema or nephrogenic diabetes insipidus. In a healthy person, the kidneys constantly filter the blood in the body. Most of the blood enters into the nephrons (everything except the big molecules like proteins) and then your body reabsorbs the things you still need, like nutrients and fluids, back …
Can thiazides be used to treat nephrogenic diabetes insipidus?
Jul 10, 2021 · Thiazides are usually prescribed as Diuretics because they inhibit the Na-Cl Cotransporter in the DCT which prevents their reabsorption and increases Osmolarity of Tubular fluid that decreases Water reabsorption and consequently the GFR. In case of NDI, our kidneys don’t respond to the ADH/Vasopressin hormone.
What is the antidiuretic effect of hydrochlorothiazide in lithium-induced nephrogenic diabetes insipidus?
Apr 05, 2018 · Thiazide diuretics change the reabsorption of certain things in your urine, making you urinate more often. Specifically, they block sodium and chloride salts from being reabsorbed, which means more of these comes out in your urine.
Why do thiazide diuretics work for nephrogenic diabetes insipidus?
In fact, the most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion (1,2,6⇓⇓). The renal sodium loss causes extracellular volume contraction leading to lowered GFR and increased proximal tubular sodium and water reabsorption.1 Nov 2004
Which diuretic is used for nephrogenic diabetes insipidus?
Nephrogenic diabetes insipidus. Treatment with the drug hydrochlorothiazide (Microzide) may improve your symptoms. Although hydrochlorothiazide is a type of drug that usually increases urine output (diuretic), it can reduce urine output for some people with nephrogenic diabetes insipidus.10 Apr 2021
How is NDI treated?
Dietary modifications and drug therapy are used to decrease urine output. Individuals with NDI may be placed on a very low sodium diet (0.5 g/d) because sodium contributes to water loss. Drugs that affect how much water is excreted in the urine (diuretics) may also be used.
How do thiazides reduce GFR?
Non-hormonal Therapy Thiazide diuretics reduce total body sodium by an initial natriuresis, resulting in decreased extracellular fluid volume and reduced glomerular filtration rate. These changes cause increased fluid reabsorption in the proximal renal tubule and reduce urine output.
How does a thiazide diuretic work?
Thiazide diuretics are drugs that cause both natriuresis (removal of sodium in the urine) and diuresis. Thiazide diuretics work by blocking sodium and chloride (Na/Cl) channels in the distal convoluted tubule of the nephron and inhibit the reabsorption of sodium and water.14 Jun 2021
What is a thiazide diuretic drug?
Thiazide diuretics are a type of diuretic (a drug that increases urine flow). They act directly on the kidneys and promote diuresis (urine flow) by inhibiting the sodium/chloride cotransporter located in the distal convoluted tubule of a nephron (the functional unit of a kidney).
What is the treatment for nephrogenic diabetes insipidus?
Treatment of Nephrogenic Diabetes Insipidus Treatment consists of ensuring adequate free water intake; providing a low-salt, low-protein diet; and correcting the cause or stopping any likely nephrotoxin. Serious sequelae are rare if patients can drink at will.
Why do diabetics get kidney disease?
How does diabetes cause kidney disease? High blood glucose, also called blood sugar, can damage the blood vessels in your kidneys. When the blood vessels are damaged, they don't work as well. Many people with diabetes also develop high blood pressure, which can also damage your kidneys.
What is the urine sodium in diabetes insipidus?
Diabetes insipidus is present when the serum osmolality is raised (>295 milliOsmol/kg) with inappropriately dilute urine (urine osmolality <700 milliOsmol/kg). The serum sodium is often elevated due to excess free water losses.
Why do thiazide diuretics produce less diuresis than the loop diuretics?
Thiazide diuretics, which are the most commonly used diuretic, inhibit the sodium-chloride transporter in the distal tubule. Because this transporter normally only reabsorbs about 5% of filtered sodium, these diuretics are less efficacious than loop diuretics in producing diuresis and natriuresis.
How do thiazide diuretics cause metabolic alkalosis?
