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Persons with nephrogenic diabetes insipidus must consume enough fluids to equal the amount of urine produced. Any underlying cause such as high blood calcium must be corrected to treat nephrogenic diabetes insipidus. The first line of treatment is hydrochlorothiazide and amiloride. [10] Patients may also consider a low-salt and low-protein diet.
Nephrogenic DI may be treated by addressing the underlying cause or by the use of a thiazide, aspirin or ibuprofen. [1] The number of new cases of diabetes insipidus each year is 3 in 100,000. [4] Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally. [2] Nephrogenic DI can begin at any age. [3]
X-linked nephrogenic diabetes insipidus type 1 [304800] V2 receptor: Xq28: XR: Hyperthermia, polyuria, polydipsia, dehydration, inability to form concentrated urine, intellectual disability if diagnosis delayed. Symptoms in infancy: Hyperosmolar plasma, dilute urine Autosomal dominant nephrogenic diabetes insipidus type 2 [192340] AQP2: 12q13 ...
A fluid or water deprivation test is a medical test [1] which can be used to determine whether the patient has diabetes insipidus as opposed to other causes of polydipsia (a condition of excessive thirst that causes an excessive intake of water). The patient is required, for a prolonged period, to forgo intake of water completely, to determine ...
Chlortalidone (or other thiazide medication) is a key component of treatment of nephrogenic diabetes insipidus. Nephrogenic diabetes insipidus occurs when the kidney is unable to concentrate urine because it has an inadequate response to vasopressin-dependent removal of free water from the renal tubular filtrate.
In the absence of diabetes mellitus, the most common causes are the decreased secretion of aldosterone due to adrenal cortical tumor, primary polydipsia (excessive fluid drinking), central diabetes insipidus, and nephrogenic diabetes insipidus. [6] Polyuria may also be due to various chemical substances, such as diuretics, caffeine, and ethanol.
Hypercalcemia usually causes symptoms that lead to chronic dehydration, such as nausea, vomiting, anorexia, and nephrogenic diabetes insipidus (inability of the kidney to concentrate the urine). IV fluid rehydration allows the kidneys to excrete more calcium, and usually lowers the calcium level by 1–2 mg/dL.
Nocturia, polyuria, and polydipsia from reduced urinary concentrating capacity (i.e. nephrogenic diabetes insipidus) as can be seen in hypercalcemia, medullary nephrocalcinosis of any cause, or in children with Bartter syndrome in whom essential tubular salt reabsorption is compromised.