🩺 Polyuria

Polyuria is the excretion of an abnormally large volume of urine (>3 litres per day in adults). It must be distinguished from urinary frequency, where volume is normal but the urge to void is frequent. It occurs when either water is not reabsorbed in the collecting ducts (water diuresis) or there is an excess of solutes being excreted (osmotic diuresis). Diabetes Mellitus is the most common cause globally. In cases of dilute urine, the differential narrows to Diabetes Insipidus or primary polydipsia. Management depends entirely on correcting the underlying metabolic or hormonal imbalance.

Confirm that the patient is passing large volumes, not just frequently. Ask about thirst (polydipsia) and whether it wakes them up at night (nocturia is common in polyuria). Enquire about dietary habits and medication, specifically Lithium or diuretics. A history of head trauma or neurosurgery points toward Cranial Diabetes Insipidus. Ask about 'stones, bones, abdominal moans, and psychic groans' to screen for hypercalcaemia. Review a 'Bladder Diary' where the patient records input and output over 24-48 hours.

Check for signs of dehydration (dry mucous membranes, reduced skin turgor) or signs of systemic disease. Inspect for features of hypercalcaemia (e.g., band keratopathy, though rare) or cushions of fat and striae (Cushing's syndrome). In cranial diabetes insipidus, look for signs of pituitary mass effects such as visual field defects (bitemporal hemianopia). Assess for signs of chronic kidney disease (skin pallor, excoriations). Check blood pressure and pulse for orthostatic changes.

Diabetes Mellitus (most common); Cranial Diabetes Insipidus (ADH deficiency); Nephrogenic Diabetes Insipidus (ADH resistance); Primary Polydipsia (excessive drinking); Hypercalcaemia / Hypokalaemia; Diuretic use.

Sudden onset of extreme thirst and polyuria (new-onset Type 1 Diabetes); Polyuria following head trauma or pituitary surgery (Cranial DI); Associated neurological symptoms or visual field loss; Severe dehydration or haemodynamic instability due to massive fluid loss.

Initial tests: Finger-prick glucose or HbA1c to exclude Diabetes Mellitus; U&Es to check renal function and potassium (hypokalaemia causes polyuria); Serum Calcium (hypercalcaemia causes nephrogenic DI). Urinalysis and urine osmolality are crucial: dilute urine (<300 mOsm/kg) in the presence of high plasma osmolality suggests Diabetes Insipidus. The definitive test for DI is the Water Deprivation Test followed by a Desmopressin (DDAVP) challenge. MRI brain may be needed if cranial DI is confirmed.

Always distinguish polyuria (increased volume >3L/day) from frequency (increased number of voids, but normal total volume). A common 'trick' is distinguishing Cranial DI from Nephrogenic DI using the water deprivation test and desmopressin response. If the patient is thirsty and drinking excessively, the primary drive may be 'psychogenic polydipsia', where the urine will eventually concentrate if water is restricted.

Relevant to 'Endocrinology' and 'Renal'. Focus on the physiology of ADH and the interpretation of the water deprivation test results for different types of DI.