Loop and thiazide diuretics can cause metabolic alkalosis due to increased excretion of chloride in proportion to bicarbonate. This is more common with loop diuretics than thiazide diuretics.
How does hydrochlorothiazide affect kidney function?
How does hydrochlorothiazide work? Hydrochlorothiazide is a diuretic (water pill) used for treating high blood pressure (hypertension) and accumulation of fluid (edema). It works by blocking salt and fluid reabsorption from the urine in the kidneys, causing increased urine output (diuresis).
How do thiazides decrease urine volume in diabetes insipidus?
How do thiazides decrease urine volume in Diabetes insipidus? Thiazides are Diuretics that act on Distal Convoluted Tubule and inhibit the NaCl cotransporter in the luminal membrane, thus decreasing the Cl and Na+ reabsorption. It has paradoxical antidiuretic action in Diabetes Insipidus (DI) An initial reduction of sodium reabsorption in the distal tubule increases sodium excretion and causes extracellular fluid volume contraction. As a result, the glomerular filtration rate decreases and the proximal tubular sodium and water reabsorption increases. Consequently, less water and sodium are delivered to the collecting tubules and, as a result, less water is excreted. Thiazides work upon the nephrons in kidney usually on the proximal part of the distal tubule. They increase the Sodium excretion and urine volume a by interference with transfer across cell membranes. The result is a reduction in blood volume. Changes in cardiac output and extracellular fluid volume are transient and, in the long-term, the major haemodynamic effect is a reduction in peripheral resistance due to subtle alterations in the contractile responses of vascular smooth muscle. Diabetes insipidus (DI) is a temporary or chronic disorder characterized by the excretion of excessive quantities of very dilute, but otherwise normal urine. In brief thiazides reduce polyuria and increase urine osmolality in DI. Continue reading >>
What is thiazide used for?
Diuretic, thiazide (Oral route, parenteral route) Thiazide or thiazide-like diuretics are commonly used to treat high blood pressure (hypertension). High blood pressure adds to the workload of the heart and arteries. If it continues for a long time, the heart and arteries may not function properly. This can damage the blood vessels of the brain, heart, and kidneys, resulting in a stroke, heart failure, or kidney failure. High blood pressure may also increase the risk of heart attacks. These problems may be less likely to occur if blood pressure is controlled. Thiazide diuretics are also used to help reduce the amount of water in the body by increasing the flow of urine. They may also be used for other conditions as determined by your doctor. Thiazide diuretics are available only with your doctor's prescription. Once a medicine has been approved for marketing for a certain use, experience may show that it is also useful for other medical problems. Although these uses are not specifically included in product labeling, thiazide diuretics are used in certain patients with the following medical conditions: For patients taking this medicine for diabetes insipidus (water diabetes): Some thiazide diuretics are used in the treatment of diabetes insipidus (water diabetes). In patients with water diabetes, this medicine causes a decrease in the flow of urine and helps the body hold water. Thus, the information given about increased urine flow will not apply to you. Tell your doctor if you have ever had any unusual or allergic reaction to medicines in this group or any other medicines. Also tell your health care professional if you have any other types of allergies, such as to foods dyes, preservatives, or animals. For non-prescription products, read the label or package ingredien Continue reading >>
What is a nephrogenic disease?
Nephrogenic diabetes insipidus (NDI) is a rare disorder that occurs when the kidneys are unable to concentrate urine. In most people, the body balances the fluids you drink with the amount of urine you excrete, or expel, from your body. However, people with NDI produce excessive amounts of urine. This is a condition known as polyuria and it causes insatiable thirst, or polydipsia. NDI occurs when the balance between fluid intake and urine excretion is disrupted. NDI can cause dehydration, among other complications, so it’s important to talk to a doctor if you’re experiencing symptoms. NDI can be fatal if you don’t get treatment for it. The earlier you receive the diagnosis, the better your outlook will be. NDI is unrelated to diabetes mellitus, which is more commonly known as diabetes. The symptoms of NDI vary with age. Infants are severely affected, but the symptoms can resemble many other disorders. As children age, the symptoms become more recognizable. If a diagnosis isn’t made, the symptoms can become severe enough to be life-threatening. You should visit your doctor as soon as possible if you’re experiencing symptoms of NDI. Symptoms in infants The symptoms in infants can include: excessive wet diapers vomiting recurring fevers that have no known cause constipation Symptoms in young children The symptoms in young children can include: bedwetting difficulties in toilet training a failure to thrive mental confusion due to dehydration Symptoms in older children Older children and teenagers can display symptoms that include: high urine output disturbed sleep and fatigue from urinating at night low body weight due to preferring water to food a failure to thrive Symptoms in adults The most common symptoms experienced by adults include: excessive thirst excessi Continue reading >>
What is the kidneys' water transport defect?
