Central diabetes insipidus (CDI) is a clinical syndrome which results from loss or impaired function of vasopressinergic neurones 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 aetiologies, although it typically develops due to neoplastic, traumatic or autoimmune destruction of AVP synthesizing/secreting neurones. 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.

Background Long-term glucocorticoid therapy is a key component of immunosuppression for kidney transplant recipients (KTR), leading to significant cumulative glucocorticoid exposure. The aims of this study are to investigate the prevalence of adrenal insufficiency (AI) in KTR taking prednisolone and to develop a screening algorithm to identify patients at highest risk of AI. Methods In this cross-sectional cohort study, 67 KTR receiving prednisolone underwent a short synacthen test (SST) and measurement of cumulative glucocorticoid exposure. Results 72% (n = 48) of participants failed the SST. Participants with AI had a higher daily prednisolone dose (4.9 vs 4.2mg/day,  p = 0.002) and greater cumulative glucocorticoid exposure (289 vs 111mg/kg,  p = 0.03) than those with intact adrenal function. Participants with AI had a lower baseline cortisol than participants with intact adrenal function (143 vs 303nmol/l,  p < 0.001). Morning cortisol of > 288nmol/l predicted a normal SST with 100% specificity (95% CI 92–100%) and 70% sensitivity (95% CI 56–78%), therefore excluding AI. Conclusions Our results suggest KTR are at higher risk for AI than previously reported. A morning serum cortisol measurement is a useful screening tool in this cohort, reducing the need for stimulatory testing by 44%. KTR with AI need education regarding glucocorticoid sick rules similar to patients with other forms of AI.

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