Unit VI Study Questions

Study Questions

Choose the ONE best answer.

VI.1. A patient taking penicillin for a bacterial infection presents with nausea and vomiting. Urinalysis reveals mild proteinuria and cell casts, suggestive of acute interstitial nephritis. Which of the following glomerular structures normally prevents cells from entering the tubule?

A. Smooth muscle cells
B. Mesangial cells
C. Capillary endothelial cells
D. Glomerular basement membrane
E. Podocytes

Best answer = C. The glomerular filtration barrier comprises capillary endothelial cells, a basement membrane, and a filtration slit diaphragm located between podocyte foot processes (25∙III∙A). Capillary walls are fenestrated to enhance plasma filtration, but the pores are small (~70 nm), effectively trapping the cells in the vasculature. Smooth muscle cells are located in glomerular arterioles, whereas mesangial cells are located between the glomerular capillaries. Although the latter regulate barrier surface area, they are not directly involved in fluid filtration.

VI.2. A 65-year-old man with a family history of nephrolithiasis presents with flank pain. A creatinine clearance assessment is performed. “Creatinine clearance” best equates with which of the following?

A. Renal blood flow
B. Renal plasma flow
C. Amount of creatinine traversing the glomerulus per minute
D. Amount of creatinine entering the urinary bladder per minute
E. Plasma volume completely cleared of creatinine per minute

Best answer = E. “Clearance” defines the kidneys’ ability to completely clear a known volume of plasma of a given substance during passage through the renal vasculature (25∙V∙A). Creatine clearance is used clinically to estimate glomerular filtration rate (25∙V∙C). Clearance of other substances (e.g., para-aminohippuric acid) can be used to estimate renal plasma flow and, if hematocrit is known, renal blood flow (25∙V∙D). A change in clearance might affect how much creatinine enters the bladder, but excretion rate does not equate with clearance. Clearance is unrelated to the amount of a substance traversing the glomerular network per unit time.

VI.3. A 17-year-old male presents with urethral burning following urination. He is asked to provide a urine sample and swabbed to test for a possible bacterial infection. Which of the following is responsible for initiating micturition when providing a urine sample?

A. Pontine micturition center
B. Uroepithelial mechanoreceptors
C. Spontaneous detrusor contractions
D. Rising intravesical pressure
E. Internal urethral sphincter relaxation

Best answer = A. Voiding is initiated and coordinated by the pontine micturition center, which relaxes the internal (involuntary) urethral sphincter and facilitates detrusor muscle contraction once voluntary relaxation of the external urethral sphincter has occurred (25∙VI∙D). Although internal sphincter relaxation is required for urine flow, it does not initiate voiding. Uroepithelial mechanoreceptors trigger spontaneous detrusor contractions when intravesical pressure rises during bladder filling, but bladder emptying is suppressed by the pontine micturition center until voiding is convenient.

VI.4. A 31-year-old male with a body mass index of 35 is found to have glycosuria during a routine physical. Elevated urinary glucose levels correlate with unmanaged type 2 diabetes mellitus. Why does glucose appear in the urine of patients with untreated diabetes?

A. Tubule glucose levels exceed transport capacity.
B. Glucose causes an osmotic diuresis that increases glucose excretion.
C. Hyperglycemia downregulates glucose transporters.
D. High plasma insulin levels are nephrotoxic.
E. High plasma insulin inhibits Na+-K+ ATPases.

Best answer = A. Transporters exhibit saturation kinetics, which limits the tubule’s ability to reabsorb solutes (26∙III∙A). Although glucose transport maximum is seldom reached in a healthy individual, the plasma ultrafiltrate of patients with untreated diabetes may contain glucose levels that exceed the tubule’s reabsorptive capability, causing it to appear in urine. Glucose can cause an osmotic diuresis, but such an event would be a consequence of exceeding transporter maximum, not the cause. Possible effects of hyperglycemia on transporter numbers and insulin-induced nephrotoxicity is not a significant physiologic concern. Insulin does modulate the Na+-K+ ATPase, but it increases pump activity rather than inhibiting it.

