Polyuria
The volume of urine produced per day varies in each individual and is affected by the amount of fluid intake, physiological requirements and insensible losses. Polyuria is arbitrarily defined as urine output of more than three litres in 24 hours.
History
General
Polyuria is often accompanied by polydipsia, and, as with all water-losing states, severe thirst is often a side-effect. Frequency of micturition (frequent passing of small amounts of urine) should be differentiated from polyuria (frequent passing of large amounts of urine). Diabetes insipidus may be hereditary and other family members may be affected.
Drug history
A detailed drug history is invaluable, as a significant number of drugs precipitate polyuria by various mechanisms. Therapeutic diuretics are used in a range of disorders, such as hypertension and cardiac failure. Opiates inhibit ADH secretion and may produce cranial diabetes insipidus, whereas drugs such as lithium and demeclocycline may produce nephrogenic diabetes insipidus. A side-effect of anticholinergics is dryness of the mouth; patients may therefore ingest excessive quantities of water, causing polyuria. Nephrotoxic drugs, such as aminoglycosides, ciclosporin, NSAIDs and ACE inhibitors, may precipitate acute tubular necrosis, which can result in severe polyuria in the recovery phase.
Past medical history
Hyperglycaemia causes an osmotic diuresis, therefore polyuria and polydipsia are common presenting features of diabetes mellitus. Malignancy and hyperparathyroidism are common causes of chronic hypercalcaemia, which can cause polyuria by an intrinsic osmotic effect or by precipitation of nephrogenic diabetes insipidus. Cranial diabetes insipidus can result from severe, blunt head injuries, craniopharyngiomas, pineal gland tumours or as a transient postoperative complication following neurosurgery. Renal ischaemia from conditions such as sepsis and haemorrhage predisposes to acute tubular necrosis. Chronic tubulointerstitial nephritis can result from reflux nephropathy, polycystic kidney disease, gout and multiple myeloma.
General Investigations
■ Urine dipstick
+++glucose with diabetes mellitus.
■ 24-hour urine collection
>3 litres confirms polyuria and helps differentiate from urinary frequency.
■ U&Es
Plasma urea and creatinine levels ↑ renal failure. Sodium ↑ with uncompensated polyuria (inadequate water intake). Sodium ↓ with urea/creatinine ↓ indicates polydipsia as the primary cause. Potassium ↓ may cause nephrogenic diabetes insipidus.
■ Urine and plasma osmolality
Urine osmolality low and plasma osmolality normal in pituitary and nephrogenic diabetes insipidus. Urine osmolality low and plasma osmolality normal to low in compulsive water drinking.
■ Serum calcium
↑ calcium causes osmotic diuresis and chronic tubulointerstitial nephritis.
The above tests may be all that is required to differentiate between osmotic diuresis, excess fluid intake and diabetes insipidus. If the differentiation between primary polydipsia and diabetes insipidus cannot be made confidently, then proceed with the following two tests. The reader is advised to consult a reference source regarding the precautions and safety measures to be observed in the water deprivation and DDAVP tests.
Do not perform this test in volume-depleted patients or in the presence of hypernatraemia.
After overnight water restriction, the plasma osmolality is measured:
Plasma osmolality ↓: primary polydipsia
Plasma osmolality ↑: stop test and measure urine osmolality
Urine osmolality ↑: no diabetes insipidus
Urine osmolality ↓ in three consecutive samples: diabetes insipidus.
Arginine vasopressin is administered:
