- What the two main sub-types of diabetes insipidus and how do you differentiate between the two?
- What are the two lesser known sub-types?
- The two main types of diabetes insipidus (DI) are central and nephrogenic. The hallmark of DI is deficiency of vasopressin and you can think of central DI as an ABSOLUTE deficiency and nephrogenic as a RELATIVE deficiency. Meaning, in central DI there is a problem with secretion of vasopressin from the posterior pituitary. The kidneys are fine, there just isn’t any vasopressin to make the kidneys hold onto water. In nephrogenic DI, there is plenty of circulating vasopressin (due to feedback to a normally functioning pituitary), but the kidneys are not responding to this stimulus. Central DI is most commonly caused by head trauma, post-neurosurgery, or autoimmune issues. Nephrogenic DI is most commonly caused by genetic defects in children, or renal problems in adults. A simple test to differentiate between central and nephrogenic DI is a desmopressin challenge. You can give desmopressin IN or SQ and measure urine osmolarity and volume every 30 minutes for 2 hours. In central DI, you should see a decrease in urine volume and increase in urine osmolarity. In nephogenic DI, nothing will change.
- There are 2 other sub-types of DI that you need to be aware of as well. Gestational DI, which is considered a form of nephrogenic DI, can occur in the second/third trimester of pregnancy. This manifests as a transient ADH resistance due to increased vasopressinase from the placenta. The other subtype of DI is dipsogenic DI, which is a result of either a defect in the thirst center of the hypothalamus, or due to mental illness, which causes near constant polydipsia and polyuria. This basically overpowers the circulating ADH
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