The renal water transport defect is located in the collecting system (i.e. the connecting tubule – CNT and the collecting duct – CD) in which vasopressin normally controls the expression and cell surface targeting of the apical water channel aquaporin-2 (AQP2) (4). The CNT and CD are also the site of amiloride-sensitive sodium reabsorption via the epithelial sodium channel (ENaC) (5). Sodium transport across ENaC may osmotically drive transepithelial water reabsorption. Consistently, both AQP2 and ENaC are regulated by vasopressin via V2-receptor-dependent cAMP production (4,5⇓). While exogenous application of vasopressin efficiently corrects the reduced AQP2 expression and the urinary concentration defect in central DI (4), the treatment of nephrogenic DI is usually less obvious and may include different approaches such as dietary sodium restriction, prostaglandin synthesis inhibitors, potassium-sparing diuretics and/or thiazide diuretics (3,6⇓). The use of diuretics for the treatment of a polyuric disease appears paradoxical, but the beneficial effect of thiazides has now been proven for more than 45 yr. In 1959, Crawford and Kennedy showed in a seminal paper that thiazides reduce polyuria and increase urine osmolality in DI (7). Since then, thiazides have become an important component in the therapeutic repertoire for treatment of D Continue reading >>
How to treat cranial diabetes insipidus?
Treatments for diabetes insipidus aim to reduce the amount of urine your body produces. Depending on the type of diabetes insipidus you have, there are several ways of treating your condition and controlling your symptoms. Cranial diabetes insipidus Mild cranial diabetes insipidus may not require any medical treatment. Cranial diabetes insipidus is considered mild if you produce approximately 3-4 litres of urine over 24 hours. If this is the case, you may be able to ease your symptoms by increasing the amount of water you drink, to avoid dehydration. Your GP or endocrinologist (specialist in hormone conditions) may advise you to drink a certain amount of water every day, usually at least 2.5 litres. However, if you have more severe cranial diabetes insipidus, drinking water may not be enough to control your symptoms. As your condition is due to a shortage of vasopressin (AVP), your GP or endocrinologist may prescribe a treatment that takes the place of AVP, known as desmopressin (see below). Desmopressin Desmopressin is a manufactured version of AVP that's more powerful and more resistant to being broken down than the AVP naturally produced by your body. It works just like natural AVP, stopping your kidneys producing urine when the level of water in your body is low. Desmopressin can be taken as a nasal spray, in tablet form or as a form that melts in your mouth, between your gum and your lip. If you're prescribed desmopressin as a nasal spray, you'll need to spray it inside your nose once or twice a day, where it's quickly absorbed into your bloodstream. If you're prescribed desmopressin tablets, you may need to take them more than twice a day. This is because desmopressin is absorbed into your blood less effectively through your stomach than through your nasal passage Continue reading >>
Is amiloride a potassium diuretic?
