Figure 841

Clinical correlates of abnormalities of tubular function in obstructive nephropathy. Acute ureteral obstruction stimulates tubular reabsorption, resulting in increased urine osmolality and reduced urine sodium concentration [60]. In contrast, obstructive nephropathy is characterized by a reduced ability to concentrate the urine, reabsorb sodium, and secrete hydrogen ions (H+) and potassium. In unilateral obstructive nephropathy, these functional abnormalities do not have a clinical correlate because of the reduced glomerular filtration rate and immaterial contribution of the obstructed kidney to total renal function. Hyperkalemic metabolic acidosis and, when the intake of free water is not adequate, hypernatremia can occur in patients with partial bilateral ureteral obstruction or partial ureteral obstruction in a solitary kidney. Similarly, postobstructive diuresis can occur only after relief of bilateral ureteral obstruction or ureteral obstruction in a solitary kidney but not after relief of unilateral obstruction [61-67]. ADH>\#209>antidiuretic hormone; ANP—atrial natriuretic peptide; ECFV— extracellular fluid volume; Na-K ATPase— sodium-potassium adenosine triphosphatase.

Urinary tract obstruction

Unilateral

Bilateral or solitary kidney

Unilateral

Bilateral or solitary kidney

Partial or complete

• Pain (dull aching

• Renin-dependent

• Polyuria, polydipsia

• Anuria • Bladder

—i renal colic)

hypertension

• Hypernatremia

• Uremia symptoms

• Susceptibility to

• Erythrocytosis

• Volume contraction

• Fluctuating

urinary tract

(rare)

• Hyperkalemic

urine

infection and

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