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QUESTIONS

DIRECTIONS: Choose the one best response to each question.

Which segment of the kidney reabsorbs the highest percentage of filtered sodium chloride?

A. Collecting duct

B. Distal convoluted tubule

C. Loop of Henle

D. Proximal convoluted tubule

The answer is D. (Chap. 303) The proximal tubule is responsible for reabsorbing ~60% of filtered sodium chloride (NaCl) and water, as well as ~90% of filtered bicarbonate and most critical nutrients such as glucose and amino acids. The proximal tubule uses both cellular and paracellular transport mechanisms. The apical membrane of proximal tubular cells has an expanded surface area available for reabsorptive work created by a dense array of microvilli called the brush border, and leaky tight junctions enable high-capacity fluid reabsorption. Approximately 15–25% of filtered NaCl is reabsorbed in the loop of Henle, mainly by the thick ascending limb. The distal convoluted tubule reabsorbs ~5% of the filtered NaCl. This segment is composed of a tight epithelium with little water permeability. The collecting duct modulates the final composition of urine. The two major divisions, the cortical collecting duct and inner medullary collecting duct, contribute to reabsorbing ~4–5% of filtered Na+ and are important for hormonal regulation of salt and water balance.

A 33-year-old woman with recently treated acute myelogenous leukemia now in remission is admitted to the hospital with lethargy, fever, and tachycardia. Blood cultures grow Pseudomonas that is resistant to cefepime. She is started on IV gentamicin. Five days after starting gentamicin, her serum creatinine rises from her baseline of 1.0 mg/dL to 2.4 mg/dL. No red or white cell casts are seen on her urinalysis. Her magnesium level is decreased at 1.5 mg/dL. Renal ultrasound is unremarkable with no hydronephrosis. Which of the following is the most likely mechanism of her acute kidney injury?

A. Acute interstitial nephritis

B. Acute tubular necrosis

C. Glomerulonephritis

D. Ischemic injury

E. Obstruction

The answer is B. (Chap. 304) Several antimicrobial agents are commonly associated with acute kidney injury (AKI). Aminoglycosides (e.g., gentamicin) and amphotericin B both cause tubular necrosis. Nonoliguric AKI (i.e., with a urine volume >400 mL/day) accompanies 10–30% of courses of aminoglycoside antibiotics, even when plasma levels are in the therapeutic range. Aminoglycosides are freely filtered across the glomerulus and then accumulate within the renal cortex, where concentrations can greatly exceed those of the plasma. AKI typically manifests after 5–7 days of therapy and can present even after ...

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