Nephrogenic diabetes insipidus results from inability of the kidneys to concentrate urine. This due to failure of the kidneys to respond to antidiuretic hormone (ADH; and also named arginine vasopressin or AVP), resulting in increased excretion of dilute urine.
The kidneys’ ability to respond to ADH can be impaired by drugs—like lithium, for example—and by chronic disorders including polycystic kidney disease, sickle cell disease, kidney failure, partial blockage of the ureters, and inherited genetic disorders.
Polyuria, with hyposthenuria, and polydipsia are the fundamental clinical manifestations of the disease.
Nephrogenic diabetes insipidus may be caused by a defect in the vasopressin-induced permeability of the distal tubules and collecting ducts to water, an insufficient buildup of the corticopapillary interstitial osmotic gradient, or to a combination of these two factors.
Nephrogenic diabetes insipidus
