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Ch. 24 The Urinary System
Amerman - Human Anatomy & Physiology 2nd Edition
Amerman2nd EditionHuman Anatomy & PhysiologyISBN: 9780136873822Not the one you use?Change textbook
All textbooksAmerman 2nd EditionCh. 24 The Urinary SystemProblem L3.A3
Chapter 24, Problem L3.A3

Deana is a 4-year-old girl with a rare genetic defect that causes the Na+/glucose symporters in the proximal tubule to reabsorb fewer glucose and sodium ions than normal. Predict the effects this defect will have on the composition and volume of Deana's urine. Explain why you would expect to see increased activity of the tubuloglomerular feedback and the renin-angiotensin-aldosterone system in Deana's kidneys.

Verified step by step guidance
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Understand the role of Na+/glucose symporters in the proximal tubule: These transporters are responsible for reabsorbing sodium (Na+) and glucose from the filtrate back into the bloodstream. A defect in these symporters means less glucose and sodium will be reabsorbed, leading to higher concentrations of these substances in the filtrate and, consequently, in the urine.
Predict the effects on urine composition: With less glucose and sodium being reabsorbed, more glucose will remain in the filtrate, leading to glucosuria (glucose in the urine). Sodium retention in the filtrate will also increase, which can lead to osmotic diuresis (increased urine volume) as water follows the solutes into the urine due to osmotic gradients.
Explain the increased activity of tubuloglomerular feedback: The macula densa cells in the distal tubule detect increased sodium levels in the filtrate. This triggers tubuloglomerular feedback, which reduces the glomerular filtration rate (GFR) to prevent excessive loss of sodium and water. However, in Deana's case, the defect in the symporters may cause persistent sodium loss, leading to sustained activation of this feedback mechanism.
Discuss the activation of the renin-angiotensin-aldosterone system (RAAS): The loss of sodium and water can lead to decreased blood volume and blood pressure. This stimulates the juxtaglomerular cells in the kidney to release renin, which activates the RAAS. The system works to increase sodium reabsorption (via aldosterone) and water retention (via antidiuretic hormone, ADH) to restore blood volume and pressure.
Summarize the overall effects: Deana's urine will likely have increased glucose and sodium concentrations, as well as a higher volume due to osmotic diuresis. The persistent sodium and water loss will lead to compensatory mechanisms, including increased tubuloglomerular feedback and activation of the RAAS, in an attempt to maintain homeostasis.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Na+/Glucose Symporters

Na+/glucose symporters are transport proteins located in the proximal tubule of the nephron that facilitate the reabsorption of glucose and sodium ions from the filtrate back into the bloodstream. In Deana's case, a defect in these symporters leads to decreased reabsorption, resulting in higher levels of glucose and sodium remaining in the urine, which can affect urine composition and volume.
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Primary Active Transport: Na+/K+ Pump

Tubuloglomerular Feedback

Tubuloglomerular feedback is a mechanism by which the kidneys regulate glomerular filtration rate (GFR) based on the composition of the fluid in the distal tubule. When sodium and chloride concentrations are low due to decreased reabsorption, the macula densa cells signal the afferent arterioles to dilate, increasing GFR to enhance sodium and fluid reabsorption, which would be heightened in Deana's condition.
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Feedback Loops: Positive Feedback Example 1

Renin-Angiotensin-Aldosterone System (RAAS)

The renin-angiotensin-aldosterone system is a hormone system that regulates blood pressure and fluid balance. In response to low sodium levels and decreased blood volume from the defect in glucose and sodium reabsorption, the kidneys release renin, leading to the production of angiotensin II and aldosterone, which promote sodium reabsorption and increase blood pressure, thus compensating for the loss of sodium in Deana's urine.
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Renin-Angiotensin-Aldosterone-System
Related Practice
Textbook Question

Mr. Gupta has been diagnosed with nephrotic syndrome, which is characterized by the loss of plasma proteins such as albumin into the urine. What impact will this have on his colloid osmotic pressure? How will this affect the net filtration pressure in his capillary beds? What effect will this likely cause?

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Textbook Question

Drugs that treat hypertension, or high blood pressure, have the following actions. Discuss the specific effect that each drug will have on the kidneys.

b. Blocking the receptor for angiotensin-II on blood vessels and in the renal tubule cells

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Textbook Question

Explain how each of the drugs in question 1 from this section would lower blood pressure.

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Textbook Question

Mark the following statements as true or false. If a statement is false, correct it to make a true statement.

b. Internally, the kidneys consist of an outer renal medulla, a middle renal pelvis, and an inner renal cortex.

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Textbook Question

Mark the following statements as true or false. If a statement is false, correct it to make a true statement.

a. The kidneys are retroperitoneal and covered by three layers of connective tissue.

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Textbook Question

Drugs that treat hypertension, or high blood pressure, have the following actions. Discuss the specific effect that each drug will have on the kidneys.

a. Blocking the action of aldosterone on the kidneys

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