I. Polyuria = >3l/d
- Difficult to distinguish from urinary frequency (check 24h output to be sure)
- Caused by DI, solute diuresis, natriuresis, and primary
- Approach to nocturia is the same but can also be caused by
- Edema from any cause
- Decreased bladder capacity from infection, tumor, stone
- Chronic partial bladder outflow obstruction
II. Diabetes insipidus
- Definition: inadequate renal H2O conservation causing polyuria and thirst
- Decreased H2O reabsorption all along distal nephron
- Get "washout" of medullary interstitium (solutes washed into vasa recta), llowering the ability to concentrate urine even in the presence of ADH
- Central: due to hypophysectomy, trauma, tumor, inflammation, infection, vasculopathy; also exist inherited form (autosomal dominant)
- Nephrogenic: due to nephropathies, e.g.
- Lithium, phenytoin, methoxyflurane, demeclocycline, propoxyphene, amphotericin
III. Solute diuresis
- Glucose, mannitol, urea (often occurs from high-protein enteral feeding), IV contrast
IV. Natriuresis: chronic Na loss from tubulointerstitial or cystic disease, e.g.
- Medullary cystic disease
- Bartter's sd.
- ATN (diuretic phase)
- Some diuretics
- Most primary renal diseases
V. Primary polyuria-secondary to high H2O intake.
- Different from DI in that extracellular volume is high or normal; basal but measurable ADH level.
- Caused by habit, hypothalamic lesions, and some drugs (anticholinergics, antipsychotics)
VI. Approach to pt with polyuria
- Distinguish between central DI, nephrogenic DI, and primary polydipsia with
- Urine osmolarity studies with H2O deprivation and ADH administration
- H2O deprivation will fail to produce concentrated urine in DI; ADH administration will distinguish between central and nephrogenic
- However, may get same results with primary polydipsia! (Because of medullary washout)