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Review
. 2022 Sep 28;107(10):2701-2715.
doi: 10.1210/clinem/dgac381.

Diagnosis and Management of Central Diabetes Insipidus in Adults

Maria Tomkins  1 , Sarah Lawless  1 , Julie Martin-Grace  1 , Mark Sherlock  1 , Chris J Thompson  1
Affiliations
Review

Diagnosis and Management of Central Diabetes Insipidus in Adults

Maria Tomkins et al. J Clin Endocrinol Metab. .

Abstract

Central diabetes insipidus (CDI) is a clinical syndrome which results from loss or impaired function of vasopressinergic neurons in the hypothalamus/posterior pituitary, resulting in impaired synthesis and/or secretion of arginine vasopressin (AVP). AVP deficiency leads to the inability to concentrate urine and excessive renal water losses, resulting in a clinical syndrome of hypotonic polyuria with compensatory thirst. CDI is caused by diverse etiologies, although it typically develops due to neoplastic, traumatic, or autoimmune destruction of AVP-synthesizing/secreting neurons. This review focuses on the diagnosis and management of CDI, providing insights into the physiological disturbances underpinning the syndrome. Recent developments in diagnostic techniques, particularly the development of the copeptin assay, have improved accuracy and acceptability of the diagnostic approach to the hypotonic polyuria syndrome. We discuss the management of CDI with particular emphasis on management of fluid intake and pharmacological replacement of AVP. Specific clinical syndromes such as adipsic diabetes insipidus and diabetes insipidus in pregnancy as well as management of the perioperative patient with diabetes insipidus are also discussed.

Keywords: adipsia; dDAVP; diabetes insipidus; hypernatremia; hyponatremia.

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Figures

Figure 1.
Figure 1.
Results of AVP responses to hypertonic saline infusion in polyuric states compared with healthy controls (shaded area). White circles represent 8 patients with cranial diabetes insipidus, black circles represent 3 patients with nephrogenic diabetes insipidus, black triangles represent 3 patients with primary polydipsia. (reproduced with permission from Thompson et al. Baillière’s Clinical Endocrinology and Metabolism 1989) (43).
Figure 2.
Figure 2.
Structure of vasopressin preprohormone.
Figure 3.
Figure 3.
Comparison of AVP and copeptin concentrations during hypertonic saline tests, rS denotes Spearman’s correlation (reproduced from Balanescu et al JCEM 2011) (7).
Figure 4.
Figure 4.
Comparison of the amino acid structures of native AVP and dDAVP.
See this image and copyright information in PMC

References

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