Figure 130

Syndromes of diminished sodium reabsorption and hypotension. Recently, a variety of syndromes associated with salt wasting, and usually hypotension, have been attributed to specific molecular defects in the distal nephron. Bartter's syndrome, which usually is accompanied by metabolic alkalosis and hypokalemia, has been found to be associated with at least three separate defects (the three transporters shown) in the thick ascending limb. These defects are at the level of the sodium-potassium-2chloride (Na+-K+-2Cl-) cotransporter, apical potassium channel, and basolateral chloride channel (see Fig. 1-17). Malfunction in any of these three proteins results in diminished sodium chloride reabsorption similar to that occurring with administration of loop diuretics. Gitelman's syndrome, which was originally described as a variant of Bartter's syndrome, represents a defect in the sodium chloride cotransport mechanism in the distal tubule. Pseudohypoaldosteronism results from a defect in the apical sodium channels in the collecting ducts. In contrast to Bartter's and Gitelman's syndromes, hyperkalemia may be present. These rare disorders illustrate that defects in sodium chloride reab-sorptive mechanisms can result in abnormally low blood pressure as a consequence of excessive sodium excretion in the urine. Although these conditions are rare, similar but more subtle defects of the heterozygous state may contribute to protection from hypertension in some persons [31]. B—basolateral side; L—lumen of tubule.

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