Amiloride is one of the four potassium sparing diuretics (others include spironolactone, eplerenone, and triamterene). Amiloride is most like triamterene in that they are both cations that directly decrease sodium channel activity in the principal cells in the cortical collecting tubule. Inhibition of sodium reabsorption at the cationic site prevents the secretion of potassium and can lead to life threatening hyperkalemia. The risk of hyperkalemia is higher when it is used concurrently with an ACE inhibitor or another potassium-sparing diuretic (most commonly spironolactone). This class of diuretics is rather weak and is usually used in conjunction with a loop or thiazide diuretic. In addition, amiloride also is a weak inhibitor of cGMP-gated channels; however, this is thought to be fairly weak. An additional use of amiloride involves its importance in patients with lithium-induced nephrogenic diabetes insipidus who have complaints of polyuria and polydipsia. In this circumstance, lithium accumulates in the collecting tubule cells and blocks movement through the sodium channels in the luminal membrane. Blocking these channels with amiloride may partially reverse and even prevent the concentrating effect. Amiloride is the best tolerated drug in its diuretic class and has few side effects aside from hyperkalemia. Continue reading >>
How do thiazides decrease urine volume in diabetes insipidus?
How do thiazides decrease urine volume in Diabetes insipidus? Thiazides are Diuretics that act on Distal Convoluted Tubule and inhibit the NaCl cotransporter in the luminal membrane, thus decreasing the Cl and Na+ reabsorption. It has paradoxical antidiuretic action in Diabetes Insipidus (DI) An initial reduction of sodium reabsorption in the distal tubule increases sodium excretion and causes extracellular fluid volume contraction. As a result, the glomerular filtration rate decreases and the proximal tubular sodium and water reabsorption increases. Consequently, less water and sodium are delivered to the collecting tubules and, as a result, less water is excreted. Thiazides work upon the nephrons in kidney usually on the proximal part of the distal tubule. They increase the Sodium excretion and urine volume a by interference with transfer across cell membranes. The result is a reduction in blood volume. Changes in cardiac output and extracellular fluid volume are transient and, in the long-term, the major haemodynamic effect is a reduction in peripheral resistance due to subtle alterations in the contractile responses of vascular smooth muscle. Diabetes insipidus (DI) is a temporary or chronic disorder characterized by the excretion of excessive quantities of very dilute, but otherwise normal urine. In brief thiazides reduce polyuria and increase urine osmolality in DI. Continue reading >>
What is thiazide used for?
Thiazide diuretics are a form of medication that is commonly used to treat water retention and increase the passage of water in urine. However, in patients with diabetes insipidus, the drug raises the concentration of urine and reduces the amount of urine passed from the body.
What is the treatment for diabetes insipidus?
In central DI and most cases of gestational DI, the primary problem is a deficiency of antidiuretic hormone (ADH)also known as arginine vasopressin (AVP)and therefore, physiologic replacement with desmopressin is usually effective.
What is the mechanism of action of NSAIDs?
Its effects are additive to those of other agents. Nonsteroidal Anti-inflammatory Agents (NSAIDs) The mechanism of action of NSAIDs is not known, but these agents may act by inhibiting prostaglandin synthesis. Inh Continue reading >>. Topical antimicrobial agents for treating foot ulcers in people with diabetes.
What is the condition where the kidneys cannot concentrate urine?
Nephrogenic Diabetes Insipidus (ndi) Nephrogenic diabetes insipidus (NDI) is a rare disorder that occurs when the kidneys are unable to concentrate urine. In most people, the body balances the fluids you drink with the amount of urine you excrete, or expel, from your body.
What is the kidneys' water transport defect?
The renal water transport defect is located in the collecting system (i.e. the connecting tubule – CNT and the collecting duct – CD) in which vasopressin normally controls the expression and cell surface targeting of the apical water channel aquaporin-2 (AQP2) (4). The CNT and CD are also the site of amiloride-sensitive sodium reabsorption via the epithelial sodium channel (ENaC) (5). Sodium transport across ENaC may osmotically drive transepithelial water reabsorption. Consistently, both AQP2 and ENaC are regulated by vasopressin via V2-receptor-dependent cAMP production (4,5⇓). While exogenous application of vasopressin efficiently corrects the reduced AQP2 expression and the urinary concentration defect in central DI (4), the treatment of nephrogenic DI is usually less obvious and may include different approaches such as dietary sodium restriction, prostaglandin synthesis inhibitors, potassium-sparing diuretics and/or thiazide diuretics (3,6⇓). The use of diuretics for the treatment of a polyuric disease appears paradoxical, but the beneficial effect of thiazides has now been proven for more than 45 yr. In 1959, Crawford and Kennedy showed in a seminal paper that thiazides reduce polyuria and increase urine osmolality in DI (7). Since then, thiazides have become an important component in the therapeutic repertoire for treatment of D Continue reading >>
What is nephrogenic di?
