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Abstract
Diabetes insipidus is one cause of hypotonic polyuria and previously was classified as either central or nephrogenic, on the basis of a water-deprivation test and the administration of vasopressin.1 But in 1970, Miller et al. noted that some patients who underwent water deprivation had a urine osmolality greater than their plasma osmolality and that the urine osmolality further increased, albeit modestly, after the injection of vasopressin -- a state they called "partial antidiuretic hormone deficiency," as diagnosed by the indirect water-deprivation test.2 In 1973, Robertson et al. developed a radioimmunoassay for vasopressin to enhance the sensitivity of the water-deprivation test, but given the short half-life of circulating vasopressin and the fact that it binds to platelets, the assay was found to be difficult to interpret clinically.3 The indirect water-deprivation test remained the only accepted method for differentiating polyuric states, despite a diagnostic accuracy of only 70%. Furthermore, polydipsia is increasingly recognized in patients with psychiatric disorders (e.g., in patients with psychogenic polydipsia or in patients taking certain psychotropic medications). [...]there is a continued need to refine the diagnostic approach to polyuria. [...]hypertonic saline infusions were consistently associated with more adverse events and higher serum sodium levels than water deprivation alone. [...]saline infusions to stimulate copeptin could be problematic; for example, they could induce congestive heart failure in high-risk patients.