Renal Physiology — MCQs

Renal Physiology Indian Medical PG Practice Questions and MCQs

Question 441: All of the following substances have decreased concentration on the luminal side of the proximal convoluted tubule except:

A. Glucose
B. Amino acids
C. Bicarbonate
D. Chloride (Correct Answer)

Explanation: ***Chloride*** - As **water and other solutes** are reabsorbed from the proximal tubule, the concentration of **chloride** actually increases in the remaining luminal fluid due to continued water reabsorption. - This increased luminal **chloride concentration** then drives passive reabsorption of chloride later in the tubule. *Glucose* - **Glucose** is almost completely reabsorbed from the tubular lumen by **secondary active transport** in the early part of the proximal tubule. - Therefore, its concentration in the remaining luminal fluid rapidly decreases. *Amino acids* - Similar to glucose, **amino acids** are extensively reabsorbed by **secondary active transport** mechanisms in the proximal tubule. - Consequently, their luminal concentration significantly decreases. *Bicarbonate* - Most **bicarbonate** is reabsorbed in the proximal tubule through a process involving **carbonic anhydrase**, converting it to CO2 and water, which then diffuse into the cell. - This efficient reabsorption results in a substantial decrease in luminal bicarbonate concentration.

Question 442: Which region of the nephron reabsorbs the highest percentage of filtered bicarbonate?

A. Collecting duct
B. Thick ascending limb
C. Distal tubule
D. Proximal tubule (Correct Answer)

Explanation: ***Proximal tubule*** - The **proximal convoluted tubule (PCT)** reabsorbs approximately 80-90% of the **filtered bicarbonate** through a process involving **carbonic anhydrase** and the **Na+/H+ exchanger**. - This vital function ensures that the majority of bicarbonate, a key buffer, is returned to the blood to maintain **acid-base balance**. *Collecting duct* - While the collecting duct does have the ability to reabsorb and secrete bicarbonate, its contribution is minor compared to the PCT, primarily for fine-tuning acid-base balance. - Cells in the collecting duct, particularly **Type A intercalated cells**, are important for secreting acid (H+) in acidosis and therefore reabsorbing bicarbonate, but not the bulk of it. *Thick ascending limb* - The primary role of the **thick ascending limb** is the reabsorption of **sodium**, **potassium**, and **chloride** to create a concentrated interstitium, not significant bicarbonate reabsorption. - It is largely impermeable to water and is relatively impermeable to bicarbonate. *Distal tubule* - The **distal convoluted tubule (DCT)** reabsorbs a small percentage of filtered bicarbonate, but its main role is regulated reabsorption of **sodium** and **calcium**, and secretion of **potassium** and **hydrogen ions**. - Its contribution to bicarbonate reabsorption is much less significant than that of the proximal tubule.

Question 443: Which mechanism primarily regulates sodium reabsorption in the collecting duct?

A. Glomerulotubular balance
B. Atrial natriuretic peptide
C. Antidiuretic hormone
D. Aldosterone (Correct Answer)

Explanation: ***Aldosterone*** - **Aldosterone** is the primary hormone that stimulates **sodium reabsorption** and **potassium secretion** in the principal cells of the collecting duct. - It acts by increasing the synthesis and activity of **ENaC channels** on the apical membrane and **Na+/K+-ATPase pumps** on the basolateral membrane. *Glomerulotubular balance* - **Glomerulotubular balance** refers to the mechanism by which the **proximal tubule** reabsorbs a constant fraction of the filtered load, regardless of changes in glomerular filtration rate (GFR). - This mechanism maintains a relatively constant delivery of fluid and solutes to downstream segments but does not primarily regulate sodium in the collecting duct. *Atrial natriuretic peptide* - **Atrial natriuretic peptide (ANP)** primarily **inhibits sodium reabsorption** in the collecting duct, leading to **natriuresis** and **diuresis**, which is the opposite of sodium reabsorption. - ANP is released in response to atrial stretch, indicating increased blood volume. *Antidiuretic hormone* - **Antidiuretic hormone (ADH)** primarily regulates **water reabsorption** in the collecting duct by increasing the insertion of **aquaporin-2 channels** into the apical membrane, making the collecting duct permeable to water. - While ADH can indirectly affect sodium concentration by influencing water movement, it does not directly regulate sodium transport to the same extent as aldosterone.

