Makindo Medical Notes

Polyuria is defined as the passage of urine volumes >3 L/day in adults (or >2 L/m²/day in children). It is a symptom rather than a disease, and the key clinical challenge is to distinguish between water diuresis (e.g. diabetes insipidus, polydipsia) and solute diuresis (e.g. hyperglycaemia, diuretics). Accurate measurement of 24-hour urine volume and osmolality is crucial.

About Polyuria 🔎

• Characterized by persistently high urine output that is disproportionate to fluid intake.
• Should not be confused with frequency (passing small amounts often).
• Often requires differentiation from nocturia and urinary urgency.

Pathophysiological Categories ⚖️

• Decreased Vasopressin Production (Cranial Diabetes Insipidus): Failure of ADH secretion from posterior pituitary.
• Decreased Renal Response to Vasopressin (Nephrogenic DI): Kidneys fail to respond to ADH due to acquired or genetic causes.
• Excessive Water Intake: Potomania (beer drinker’s potomania) or psychogenic polydipsia → low solute intake prevents urine concentration.
• Excessive Solute Load: Glucose (uncontrolled diabetes), mannitol, high urea states, or diuretic misuse.

Causes 💡

• Cranial Diabetes Insipidus: Head trauma, pituitary surgery, tumours (craniopharyngioma), sarcoidosis, idiopathic.
• Nephrogenic Diabetes Insipidus:
  • Congenital (X-linked mutation in vasopressin receptor V2 gene).
  • Acquired: Hypercalcaemia, hypokalaemia, lithium therapy, CKD, post-obstructive uropathy.
• Psychogenic Polydipsia: Seen in psychiatric illness (schizophrenia, mood disorders).
• Solute Diuresis: Hyperglycaemia (osmotic diuresis), high-protein feeds, mannitol therapy, diuretics.
• Cardiac Causes: Post-SVT or atrial stretch → release of atrial natriuretic peptide.

Investigations 🔬

• 24-hour urine collection: Confirms polyuria (>3L/day in adults).
• Urine osmolality & serum osmolality: Distinguishes solute vs water diuresis.
• Water Deprivation Test:
  • In DI → urine fails to concentrate despite rising serum osmolality.
  • After desmopressin: concentration improves in cranial DI but not in nephrogenic DI.
• Bloods: U&E, calcium, glucose, potassium, renal function.
• MRI pituitary if cranial DI suspected.

Management 💊

• Cranial DI: Desmopressin (DDAVP) intranasal/oral/parenteral → replaces deficient ADH.
• Nephrogenic DI: Thiazide diuretics + low-salt, low-protein diet → reduce urine volume via paradoxical effect.
• Amiloride in lithium-induced nephrogenic DI (blocks lithium entry into collecting duct cells).
• Treat underlying cause:
  • Correct hypercalcaemia/hypokalaemia.
  • Review drug history (stop lithium, diuretics where possible).
  • Manage hyperglycaemia in diabetes mellitus.
• Ensure adequate hydration to prevent hypernatraemia.

Key Clinical Pearls 📝

• Polyuria + polydipsia + weight loss → always exclude diabetes mellitus first (check glucose, HbA1c).
• Cranial DI: responds to desmopressin; Nephrogenic DI: does not.
• Psychogenic polydipsia: urine osmolality remains very low, risk of hyponatraemia if unchecked.
• Unexplained high-output urine in hospitalised patients: always think of diuretics (prescribed or surreptitious).

References 📚

• BMJ Best Practice: Diabetes Insipidus and Polyuria
• UpToDate: Polyuria in Adults

🧑‍⚕️ Case Examples — Polyuria

• Case 1 (Diabetes Mellitus — osmotic diuresis): 🍭 A 52-year-old man presents with excessive thirst, nocturia, and weight loss. Blood glucose is 18 mmol/L, urine dip positive for glucose and ketones. Analysis: Hyperglycaemia → osmotic diuresis → polyuria and polydipsia. Diagnosis: New-onset type 2 diabetes with osmotic diuresis. Management: Lifestyle modification, metformin, glycaemic control; fluids if dehydrated.
• Case 2 (Diabetes Insipidus — central): 💧 A 24-year-old woman reports drinking >8 L water/day and passing copious dilute urine, even at night. Serum sodium 150 mmol/L, urine osmolality 100 mOsm/kg. Water deprivation test fails to concentrate urine, but improves with desmopressin. Analysis: Lack of ADH secretion from posterior pituitary. Diagnosis: Central diabetes insipidus. Management: Desmopressin (DDAVP), treat underlying cause (e.g., pituitary pathology).
• Case 3 (Diabetes Insipidus — nephrogenic): 🧬 A 35-year-old man on long-term lithium for bipolar disorder presents with persistent polyuria and polydipsia. Serum sodium 148 mmol/L, urine osmolality remains low even after desmopressin. Analysis: Kidneys resistant to ADH → nephrogenic DI. Diagnosis: Lithium-induced nephrogenic diabetes insipidus. Management: Stop lithium if possible, thiazide diuretic, low-salt diet, amiloride if lithium cannot be stopped.
• Case 4 (Primary polydipsia): 🚰 A 40-year-old woman presents with urinary frequency and excessive water intake, claiming to drink “constantly.” Serum sodium is 132 mmol/L, urine osmolality is low. Water deprivation test shows gradual urine concentration without desmopressin. Analysis: Excessive fluid intake → dilute urine, mild hyponatraemia. Diagnosis: Primary polydipsia (psychogenic). Management: Behavioural modification, psychiatric support, monitor sodium.