INTRODUCTION Nephrogenic diabetes insipidus (nephrogenic DI) results from partial or complete resistance of the kidney to the effects of antidiuretic hormone (ADH). As a result, patients with this disorder are not likely to have a good response to hormone administration (as desmopressin [dDAVP]) or to drugs that increase either the renal response to ADH or ADH secretion. Nephrogenic DI can be hereditary or acquired. In adults, a concentrating defect severe enough to produce polyuria due to nephrogenic DI is most often due to chronic lithium use or hypercalcemia and less frequently to other conditions that impair tubular function, such as Sjögren's syndrome [1]. Release of ureteral obstruction is often associated with a diuresis, but this is short lived and does not require specific therapy other than maintenance fluids. (See "Clinical manifestations and causes of nephrogenic diabetes insipidus" and "Clinical manifestations and diagnosis of urinary tract obstruction and hydronephrosis", section on 'Prognosis and recovery of renal function'.) Hereditary nephrogenic DI, which is largely an X-linked disease, may also be seen by internists since early recognition and treatment in infancy has led to survival to adulthood [2,3]. In addition, affected women may be carriers with few or no symptoms until pregnancy or other stress. In infants with hereditary nephrogenic DI, treatment is aimed at minimizing the polyuria and avoiding hypernatremia and volume depletion. In adults, therapy is usually aimed at correcting the underlying disorder or discontinuing an offending drug. In hypercalcemic patients, for example, normalization of the plasma calcium concentration usually leads to amelioration of polyuria. By contrast, lithium-induced nephrogenic DI may be irreversible if the pati Continue reading >>
How do thiazides decrease urine volume in diabetes insipidus?
How do thiazides decrease urine volume in Diabetes insipidus? Thiazides are Diuretics that act on Distal Convoluted Tubule and inhibit the NaCl cotransporter in the luminal membrane, thus decreasing the Cl and Na+ reabsorption. It has paradoxical antidiuretic action in Diabetes Insipidus (DI) An initial reduction of sodium reabsorption in the distal tubule increases sodium excretion and causes extracellular fluid volume contraction. As a result, the glomerular filtration rate decreases and the proximal tubular sodium and water reabsorption increases. Consequently, less water and sodium are delivered to the collecting tubules and, as a result, less water is excreted. Thiazides work upon the nephrons in kidney usually on the proximal part of the distal tubule. They increase the Sodium excretion and urine volume a by interference with transfer across cell membranes. The result is a reduction in blood volume. Changes in cardiac output and extracellular fluid volume are transient and, in the long-term, the major haemodynamic effect is a reduction in peripheral resistance due to subtle alterations in the contractile responses of vascular smooth muscle. Diabetes insipidus (DI) is a temporary or chronic disorder characterized by the excretion of excessive quantities of very dilute, but otherwise normal urine. In brief thiazides reduce polyuria and increase urine osmolality in DI. Continue reading >>
What is thiazide used for?
Thiazide diuretics are a form of medication that is commonly used to treat water retention and increase the passage of water in urine. However, in patients with diabetes insipidus, the drug raises the concentration of urine and reduces the amount of urine passed from the body.
What is diabetes insipidus?
Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst. [1] . The amount of urine produced can be nearly 20 liters per day. [1] . Reduction of fluid has little effect on the concentration of the urine. [1] .
How to treat cranial diabetes insipidus?
