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Primary polydipsia may have physiological causes, such as autoimmune hepatitis. Since primary polydipsia is a diagnosis of exclusion, the diagnosis may be made for patients who have medically unexplained excessive thirst, and this is sometimes incorrectly referred to as psychogenic rather than primary polydipsia.
Zinc is also known to reduce symptoms of polydipsia by causing the body to absorb fluids more efficiently (reduction of diarrhea, induces constipation) and it causes the body to retain more sodium; thus a zinc deficiency can be a possible cause. The combination of polydipsia and (nocturnal) polyuria is also seen in (primary) hyperaldosteronism ...
The most obvious cause is a kidney or systemic disorder, including amyloidosis, [2] polycystic kidney disease, [3] electrolyte imbalance, [4] [5] or some other kidney defect. [2] The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are lithium toxicity and high blood calcium.
Dipsogenic DI or primary polydipsia results from excessive intake of fluids as opposed to deficiency of arginine vasopressin. It may be due to a defect or damage to the thirst mechanism, located in the hypothalamus, [11] or due to mental illness. Treatment with desmopressin may lead to water intoxication. [12]
It differentiates primary polydipsia from diabetes insipidus and central diabetes insipidus from nephrogenic diabetes insipidus. Diabetes insipidus is treated by restoring free water deficit, replacing the missing hormone, and addressing the underlying ailment. Desmopressin, an arginine vasopressin analog, is used to treat central diabetes ...
Polyuria (excessive urine production) of which, in turn, the most frequent causes are: uncontrolled diabetes mellitus, primary polydipsia (excessive fluid drinking), central diabetes insipidus and nephrogenic diabetes insipidus. [20] Polyuria generally causes urinary urgency and frequency, but does not necessarily lead to incontinence.
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Syndrome of inappropriate antidiuretic hormone secretion (SIADH), also known as the syndrome of inappropriate antidiuresis (SIAD), [2] is characterized by a physiologically inappropriate release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an ectopic non-pituitary source, such as an ADH-secreting tumor in the lung. [1]