@article{Abbas_Iqbal_Iqbal_Javaid_Ashraf_2016, title={Diabetes insipidus: the basic and clinical review}, volume={4}, url={https://www.msjonline.org/index.php/ijrms/article/view/438}, DOI={10.18203/2320-6012.ijrms20160002}, abstractNote={<p class="abstract">Diabetes insipidus (DI) is a complex disease. DI is inability of the body to conserve water. Polydipsia and polyuria are the major manifestations of DI. DI has various variants including central diabetes insipidus (due to defect in ADH secretion), nephrogenic diabetes insipidus (due to defect in ADH receptors or urea receptors), gestational diabetes insipidus (due to catabolism of ADH by placental vasopressinase) and primary polydipsia (due to massive fluid intake). The cause of various variants of DI is either acquired or congenital. High plasma osmolality due to hypotonic urine excretion can be fatal because it can cause psychosis, lethargy, seizures, coma or even death. Polyuria and polydipsia help in the diagnosis of DI. Differential diagnosis of various variants of DI can be carried out on the basis of water deprivation test, MRI and other radiological techniques. The proper management of DI is the replenishment of water loss and correction of clinical presentations produced as a result of DI, major is hypernatremia. The best management for primary polydipsia is fluid restriction while fluid intake is used for adipsic diabetes insipidus. ADH replacement therapy is widely used to treat DI. DDAVP or desmopressin is mostly preferred ADH analogue because it has less side effects and resistant to placental vasoprssinase.</p>}, number={1}, journal={International Journal of Research in Medical Sciences}, author={Abbas, Muhammad Waseem and Iqbal, Muhammad Arslan and Iqbal, Muhammad Nouman and Javaid, Rukhsar and Ashraf, Muhammad Aizaz}, year={2016}, month={Dec.}, pages={5–11} }