Excessive thirst (polydipsia)

Polydipsia means drinking far more than the body needs — typically 3 litres or more per day, often accompanied by polyuria (urinating large volumes frequently). The healthy thirst mechanism is triggered when plasma osmolality rises by ~1%; any process that either raises osmolality (high glucose, high sodium) or prevents the kidneys from concentrating urine (low antidiuretic hormone, kidney resistance to ADH) will produce sustained polydipsia. The clinical short-list: type 1 or type 2 diabetes mellitus with glucose spilling into urine and pulling water with it (the textbook polyuria + polydipsia + weight loss triad); central diabetes insipidus (post-pituitary surgery, head trauma, infiltrative); nephrogenic diabetes insipidus (lithium toxicity, hypercalcaemia, hypokalaemia); primary polydipsia / psychogenic polydipsia (often psychiatric); medications (diuretics, lithium); sometimes pregnancy. Hypercalcaemia from primary hyperparathyroidism or malignancy is an easily-missed driver.

• Diabetes mellitus (T1 / T2) — by far the commonest; glucose >11 mmol/L (200 mg/dL) spills into urine.
• Diabetes insipidus — central (low ADH) or nephrogenic (kidney resistance); urine remains dilute despite thirst.
• Hypercalcaemia — primary hyperparathyroidism, malignancy; blunts ADH effect on kidney.
• Hypokalaemia — same mechanism.
• Lithium toxicity — nephrogenic DI.
• Diuretic use — particularly loops.
• Psychogenic polydipsia — often with schizophrenia or compulsive behaviour.
• Pregnancy — increased total body water demand.

First-line: fasting glucose + HbA1c (rule out diabetes), basic metabolic panel (sodium, potassium, calcium, creatinine), urine specific gravity. If diabetes is excluded and polydipsia continues, a supervised water-deprivation test or copeptin measurement distinguishes central from nephrogenic DI from primary polydipsia. Mediora.AI flags the high-glucose + osmotic-pattern cluster; primary diabetes insipidus diagnosis is endocrinology territory.