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2018 brings new insights into the differential diagnosis of patients with hypotonic polyuria syndrome. Exact localization of the antidiuretic defect in patients with hypotonic polyuria can be challenging, especially the distinction of primary polydipsia from partial pituitary or renal forms of diabetes insipidus. However, diagnostic precision is vital since therapeutic management differs substantially and false treatment may result in serious consequences.A main limitation of the indirect water deprivation test is its limited accuracy to correctly distinguish between the pathophysiologically distinct forms of hypotonic polyuria with a residual antidiuretic capacity. Direct detection of the osmotically-sensitive AVP reserve may be diagnostically superior but is technically difficult and not available for clinical routine, having left indirect diagnostic readouts the only accepted method for differentiating polyuric states, despite a diagnostic accuracy of only 70 %.New data demonstrate that selective measurement of plasma copeptin, a reliable AVP surrogate, not only captures patients with underlying renal defect, but critically improves diagnostic differentiation between primary polydipsia and pituitary forms of central diabetes insipidus.This manuscript presents the novel findings in the field and interprets their clinical consequences., Competing Interests: Disclosure The authors report no conflicts of interest in this work., (© Georg Thieme Verlag KG Stuttgart · New York.)

Intensive care patients often suffer from hypo- or hypernatremia. These dysnatremias reflect an antidiuretic-hormone (ADH)-related water imbalance and are the result of the underlying disease. However, they are often triggered by drug side effects and exacerbated by an intentional or unintentional sodium imbalance. Dysnatremias are also caused by artificial ventilation; however, the mechanisms behind this are beyond the scope of this article. Considerations regarding etiology, water and sodium balance and, in particular, the variable in urine dilution or concentration, take priority over a brisk normalization of sodium concentration. Therefore, the 3 most important factors are: 1) delivery of water and sodium to the collecting duct; 2) generation and maintenance of an osmotic pressure gradient exerted by solutes present in the renal medullary interstitium; 3) the regulated water permeability of collecting duct cells under the control of antidiuretic hormone. With these, most disorders can already be identified from patient history and simple factors such as body weight and serum and urine osmolality.

We know that the symptoms of diabetes insipidus develop only in a state of functional capacity of the neurohypophysis. The symptomatology of diabetes insipidus disappears, when the pars anterior of the hypophysis is destructed, whereas the two lobes have antagonistic effects in respect of water metabolism. Describing two cases the authors remember to F. v. Hann as the first describer of this syndroms' complex and postulate the corresponding nomination.

A radioimmunoassay specific for arginine-vasopressin (AVP) developed in recent years has been applied to measurement of urinary AVP during physiological and clinical studies. Daily excretion of AVP was 34 +/- 10 ng (mean +/- SD) in 17 female normals and 69 +/- 45 ng in 17 male normals, this being a significant difference (p less than 0.01). After osmolar load (Carter-Robbins test) hourly excretion of AVP increased significantly in 7 males from 1.3 to 3.1 ng/h and in 6 females from 1.7 to 6.5 ng/h. Again the difference between male and female normals was significant. In both sexes a significant correlation between AVP excretion and either plasma osmolality or free-water clearance was found. When the osmolar load test was performed under constant angiotensin II perfusion in male subjects, their AVP excretion was significantly more elevated; this confirmed in man the hypothesis that angiotensin II is a stimulus to AVP secretion. Preliminary results of AVP excretion and response to osmolar load in diabetes insipidus are reported. Exceedingly high rate of excretion of AVP up to 55 330 ng/24 h have been found in cases of bronchial carcinoma with dilutional hyponatremia.