VI.5. Fanconi syndrome is associated with proximal tubule (PT) dysfunction, the symptoms including polyuria, glycosuria, hypocalcemia, hypomagnesemia, and hypophosphatemia. A healthy PT normally recovers ~100% of which of the following filtered solutes

A. Peptides
B. Uric acid
C. Ca2+
D. PO4 3−
E. Na+

Best answer = A. The proximal tubule (PT) reabsorbs a high percentage of most materials filtering from blood, including Ca2+, PO4 3−, and Na+, but it is the principal site for reabsorption of 100% of proteins, peptides, amino acids, and glucose (26∙III). The PT recovers 65% of Ca2+, the remainder being recovered in the thick ascending limb and distal segments. The PT recovers 80% of the PO4 3− filtered load, with the remainder being recovered distally. The PT recovers 67% of Na+, although this amount can increase in the presence of angiotensin II. The PT secretes uric acid, oxalate, and other wastes (26∙IV).

VI.6. A 66-year-old woman receiving cisplatin therapy for metastatic ovarian cancer develops proximal tubule (PT) nephrotoxicity and symptoms associated with renal impairment. Which of the following best describes PT function in a healthy person?

A. Antidiuretic hormone is a primary regulator.
B. Aldosterone is a primary regulator.
C. It accomplishes isosmotic fluid reabsorption.
D. It creates the corticopapillary gradient.
E. The tubule has a high electrical resistance.

Best answer = C. The proximal tubule (PT) epithelium actively takes up many organic solutes (including drugs such as cisplatin) from blood and excretes them into the tubule (26∙IV). Concentrating such materials through uptake can cause them to rise to toxic levels. The PT is also specialized for isosmotic fluid reabsorption, which gives the epithelium a low electrical resistance (26∙II∙A). Antidiuretic hormone acts principally on the collecting ducts (27∙V∙C), whereas aldosterone targets the distal tubule segments (27∙IV). The corticopapillary osmotic gradient is established by the loop of Henle (27∙II∙C).

VI.7. Increasing which of the following variables would decrease the magnitude of the renal corticopapillary osmotic gradient that allows for urine concentration?

A. Renin release from the afferent arteriole
B. Thick ascending limb Na+-K+-2Cl− cotransport
C. Urea reabsorption by the collecting ducts
D. Blood flow through the vasa recta
E. Sympathetic nervous system activation

Best answer = D. The corticopapillary osmotic gradient is established by countercurrent multiplication in the loop of Henle (27∙II∙C). The countercurrent multiplier relies on Na+-K+-2Cl− cotransport by the thick ascending limb, so the gradient collapses when the cotransporter is inhibited by loop diuretics. Increasing flow through the vasa recta washes ions out of the medulla, thereby diminishing the osmotic gradient. Renin is released when arterial pressure falls or when the sympathetic nervous system activates, conditions that signal a likely need to conserve water. Gradient magnitude increases as a result, in part through increased urea reabsorption from the collecting ducts.\

VI.8. Genetic evaluation of a 6-year-old boy with growth and mental retardation identified alleles associated with Bartter syndrome. Bartter syndrome mimics loop diuretics by causing thick ascending limb (TAL) dysfunction. Which of the following best describes the TAL in healthy individuals?

A. Fluid leaves the thick ascending limb at ~600 mOsm/kg.
B. It is known as the “concentrating segment.”
C. It has a high water permeability.
D. It is the primary site of Ca2+ reabsorption.
E. It extracts Na+, K+, and Cl− from the lumen.

Best answer = E. The thick ascending limb (TAL) reabsorbs Na+, K+, and Cl− from the tubule lumen via Na+-K+-2Cl− cotransport and transfers these ions to the interstitium, where they help form the corticopapillary osmotic gradient (27∙II∙B). The TAL has a low water permeability that prevents H2O from following ions into the interstitium, so the tubule fluid becomes relatively dilute (<300 mOsm/kg). The TAL may be referred to as the “diluting (not “concentrating”) segment” for this reason. Ca2+ is reabsorbed primarily in the proximal tubule, with regulated reabsorption occurring in the distal tubule (27∙III∙C).

VI.9. A 77-year-old woman is taking a thiazide diuretic to treat hypertension but has become hypercalcemic. Thiazides inhibit Na+-Cl− reabsorption by the distal convoluted tubule. Why do thiazide diuretics also cause hypercalcemia?

