
Health Dictionary
Reliable, easy-to-read patient information on common medical conditions โ written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Diabetes insipidus laboratory findings
Introduction
Overview
Overview
Laboratory findings consistent with the diagnosis of diabetes insipidus include abnormal urine osmolality, abnormal urine output, and abnormal plasma and urine ADH levels as rise in plasma/urine ADH
Laboratory Findings
Laboratory Findings
Measurement of the plasma sodium concentration and the urine osmolality is helpful in distinguishing between the 3 types of diabetes insipidus. Each of the three causes of polyuria โ primary polydipsia, central DI, and nephrogenic DI โ is associated with an increase in water output and the excretion of a relatively dilute urine. In primary polydipsia, the polyuria is an appropriate response to enhanced water intake but on the contrary the water loss is inappropriate with central and nephrogenic DI.[1]
Some of the investigations that can be done to appropriately diagnose diabetes insipidus are:
Plasma sodium and urine osmolality:
- Plasma sodium concentration that is less than 137 meq/L associated with a low urine osmolality indicates water overload due to primary polydipsia.
- Plasma sodium concentration greater than 142 meq/L, due to water loss indicates diabetes insipidus diabetes insipidus.
Measurement of urine output:
- Clarity and usefulness of the sample collection is uncertain.
Water deprivation test:
- Water restriction or the administration of hypertonic saline (0.05 mL/kg per min for no more than two hours) can be used to differentiate central DI from primary polydipsia.
Plasma and urine ADH measurement[2][3]
- Rise in plasma/urine ADH in response to the rising plasma osmolality levels rules out central DI.
- An appropriate rise in urine osmolality as ADH secretion is increased rules out nephrogenic DI.
References
References
- โ Arthus MF, Lonergan M, Crumley MJ, Naumova AK, Morin D, De Marco LA, Kaplan BS, Robertson GL, Sasaki S, Morgan K, Bichet DG, Fujiwara TM (2000). “Report of 33 novel AVPR2 mutations and analysis of 117 families with X-linked nephrogenic diabetes insipidus”. J. Am. Soc. Nephrol. 11 (6): 1044โ54. PMIDย 10820168.
- โ Zerbe RL, Robertson GL (1981). “A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria”. N. Engl. J. Med. 305 (26): 1539โ46. doi:10.1056/NEJM198112243052601. PMIDย 7311993.
- โ Diederich S, Eckmanns T, Exner P, Al-Saadi N, Bรคhr V, Oelkers W (2001). “Differential diagnosis of polyuric/polydipsic syndromes with the aid of urinary vasopressin measurement in adults”. Clin. Endocrinol. (Oxf). 54 (5): 665โ71. PMIDย 11380498.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2]
