I. Polyuria = >3l/d

  1. Difficult to distinguish from urinary frequency (check 24h output to be sure)
  2. Caused by DI, solute diuresis, natriuresis, and primary
  3. Approach to nocturia is the same but can also be caused by
  1. Edema from any cause
  2. Decreased bladder capacity from infection, tumor, stone
  3. Chronic partial bladder outflow obstruction

II. Diabetes insipidus

  1. Definition: inadequate renal H2O conservation causing polyuria and thirst
  2. Decreased H2O reabsorption all along distal nephron
  3. Get "washout" of medullary interstitium (solutes washed into vasa recta), llowering the ability to concentrate urine even in the presence of ADH
  4. Central: due to hypophysectomy, trauma, tumor, inflammation, infection, vasculopathy; also exist inherited form (autosomal dominant)
  5. Nephrogenic: due to nephropathies, e.g.
  1. Hypercalcemia
  2. Hypokalemia
  3. Lithium, phenytoin, methoxyflurane, demeclocycline, propoxyphene, amphotericin
  4. EtOH

III. Solute diuresis

  1. Glucose, mannitol, urea (often occurs from high-protein enteral feeding), IV contrast

IV. Natriuresis: chronic Na loss from tubulointerstitial or cystic disease, e.g.

  1. Medullary cystic disease
  2. Bartter's sd.
  3. ATN (diuretic phase)
  4. Some diuretics
  5. Most primary renal diseases

V. Primary polyuria-secondary to high H2O intake.

  1. Different from DI in that extracellular volume is high or normal; basal but measurable ADH level.
  2. Caused by habit, hypothalamic lesions, and some drugs (anticholinergics, antipsychotics)

VI. Approach to pt with polyuria

  1. Distinguish between central DI, nephrogenic DI, and primary polydipsia with
  2. Urine osmolarity studies with H2O deprivation and ADH administration
  3. H2O deprivation will fail to produce concentrated urine in DI; ADH administration will distinguish between central and nephrogenic
  4. However, may get same results with primary polydipsia! (Because of medullary washout)