Question 444: Which transport mechanism is primarily responsible for calcium reabsorption in the proximal tubule?

A. Paracellular transport (Correct Answer)
B. Facilitated diffusion
C. Active transport
D. Antiport with sodium

Explanation: ***Paracellular transport*** - In the **proximal tubule**, approximately 60-70% of filtered calcium is reabsorbed primarily through the **paracellular pathway**, driven by the electrochemical gradient and solvent drag. - This transport occurs between cells, moving through the **tight junctions**, and is passive, following the reabsorption of water. *Facilitated diffusion* - While a type of passive transport, **facilitated diffusion** typically involves membrane proteins and occurs across the cell membrane, not primarily between cells in the proximal tubule for calcium. - This mechanism is prominent for calcium reabsorption in other nephron segments like the **distal convoluted tubule** via **TRPV5/6 channels**, but not the main route in the proximal tubule. *Active transport* - **Active transport** of calcium, mainly via **calcium ATPase** and the **Na+/Ca2+ exchanger**, occurs across the luminal and basolateral membranes, respectively, in specific nephron segments. - However, in the **proximal tubule**, the bulk of calcium reabsorption is passive and paracellular, not ATP-dependent active transport across cell membranes. *Antiport with sodium* - The **Na+/Ca2+ exchanger (NCX)** is an antiport mechanism that plays a crucial role in extruding calcium from the cell into the interstitium, particularly in the basolateral membrane of the distal tubule. - However, it is not the primary mechanism for overall tubular reabsorption of calcium in the **proximal tubule**, where paracellular movement dominates.

Question 445: Which factor most strongly influences protein filtration at the glomerulus?

A. Electrical charge
B. Molecular size (Correct Answer)
C. Shape
D. Temperature

Explanation: ***Molecular size*** - The glomerular filtration barrier, particularly the **slit diaphragms** between podocytes, acts as a size-selective filter, restricting the passage of larger molecules. - Proteins like **albumin** (molecular radius ~36 Å, molecular weight ~69 kDa) are significantly large, making them difficult to pass through the filtration barrier. - Size selectivity is the **primary and most important** factor in protein filtration. *Electrical charge* - The glomerular basement membrane contains **negatively charged proteoglycans** (heparan sulfate), which repel negatively charged proteins like albumin, contributing to their retention. - While important, the role of electrical charge is **secondary** to molecular size in preventing the bulk passage of most proteins. *Shape* - While abnormal protein shapes (e.g., **amyloid fibrils**) can impact filtration in specific disease states, the typical physiological filtration of most proteins is primarily governed by size and charge. - The inherent shape of normal globular proteins plays a less direct role compared to their overall size. *Temperature* - **Physiological temperature** is relatively constant in the body and does not directly influence the molecular interactions and physical properties of the glomerular filtration barrier in a way that significantly alters protein filtration. - Temperature changes would lead to denaturation or aggregation, which are not the primary determinants of normal protein filtration.

Question 446: What is the best stimulus for release of vasopressin?

A. Hypotension
B. Hypertension
C. Hyperosmolality of extracellular fluid (Correct Answer)
D. Decreased plasma volume

Explanation: ***Hyperosmolality of extracellular fluid*** - **Hyperosmolality** is sensed by **osmoreceptors** in the hypothalamus, which then stimulate the release of vasopressin (ADH). - This response is crucial for **water conservation** to dilute the extracellular fluid and restore normal osmolality. *Hypotension* - While hypotension does stimulate vasopressin release, its effect is less potent than that of hyperosmolality in terms of triggering release. - Baroreceptors sense a decrease in blood pressure, leading to an increase in **ADH** to help maintain blood volume and pressure. *Hypertension* - **Hypertension** would typically inhibit vasopressin release, as the body would attempt to excrete more water to lower blood volume and pressure. - Increased blood pressure signals stretch receptors, leading to a decrease in **ADH** secretion. *Decreased plasma volume* - A decrease in **plasma volume** (hypovolemia) also stimulates ADH release, but this is often accompanied by changes in osmolality. - The primary stimulus for ADH is usually the resulting **increase in plasma osmolality** due to water loss, or significant drops in blood pressure detected by baroreceptors.

