Nephrogenic Diabetes Insipidus (NDI)

The NPO order is the perioperative problem - These patients compensate by drinking, sometimes 20 L a day. Fasting, sedation, and anesthesia remove that compensation, and patients without an intact thirst mechanism develop severe hypernatremia. Minimize fasting time, keep an IV running, and start replacing losses before induction.

Preop labs that decide the plan - Serum sodium and plasma osmolality, urine osmolality or specific gravity, and serum calcium and potassium. Urine osmolality below 300 mOsm/kg with a serum sodium above 146 mmol/L points at DI; urine osmolality above 800 mOsm/kg rules it out and sends you looking for another cause of polyuria.

Desmopressin is not your rescue - DDAVP minimally raises urine osmolality in partial NDI and does not raise it at all in complete NDI. Unlike central DI, you cannot fix the urine output pharmacologically in the room — you replace what comes out.

Replace measured losses - Match ongoing urinary output with an hourly Foley and serial serum sodium and plasma osmolality. Untreated, the endpoint is hypovolemia, dehydration, and electrolyte imbalance, and in children and older patients cardiovascular collapse, fever, and hypernatremia.

Not all intraoperative polyuria is DI - Excess administered fluid, mannitol, and glucocorticoid-induced hyperglycemia with glucosuria all produce osmotic diuresis. Urine osmolality separates osmotic diuresis (isotonic or hypertonic urine) from a water diuresis (below 300 mOsm/kg).

Treat the reversible causes - Stop lithium where the psychiatric picture allows, though NDI can be permanent even after discontinuation. Correct hypercalcemia — the concentrating defect usually reverses once calcium normalizes, unless there is permanent medullary damage. Correct severe hypokalemia, which itself impairs concentrating ability.

Home regimen to expect - Low-solute diet (low salt, low protein), thiazide diuretics, and NSAIDs. Thiazides cut urine volume by promoting endogenous aldosterone release so less water reaches the collecting tubule; NSAIDs work by inhibiting the prostaglandins that antagonize ADH. A patient on both may arrive volume depleted.

Watch the sodium in both directions - Hypernatremia is the expected failure mode from unreplaced water loss, but overcorrecting with free water carries its own risk. Follow serial sodium rather than urine volume alone.

Nephrogenic diabetes insipidus (NDI) is failure of the kidney to respond to antidiuretic hormone (ADH). The defect is resistance at the V2 receptor in the collecting tubule, a defective aquaporin-2 water channel, or interference with the medullary countercurrent mechanism from medullary injury or reduced sodium chloride reabsorption in the thick ascending limb. The result is hypotonic polyuria — urine osmolality below 300 mOsm/kg with intakes up to 20 L/day driven by thirst.

Roughly 90% of hereditary NDI is X-linked AVPR2 mutation; the common acquired causes in adults are chronic lithium (about 20% of chronic lithium patients develop polyuria), hypercalcemia persistently above 11 mg/dL, and severe hypokalemia. As long as the patient can drink, they hold their sodium normal. Take away access to water and they go straight to hypovolemia and hypernatremia.