ADH axis, DI and SIADH: physiology, differentiation, and management

Apuntes

Good. Now we shift from structure to control logic. If you do not understand water physiology, SIADH and Diabetes Insipidus feel like lab-value trivia. So forget the names for a moment. Everything revolves around one hormone: ADH (vasopressin) ADH’s job is simple: It tells the collecting duct: “Insert aquaporin-2 channels. Reabsorb water.” More ADH → more water reabsorbed → urine concentrated → plasma diluted. Less ADH → less water reabsorbed → urine dilute → plasma concentrated. That is the entire axis. Now let’s break it. ⸻ DIABETES INSIPIDUS – TOO LITTLE EFFECT OF ADH Start with physiology. If ADH is absent or ineffective: The kidney cannot reabsorb free water. Water is lost in urine. Sodium stays behind in plasma. So plasma becomes hypernatremic and hyperosmolar. Urine becomes very dilute. Now differentiate mechanisms. CENTRAL DI Problem: low ADH production or release. Cause: hypothalamic or posterior pituitary damage (surgery, trauma, tumor). Mechanism: No ADH → no aquaporin insertion → massive water loss. Labs: High serum sodium High serum osmolality Low urine osmolality NEPHROGENIC DI Problem: ADH present, kidney resistant. Causes tested: Lithium Hypercalcemia Chronic kidney...