Abstract
Diabetes insipidus (DI) is an endocrine condition involving the posterior pituitary peptide hormone, antidiuretic hormone (ADH). ADH exerts its effects on the distal convoluted tubule and collecting duct of the nephron by upregulating aquaporin-2 channels (AQP2) on the cellular apical membrane surface. DI is marked by expelling excessive quantities of highly dilute urine, extreme thirst, and craving for cold water. The two main classifications of DI are central diabetes insipidus (CDI), characterized by a deficiency of the posterior pituitary gland to release ADH, and nephrogenic diabetes insipidus (NDI), characterized by the terminal distal convoluted tubule and collecting duct resistance to ADH. The two less common classifications include dipsogenic DI, characterized by excessive thirst due to a low osmotic threshold, and gestational DI, characterized by increased concentration of placental vasopressinase during pregnancy. Treatment of DI is dependent on the disease classification, but severe complications may arise if not tended to appropriately. The most important step in symptom management is maintaining fluid intake ahead of fluid loss with emphasis placed on preserving the quality of life. The most common treatment of CDI and gestational DI is the administration of synthetic ADH, desmopressin (DDAVP). Nephrogenic treatment, although more challenging, requires discontinuation of medications as well as maintaining a renal-friendly diet to prevent hypernatremia. Treatment of dipsogenic DI is mainly focused on behavioral therapy aimed at regulating water intake and/or administration of antipsychotic pharmaceutical therapy. Central and nephrogenic subtypes of DI share a paradoxical treatment in thiazide diuretics.
Highlights
BackgroundDiabetes insipidus (DI) is a rare disorder, affecting roughly 1 in 25,000 people or about 0.004% of the global population [1]
A deficiency in the release of antidiuretic hormone (ADH) from the posterior pituitary gland leads to central diabetes insipidus (CDI)
Similar to CDI, dipsogenic DI and GDI can be characterized by a deficiency in ADH
Summary
Diabetes insipidus (DI) is a rare disorder, affecting roughly 1 in 25,000 people or about 0.004% of the global population [1]. Dipsogenic DI, known as primary polydipsia, is classified as having an abnormally low osmotic thirst threshold (see Figure 5) [13] This leads to increased fluid intake causing physiological suppression of ADH secretion, excretion of large amounts of dilute urine exceeding 40-50 ml/kg body weight, and risk of hyponatremia [14]. Unlike nephrogenic and central DI, there is an increase in body water leading to a decrease in plasma osmolarity, but like nephrogenic and central DI there is a decrease in ADH secretion and urine concentration This form of DI is most commonly seen in patients with psychotic or neurodevelopmental disorders [1]. Baroreceptor stimulation of ADH takes precedence over osmoregulation [21]
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