POLYURIA

Polyuria is an absolute increase in the urine output in a 24-hour period. The average individual excretes 1,500 mL of urine a day. Many physiologic conditions increase the output of urine (stress, exercise, and warm weather associated with copious drinking). From a pathophysiologic standpoint, polyuria results from one of four mechanisms: (a) increased intake of fluids, (b) increased glomerular filtration rate, (c) increased output of solutes such as sodium chloride and glucose, and (d) inability of the kidney to reabsorb water in the distal tubule.

POLYURIA

1. Increased intake of fluid. As already mentioned, increased intake can occur under stress and nervous tension. It becomes pathologic in psychogenic diabetes insipidus when 6 to 10 L of fluid may be ingested each day.
2. Increased glomerular filtration rate. This is a factor in the polyuria of hyperthyroidism and fever of any cause.
3. Increased output of solutes. Uncontrolled diabetes mellitus (where the solute is glucose) and hyperthyroidism (where the solute may be glucose or urea) are examples of this type of polyuria. Hyperparathyroidism is another important cause (increased calcium output). Diuretics are a significant cause of this type of polyuria because they increase the amount of solute arriving at the distal tubule and hold onto the water that would otherwise be absorbed.
4. Decreased reabsorption of water in the distal tubule. This, the most common cause of polyuria, is divided into two groups: Conditions in which there is inadequate or blocked output of ADH and those in which the distal tubule and collecting ducts are unable to respond to the ADH. Decreased output of ADH occurs in diabetes insipidus from pituitary tumors, infarcts, Hand–Schüller–Christian disease, and sarcoidosis among other causes. It also results from alcohol intoxication and hypothalamus lesions. The inability of the distal tubule to respond to ADH occurs in aldosteronism, chronic glomerulonephritis, polycystic kidneys, pyelonephritis, lithium and demeclocycline (Declomycin) therapy, and idiopathic nephrogenic diabetes insipidus. Diuretics operate somewhat in this manner.

Cases of myxedema with polyuria have been reported, but the mechanism is unclear.

Approach to the Diagnosis

The diagnosis of polyuria depends largely on the association of other symptoms. Polyuria, polyphagia, and polydipsia suggest diabetes mellitus and hyperthyroidism. Polyuria with only polydipsia suggests psychogenic or idiopathic diabetes insipidus; the Hickey–Hare test will differentiate the two. Polyuria with polydipsia and weakness but with no significant weight loss suggests hypercalcemia and possible hyperparathyroidism. Chronic nephritis will be diagnosed by examination of the urine sediment and a specific gravity that remains at 1.010. Nephrogenic diabetes insipidus can be differentiated from neurogenic diabetes insipidus by the inability of the kidney to respond to a pitressin injection.

Other Useful Tests

1. Thyroid profile (hyperthyroidism)
2. Glucose tolerance test (diabetes mellitus)
3. 24-hour intake and output (diabetes insipidus)
4. Addis count (chronic nephritis)
5. Serum ADH assay (diabetes insipidus)
6. Serum and urine osmolality (pituitary diabetes insipidus, nephrogenic diabetes insipidus)
7. Spot urine sodium (diabetes insipidus)
8. CT scan of the brain (diabetes insipidus)
9. PTH assay (hyperparathyroidism)
10. Endocrine consult

Book Source Details

• Book Title: Differential Diagnosis in Primary Care
• Author(s): R. Douglas Collins
• Year of Publication: 2007
• Copyright Details: Differential Diagnosis in Primary Care, Copyright © 2007 Lippincott Williams & Wilkins.

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More About This Book: Title: Differential Diagnosis in Primary Care Authors: R. Douglas Collins Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-7817-6812-8

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