Treatments for diabetes insipidus aim to reduce the amount of urine your body produces. Depending on the type of diabetes insipidus you have, there are several ways of treating your condition and controlling your symptoms. Cranial diabetes insipidus Mild cranial diabetes insipidus may not require any medical treatment. Cranial diabetes insipidus is considered mild if you produce approximately 3-4 litres of urine over 24 hours. If this is the case, you may be able to ease your symptoms by increasing the amount of water you drink, to avoid dehydration. Your GP or endocrinologist (specialist in hormone conditions) may advise you to drink a certain amount of water every day, usually at least 2.5 litres. However, if you have more severe cranial diabetes insipidus, drinking water may not be enough to control your symptoms. As your condition is due to a shortage of vasopressin (AVP), your GP or endocrinologist may prescribe a treatment that takes the place of AVP, known as desmopressin (see below). Desmopressin Desmopressin is a manufactured version of AVP that's more powerful and more resistant to being broken down than the AVP naturally produced by your body. It works just like natural AVP, stopping your kidneys producing urine when the level of water in your body is low. Desmopressin can be taken as a nasal spray, in tablet form or as a form that melts in your mouth, between your gum and your lip. If you're prescribed desmopressin as a nasal spray, you'll need to spray it inside your nose once or twice a day, where it's quickly absorbed into your bloodstream. If you're prescribed desmopressin tablets, you may need to take them more than twice a day. This is because desmopressin is absorbed into your blood less effectively through your stomach than through your nasal passage Continue reading >>
What is central di?
Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone). [1] . This can be due to damage to the hypothalamus or pituitary gland or genetics. [1] . Nephrogenic diabetes insipidus (NDI) occurs when the kidneys do not respond properly to vasopressin. [1] . Dipsogenic DI is due to abnormal thirst mechanisms in ...
What is the diagnosis of diabetes mellitus?
[1] . Diabetes mellitus is a separate condition with an unrelated mechanism, though both can result in the production of large amounts of urine. [1] . Treatment involves drinking sufficient fluids to prevent dehydration. [1] .
What is the name of the condition where the kidneys are unable to concentrate urine?
Diabetes insipidus (DI) is a condition in which the kidneys are unable to concentrate urine. Central DI, the most common form of diabetes insipidus, is caused by insufficient levels of circulating antidiuretic hormone (ADH); nephrogenic DI, however, is characterized by defective renal ADH receptors in the kidneys.
What is the kidneys' water transport defect?
The renal water transport defect is located in the collecting system (i.e. the connecting tubule – CNT and the collecting duct – CD) in which vasopressin normally controls the expression and cell surface targeting of the apical water channel aquaporin-2 (AQP2) (4). The CNT and CD are also the site of amiloride-sensitive sodium reabsorption via the epithelial sodium channel (ENaC) (5). Sodium transport across ENaC may osmotically drive transepithelial water reabsorption. Consistently, both AQP2 and ENaC are regulated by vasopressin via V2-receptor-dependent cAMP production (4,5⇓). While exogenous application of vasopressin efficiently corrects the reduced AQP2 expression and the urinary concentration defect in central DI (4), the treatment of nephrogenic DI is usually less obvious and may include different approaches such as dietary sodium restriction, prostaglandin synthesis inhibitors, potassium-sparing diuretics and/or thiazide diuretics (3,6⇓). The use of diuretics for the treatment of a polyuric disease appears paradoxical, but the beneficial effect of thiazides has now been proven for more than 45 yr. In 1959, Crawford and Kennedy showed in a seminal paper that thiazides reduce polyuria and increase urine osmolality in DI (7). Since then, thiazides have become an important component in the therapeutic repertoire for treatment of D Continue reading >>
What is a nephrogenic disease?
Nephrogenic diabetes insipidus (NDI) is a rare disorder that occurs when the kidneys are unable to concentrate urine. In most people, the body balances the fluids you drink with the amount of urine you excrete, or expel, from your body. However, people with NDI produce excessive amounts of urine. This is a condition known as polyuria and it causes insatiable thirst, or polydipsia. NDI occurs when the balance between fluid intake and urine excretion is disrupted. NDI can cause dehydration, among other complications, so it’s important to talk to a doctor if you’re experiencing symptoms. NDI can be fatal if you don’t get treatment for it. The earlier you receive the diagnosis, the better your outlook will be. NDI is unrelated to diabetes mellitus, which is more commonly known as diabetes. The symptoms of NDI vary with age. Infants are severely affected, but the symptoms can resemble many other disorders. As children age, the symptoms become more recognizable. If a diagnosis isn’t made, the symptoms can become severe enough to be life-threatening. You should visit your doctor as soon as possible if you’re experiencing symptoms of NDI. Symptoms in infants The symptoms in infants can include: excessive wet diapers vomiting recurring fevers that have no known cause constipation Symptoms in young children The symptoms in young children can include: bedwetting difficulties in toilet training a failure to thrive mental confusion due to dehydration Symptoms in older children Older children and teenagers can display symptoms that include: high urine output disturbed sleep and fatigue from urinating at night low body weight due to preferring water to food a failure to thrive Symptoms in adults The most common symptoms experienced by adults include: excessive thirst excessi Continue reading >>
Is HCTZ a diuretic?
Hydrochlorothiazide (HCTZ) is the most frequently used thiazide diuretic in the United States, although chlorthalidone is the diuretic that was used in many of the landmark clinical outcomes trials.1 Nazeer Ahmed1, ... Catherine Kiruthi, in Side Effects of Drugs Annual , 2015 Hydrochlorothiazide was examined as a putative chronic antigen in a cohort of prospectively staged patients after patients were observed with HCTZ-associated common cutaneous T cell lymphomas (CTCL). Patients with hypertensive CTCL were divided into two groups based on whether they were treated with HCTZ or not. Association between HCTZ use and CTCL was analyzed and about 30% of patients experienced complete remission after discontinuing HCTZ. Three patients were rechallenged and developed lesions that resolved or improved with discontinuation of the medication. HCTZ is commonly prescribed and may be a putative antigen in a small subset of patients with mycosis fungoides [35c]. Vassilios Fanos, Laura Cuzzolin, in Comprehensive Pediatric Nephrology , 2008 Hydrochlorothiazide is used in combination with beta blockers for treatment of hypertensive children (with digoxin or ACE inhibitors in heart failure, and with indomethacin or amiloride in the treatment of nephrogenic diabetes insipidus to reduce polyuria and avoid dehydration and hypernatremia). As also reported with furosemide, hydrochlorothiazide can decrease vascular volume and induce electrolyte deficits.71 The effects of hydrochlorothiazide on renal calcium excretion in 30 children with hypercalciuria were evaluated. It was found that 1 mg/kg/day of the diuretic caused a rapid and long-lasting correction of hypercalciuria and prevented the formation of new urinary stones. Other authors do not recommend hydrochlorothiazide in all children dia Continue reading >>
Diabetes Insipidus Treatment
For most patients with diabetes insipidus, treatment often involves a few lifestyle changes and the regular consumption of fluids to prevent dehydration. Each patient will be given a customized treatment plan when this disease is diagnosed and it will be based on the type of diabetes insipidus that is present.
Use Of Acetazolamide In Lithium-induced Nephrogenic Diabetes Insipidus: A Case Report - Edm Case Reports
Use of acetazolamide in lithium-induced nephrogenic diabetes insipidus: a case report Ricardo A Macau 1, * , Tiago Nunes da Silva 2, * , Joana Rego Silva 1 , Ana Gonalves Ferreira 2 and Pedro Bravo 1 [1] Nephrology DepartmentHospital Garcia de Orta [2] Endocrinology DepartmentHospital Garcia de Orta, Almada, Portugal Endocrinology, Diabetes & Metabolism Case Reports, 02 2018, EDM-17-0154, 10.1530/EDM-17-0154 .
Diabetes Insipidus: Causes, Symptoms And Treatment
Diabetes insipidus is a condition where the body loses too much fluid through urination, causing a significant risk of dangerous dehydration as well as a range of illnesses and conditions. There are two forms of the disease: nephrogenic diabetes insipidus and central diabetes insipidus (also known as neurogenic diabetes insipidus).
