Chapter 552 Diabetes Insipidus
Diabetes insipidus (DI) manifests clinically with polyuria and polydipsia and can result from either vasopressin deficiency (central DI) or vasopressin insensitivity at the level of the kidney (nephrogenic DI). Both central DI and nephrogenic DI can arise from inherited defects of congenital or neonatal onset or can be secondary to a variety of causes (Table 552-1).
Physiology of Water Balance
The control of extracellular tonicity (osmolality) and volume within a narrow range is critical for normal cellular structure and function (Chapter 52). Extracellular fluid tonicity is regulated almost exclusively by water intake and excretion, whereas extracellular volume is regulated by sodium intake and excretion. The control of plasma tonicity and intravascular volume involves a complex integration of endocrine, neural, behavioral, and paracrine systems (Fig. 552-1). Vasopressin, secreted from the posterior pituitary, is the principal regulator of tonicity, with its release largely stimulated by increases in plasma tonicity. Volume homeostasis is largely regulated by the renin-angiotensin-aldosterone system, with contributions from both vasopressin and the natriuretic peptide family.