An edematous patient is taking therapeutic doses of a loop diuretic. Which of the following would you expect to occur along with the increased urine volume?
|C||Reduced net excretion of Cl-|
a. Recall one of the main mechanisms by which a concentrated urine is formed: a hypertonic milieu in the renal medulla—and a medullary-to-cortical osmotic gradient—osmotically withdraws water (but not solute) from the tubular fluid as it passes through the collecting ducts.
b. What creates that hypertonic medullary-to-cortical gradient? Reabsorption of Na and Cl- as tubular fluid ascends the loop of Henle, which ultimately increases interstitial osmolality However, that process of ion resorption is impaired by loop diuretics.
c. That reduces osmolality in the medullary interstitium, thereby dramatically reducing the osmotic gradient that enables the tubular fluid to become hypertonic as water is lost in the distal nephron. Thus, in the presence of a loop diuretic the urine remains dilute and hypotonic.
d. Metabolic acidosis from increased bicarbonate excretion doesn’t occur. Recall that the main anion excreted (along with Na K etc.) is chloride. Bicarbonate tends to be reabsorbed. So, if there is any change of blood pH, it’s one that can be characterized as alkalosis. Indeed, hypochloremic alkalosis is one potential adverse response of loop diuretics.
e. Loop diuretics do not lower serum urate concentrations. Rather, urate levels tend to rise, in part, because of reduced urate excretion combined with a “concentration” of urate in the blood owing to increased free water loss via the urine.
f. Hypercalcemia is not an expected accompaniment. Loop diuretics (in contrast with thiazides) increase renal Calcium elimination.
g. Serum uric acid concentration tends to rise. The loop diuretics reduce urate excretion. In addition, the proportionally large extra free water loss shrinks blood volume and tends to increase solute concentration, independent of any renal tubular effects on urate elimination.