A. Thiazide diuretics also inhibit Ca2+ ATPases.
B. The Na+-Cl− cotransporter also carries Ca2+.
C. Apical Na+-Ca2+ exchange increases.
D. The gradient driving Ca2+ uptake steepens.
E. Paracellular Ca2+ uptake increases.

Best answer = D. Ca2+ reabsorption by the distal convoluted tubule (DCT) is mediated by a Ca2+ channel (a transient receptor-potential channel, TRPV5) and driven by the electrochemical gradient across the tubule epithelium’s apical membrane (27∙III∙C). Inhibiting the Na+-Cl−cotransporter reduces Na+ influx into the epithelial cell, so the interior becomes more negative. This negativity increases the driving force for Ca2+ reabsorption and causes hypercalcemia. Thiazides have no significant effect on Ca2+ ATPases. The DCT does not reabsorb significant amounts of Ca2+ via the Na+-Cl− cotransporter, an apical Na+-Ca2+ exchanger, or paracellularly.

VI.10. A researcher observes a consistent 75% decrease in renal blood flow in subjects performing maximal exercise. Which of the following best accounts for the decreased flow?

A. Decrease in mean arterial pressure
B. Decrease in renal arterial pressure
C. Sweat-induced hypovolemia
D. Increased renal sympathetic nerve activity
E. Antidiuretic hormone release

Best answer = D. The sympathetic nervous system (SNS) increases cardiac output and decreases flow to nonessential organs (such as the kidney) to sustain mean arterial pressure (MAP) during skeletal muscle vasodilation (28∙III∙C; 39∙V). The SNS reduces renal blood flow by constricting resistance vessels (arterioles, including glomerular arterioles, and small arteries). Renal arterial pressure, which is closely tied to MAP, should not be affected to a significant degree. Although antidiuretic hormone can vasoconstrict under some circumstances, these effects are secondary to SNS activation. Hypovolemia may potentiate SNS effects on renal flow during exercise, but, again, this is secondary to SNS effects.

VI.11. A physician notes that an underweight teenage girl’s tooth enamel is eroded. A basic metabolic panel reveals hypokalemia and metabolic alkalosis, suggestive of an eating disorder and repeated purging. Which of the following would also be consistent with such a diagnosis?

A. Renal tubular acidosis
B. Decreased β-intercalated cell activity
C. Hypoventilation
D. Increased NH4 + excretion
E. High plasma aldosterone levels

Best answer = C. Loss of stomach acid during repeated vomiting leaves an HCO3 − excess that manifests as metabolic alkalosis (28∙VI∙F). The respiratory centers help compensate by decreasing volatile acid (H2CO3) transfer to the environment by decreasing ventilation (hypoventilation). Renal tubular acidosis is a metabolic acidosis that may have a number of underlying causes. NH4 + excretion helps dispose of nonvolatile acid, so excretion rates would fall during alkalosis. β-Intercalated cells secrete HCO3 − into the tubule lumen, and, thus, their activity would be increased during alkalosis. Aldosterone is involved in Na+ balance, not pH balance.

VI.12. A 25-year-old patient with recurrent flash (rapid onset) pulmonary edema is evaluated for renal hypertension using Doppler ultrasonography. Tests confirm renal artery stenosis. An angiotensin-converting enzyme inhibitor might have which of the following effects in this patient?

A. Unchanged hypertension
B. Increased plasma creatinine
C. Decreased plasma renin
D. Increased glomerular filtration rate
E. Increased systemic vascular resistance

Best answer = B. Renal artery stenosis impairs glomerular perfusion and decreases ultrafiltration pressure (PUF). The afferent arteriole responds by releasing renin (28∙IV∙C). Plasma angiotensin II (Ang-II) levels rise as a result, causing systemic vasoconstriction and a rise in mean arterial pressure (MAP). The MAP increase helps restore glomerular flow and PUF rises. Ang-II also constricts the efferent arteriole to potentiate a rise in PUF (25∙IV∙C). Angiotensin-converting enzyme (ACE) inhibition would, thus, decrease PUF and glomerular filtration rate, which would allow plasma creatinine levels to rise. The afferent arteriole would respond with increased renin release. An ACE inhibitor would also attenuate Ang-II effects on systemic vessels, decreasing systemic vascular resistance, thereby reducing MAP.


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