Abstract
Old female mice of the SWV strain have an hereditary polydipsia–polyuria defect with a severe increase in water turnover and with hypotonic urine which contains no glucose, blood, or protein; that is, they have diabetes insipidus. Their responses to exogenous vasopressin (negative) and water deprivation (positive) and the normal amount of neurosecretory material in their posterior pituitaries indicate that they have nephrogenic diabetes insipidus. The females also have a progressive kidney defect which, although it resembles nephronophthisis in some aspects and hypokalemia in others, is unique. There is a progressive anemia. Amyloid kidneys, polycystic kidneys, diabetes mellitus, and nephronophthisis have been ruled out as the cause of the defect but hypokalemia and hypercalcemia are still possibilities. The SWV males have a milder form of the defect which develops at an older age and shows no signs of histopathology.
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