Abstract

BackgroundThe treatment of central diabetes insipidus (DI) with desmopressin in the neonatal period is challenging because of the significant risk of hyponatremia with this agent. The fixed anti-diuresis action of desmopressin and the obligate high fluid intake with milk feeds lead to considerable risk of water intoxication and hyponatremia. To reduce this risk, thiazide diuretics, part of the treatment of nephrogenic DI, were used in conjunction with low renal solute feed and were effective in a single case series of neonatal central DI.Aim We evaluated the efficacy of early treatment of neonatal central DI with hydrochlorothiazide with low solute feed and investigated the clinical indicators for transition to desmopressin during infancy.MethodsA retrospective chart review was conducted at Princess Margaret Hospital, Perth of neonates diagnosed with central DI and treated with hydrochlorothiazide, between 2007 and 2013. Four newborns were identified. Mean sNa and mean change in sNa with desmopressin and hydrochlorothiazide treatment were recorded along with episodes of hyponatremia and hypernatremia. Length and weight trajectories during the first 12 months were assessed.ResultsThe mean change in sNa per day with hydrochlorothiazide and low renal solute feed was 2.5 - 3 mmol/L; on desmopressin treatment, the mean change in sNa was 6.8-7.9 mmol/L. There was one episode of symptomatic hyponatremia with intranasal desmopressin with no episodes of hyponatremia or hypernatremia during treatment with hydrochlorothiazide or following transition to oral desmopressin. Transition to oral desmopressin between 3 to 12 months of age was associated with good control of DI. Following introduction of solids, sNa remained stable but weight gain was slow. This improved following transition to desmopressin in one infant.ConclusionsHydrochlorothiazide with low renal solute feed is a safe and effective treatment option in neonatal central DI. However, transition to desmopressin should be considered early in infancy following initiation of solids to facilitate growth.

Highlights

  • Central Diabetes Insipidus (DI) in newborns and infants is due to the deficiency of arginine vasopressin (AVP) from the posterior pituitary and is associated with septo-optic dysplasia and other midline malformations [1]

  • There were 4 newborns treated for central diabetes insipidus (DI) with thiazide diuretics

  • Wide fluctuations in sNa levels on desmopressin initiated a change to hydrochlorothiazide with low renal solute load feed and led to stabilisation of sNa levels

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Summary

Introduction

Central Diabetes Insipidus (DI) in newborns and infants is due to the deficiency of arginine vasopressin (AVP) from the posterior pituitary and is associated with septo-optic dysplasia and other midline malformations [1]. The fixed anti-diuresis action of desmopressin and the high fluid intake necessary to meet caloric requirements of newborns with milk feeds [4] increase the risk of hyponatremia and make the management of newborns with central DI challenging and difficult. The fixed anti-diuresis action of desmopressin and the obligate high fluid intake with milk feeds lead to considerable risk of water intoxication and hyponatremia. To reduce this risk, thiazide diuretics, part of the treatment of nephrogenic DI, were used in conjunction with low renal solute feed and were effective in a single case series of neonatal central DI

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