Nephrogenic Diabetes Insipidus (ndi)
Nephrogenic diabetes insipidus (NDI) is a rare disorder that occurs when the kidneys are unable to concentrate urine. In most people, the body balances the fluids you drink with the amount of urine you excrete, or expel, from your body. However, people with NDI produce excessive amounts of urine.
Diuretic Action Of Three Sulfonylurea Drugs
Diuretic Action of Three Sulfonylurea Drugs ARNOLD M. MOSES, M.D., F.A.C.P.; JOAN HOWANITZ, M.D.; MYRON MILLER, M.D., F.A.C.P. The effect of three sulfonylurea drugs, acetohexamide, tolazamide, and glyburide, on water excretion in hydrated normal subjects was investigated and compared with that of chlorpropamide.
Payperview: Hydrochlorothiazide-amiloride In The Treatment Of Congenital Nephrogenic Diabetes Insipidus - Karger Publishers
I have read the Karger Terms and Conditions and agree. The effects of treatment with hydrochlorothiazide combined with amiloride were compared to hydrochlorothiazide treatment alone in 2 brothers with congenital nephrogenic diabetes insipidus.
Nephrogenic Diabetes Insipidus
In nephrogenic diabetes insipidus, the kidneys produce a large volume of dilute urine because the kidney tubules fail to respond to vasopressin (antidiuretic hormone) and are unable to reabsorb filtered water back into the body. Often nephrogenic diabetes insipidus is hereditary, but it can be caused by drugs or disorders that affect the kidneys.
Where do thiazides inhibit?
The principal site of thiazide action is the distal convoluted tubule, where they inhibit the NaCl cotransporter in the luminal membrane, thus decreasing the Cl − and Na + reabsorption. In 1990 Tran et al. [ 2] studied metolazone, a thiazide type diuretic and suggested that thiazides occupy the Cl − binding site of the Na + Cl − cotransporter. In this position, metolazone impedes the chloride entrance into the transporter molecule, thus blocking the reabsorption of the ion. The principal adverse effect produced by thiazides is potassium loss with consecutive hypokalaemia. Such potassium loss is basically due to (i) enhanced delivery of sodium to late nephron segments, (ii) inhibition of carbonic anhydrase with a consecutive decrease of the distal delivery of chloride, and (iii) stimulation of the apical K‐Cl symporter in principal cells of the distal tubule.
What are the causes of NDI?
Drugs are the most important causes of NDI [ 3 ]. This condition is characterized by unresponsiveness of the kidney to the action of vasopressin. Thus, the administration of desmopressin (dDAVP, a vasopressin analogue acting on the V 2 type vasopressin receptor only) or of other drugs that potentiate arginine–vasopressin, such as carbamazepine, are not effective in NDI. In drug‐induced NDI, the treatment of choice is obviously elimination of the responsible drug [ 3 ]. Nevertheless, in many cases, such as lithium therapy for affective disorders, discontinuance of the drug is often not feasible because alternative drugs with comparable therapeutic effect are not available. In this psychiatric illness, apart from the bothersome symptoms of diabetes insipidus, persistence of polyuria carries the risk of dehydration with decreased lithium clearance and conversely increased serum lithium concentrations and the potential risk of lithium intoxication. The only therapeutic approach is sodium restriction or administration of thiazide diuretics or both. In 1905, Meyer (in [ 4 ]) was the first to observe that diuretics decrease urinary volume in diabetes insipidus, but it was only in 1959 that Crawford and Kennedy [ 5] used thiazides to treat this form of diabetes insipidus in rats. In 1961 the same authors administered thiazides to patients with NDI [ 6 ]. Since that time, thiazides have been an important element in the treatment of NDI [ 7 ]. Although it seems paradoxical to treat polyuria with a diuretic, a net decrease of urine flow occurs with lowering of urine volumes to normal or only slightly elevated values (e.g. typically from 8–10 litres to 4 litres or less per day).
Can thiazides cause polyuria?
First, the clinician has to be aware that there is more than one reason to explain polyuria. When thiazides are used in primary NDI or patients on lithium treatment, potassium depletion may occur. Potassium depletion per se causes polydipsia and vasopressin‐resistant polyuria.