Polyuria and polydipsia

Polyuria and polydipsia together describe a syndrome every general paediatrician meets: a child who passes large volumes of urine and is driven to drink to keep up. The complaint sounds simple, but it conceals a fork that, once taken wrongly, causes real harm. The single most common cause of polyuria in a child is uncontrolled diabetes mellitus, where glucose spills into the urine and drags water with it — an osmotic diuresis. [1] [3] That diagnosis is missed by going straight to rare endocrine causes, so the discipline of this topic is to exclude glucose first, every time, before ever thinking about the water-balance disorders.

When the glucose is normal, the question becomes whether the kidney is failing to concentrate urine at all — a water diuresis — or whether it is being asked to excrete a load of solute. The urine osmolality answers that in a single number: dilute urine below 300 mOsm per kg is a water diuresis and leads to the three diabetes insipidus disorders. [1] [10] This page owns that diagnostic fork and the fluids-and-electrolytes consequences, while the companion endocrinology page carries the deep pituitary-tumour and congenital detail. The teaching spine is glucose first, osmolality second, sodium third, desmopressin response fourth, and slow correction of the sodium throughout.

Overview & Definition

Polyuria is defined quantitatively. In a child it means a urine output over 2 litres per square metre of body-surface area per day, or more simply over 40 to 50 mL per kilogram per day. [1] [3] Polydipsia is the compensatory intake that follows, because the body is defending its serum osmolality. The two together form the polyuria-polydipsia syndrome, and the first task is to decide whether the kidney is producing dilute urine because it cannot concentrate it (a water diuresis) or because it is being flooded with solute it must excrete (an osmotic or solute diuresis). [10] [5]

The urine osmolality is the single number that separates these. A water diuresis produces urine that is genuinely dilute — osmolality below 300 mOsm per kg — because the kidney cannot retain water against its concentration gradient. [1] [6] An osmotic diuresis produces a high volume of urine that is not dilute at all, because the obligate excretion of glucose, mannitol or urea carries water but keeps the urine relatively concentrated. This distinction is why a urine osmolality is measured alongside the glucose at first contact, rather than later. [5] [10]

Within the water diuresis sits diabetes insipidus, named centuries ago for the tasteless (insipid) urine that distinguished it from the sweet urine of diabetes mellitus. The 2022 Working Group position statement renamed central diabetes insipidus as arginine vasopressin deficiency (AVP-D) and nephrogenic disease as arginine vasopressin resistance (AVP-R), to remove confusion with diabetes mellitus and to describe mechanism rather than anatomy, though the older names remain in wide clinical use. [2] [1] Both describe a kidney that cannot concentrate urine; the difference is whether the problem is a lack of the hormone or a failure of the kidney to respond to it.

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1. [1]Christ-Crain M; Bichet DG; Fenske WK; Goldman MB; Rittig S; Verbalis JG Diabetes insipidus. Nat Rev Dis Primers, 2019.PMID 31395885
2. [2]Arima H, Cheetham T, Christ-Crain M, et al. Changing the name of diabetes insipidus: a position statement of The Working Group for Renaming Diabetes Insipidus. Eur J Endocrinol, 2022.PMID 36239119
3. [3]Dabrowski E; Kadakia R; Zimmerman D Diabetes insipidus in infants and children. Best Pract Res Clin Endocrinol Metab, 2016.PMID 27156767
4. [4]Di Iorgi N; Napoli F; Allegri AE; Olivieri I; Bertelli E; Gallizia A; Rossi A; Maghnie M Diabetes insipidus--diagnosis and management. Horm Res Paediatr, 2012.PMID 22433947
5. [5]Fenske W; Allolio B Clinical review: Current state and future perspectives in the diagnosis of diabetes insipidus: a clinical review. J Clin Endocrinol Metab, 2012.PMID 22855338
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7. [7]Fenske W; Refardt J; Chifu I; Schnyder I; Winzeler B; Drummond J; Rutishauser J; Kopp P; Landgraf R; Luger A; Christ-Crain M A Copeptin-Based Approach in the Diagnosis of Diabetes Insipidus. N Engl J Med, 2018.PMID 30067922
8. [8]Winzeler B; Cesana-Nigro N; Refardt J; Vogt DR; Chifu I; Bassetti CL; Fenske WK; Kopp P; Christ-Crain M Arginine-stimulated copeptin measurements in the differential diagnosis of diabetes insipidus: a prospective diagnostic study. Lancet, 2019.PMID 31303316
9. [9]Bockenhauer D; Bichet DG Pathophysiology, diagnosis and management of nephrogenic diabetes insipidus. Nat Rev Nephrol, 2015.PMID 26077742
10. [10]Robertson GL Diabetes insipidus: Differential diagnosis and management. Best Pract Res Clin Endocrinol Metab, 2016.PMID 27156759
11. [11]Djermane A; Elmaleh M; Simon D; Poidvin A; Souberbielle JC; Beltrand J; Brassier G; Houang M; Carel JC; Chomton M; Leger J Central Diabetes Insipidus in Infancy With or Without Hypothalamic Adipsic Hypernatremia Syndrome: Early Identification and Outcome. J Clin Endocrinol Metab, 2016.PMID 26588450
12. [12]Zieg J Diagnosis and management of hypernatraemia in children. Acta Paediatr, 2022.PMID 34716953