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Dr Farah Rao, Dr Hafsa Shabbir, Dr Hafza Sarah Tariq


Diabetes inspidius is defined as incapability to focus urine secondary to vasopressin deficiency or to vasopressin resistance which outcome is polyuria. The prevalence of DI is approximately 1:25,000 less than 10% of cases are hereditary naturally. Certainly diabetes inspidius is very infrequent. More than 90% of reported cases are from Central DI (CDI) depending on the cause it can occur at any age. Since now no hereditary prevalence of CDI has been confirmed. Whereas Nephrogenic DI is less resistant than CDI. DI can be defined as CDI or NDI [1]. In the magnocellular neurons of the paraventricular and supraoptic nuclei of the hypothalamus Vasopressin is produced which send axons to the posterior pituitary. The vasopressin is then excreted into the bloodstream via posterior pituitary. The neurons which release vasopressin are damaged in case of CDI. Whereas in case of NDI, there is normal production of vasopressin but at kidney level there is no response of the hormone. At the basolateral membrane of the collecting duct of the kidney Vasopressin acts at V2 receptors. Management of DI in patients requiring intravenous fluids needs further attention as no evidence based studies exist to determine optimal fluid choice and fluid rates. NDI is currently managed with thiazide diuretics; however additional research is necessary to optimize management and promising alternatives are on the horizon.


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