Question 447: NaCl symporter is present in which part of the nephron?

A. PCT
B. DCT (Correct Answer)
C. Loop of Henle
D. Collecting duct

Explanation: ***DCT*** - The **NaCl symporter** (also known as the **Na-Cl co-transporter** or NCC) is located in the **luminal membrane** of cells in the **distal convoluted tubule (DCT)**. - This transporter is responsible for reabsorbing approximately 5-10% of filtered sodium and chloride, and it is the target of **thiazide diuretics**. *PCT* - The **proximal convoluted tubule (PCT)** is responsible for bulk reabsorption of Na+ through various mechanisms, including Na+/H+ exchangers and Na+-glucose co-transporters, but not the specific NaCl symporter found in the DCT. - While significant NaCl reabsorption occurs here, it is primarily driven by different transport proteins. *Loop of Henle* - The **thick ascending limb of the loop of Henle** uses the **Na-K-2Cl co-transporter (NKCC2)** for Na+ reabsorption, which is distinct from the NaCl symporter. - This segment is the target for **loop diuretics**. *Collecting duct* - The **collecting duct** reabsorbs Na+ primarily through the **epithelial sodium channel (ENaC)**, which is regulated by aldosterone. - While reabsorption of sodium occurs, the specific NaCl symporter is not present in this segment.

Question 448: A healthy 22-year-old female medical student with normal kidneys decreases her sodium intake by 50% for a period of 2 months. Which of the following parameters is expected to increase in response to the reduction in sodium intake?

A. Atrial natriuretic peptide release
B. Extracellular fluid volume
C. Arterial pressure
D. Renin release (Correct Answer)

Explanation: ***Renin release*** - A reduction in **sodium intake** leads to decreased extracellular fluid volume and **reduced renal perfusion pressure**, which stimulates **renin release** from the juxtaglomerular cells. - Renin initiates the **renin-angiotensin-aldosterone system (RAAS)**, leading to **angiotensin II** formation and increased **aldosterone** secretion, aimed at sodium and water retention. *Atrial natriuretic peptide release* - **Atrial natriuretic peptide (ANP)** release is stimulated by **atrial stretch** due to increased blood volume and pressure, which would decrease with reduced sodium intake. - Therefore, ANP release would likely **decrease** or remain unchanged, not increase, in response to chronic sodium restriction. *Extracellular fluid volume* - A decrease in sodium intake directly leads to a **reduction in total body sodium**, which is the primary determinant of **extracellular fluid volume**. - The body attempts to maintain fluid balance, but chronic sodium restriction will ultimately lead to a **decrease** in extracellular fluid volume as the kidneys excrete less water to match the lower sodium intake. *Arterial pressure* - Reduced sodium intake typically leads to a **decrease in extracellular fluid volume** and **cardiac output**, which in turn causes a **reduction in arterial blood pressure**. - The activation of the RAAS aims to mitigate this drop but usually does not fully compensate to increase pressure above baseline in this scenario.

Question 449: Escape phenomenon in mineralocorticoid excess occurs due to:

A. Angiotensin II
B. Renin
C. Mineralocorticoid-like action of cortisol
D. ANP (Atrial Natriuretic Peptide) (Correct Answer)

Explanation: ***ANP (Atrial Natriuretic Peptide)*** - The **escape phenomenon** in mineralocorticoid excess is an adaptive mechanism where initial sodium and water retention is followed by a return to near-normal sodium balance, primarily due to increased release of **ANP**. - **ANP** promotes natriuresis (sodium excretion) and diuresis (water excretion), counteracting the effects of prolonged mineralocorticoid action. *Angiotensin II* - **Angiotensin II** stimulates aldosterone secretion and promotes sodium and water reabsorption, directly opposing the "escape" from mineralocorticoid-induced fluid retention. - Its actions would exacerbate, rather than mitigate, the effects of mineralocorticoid excess. *Renin* - In mineralocorticoid excess, high sodium and fluid volume typically **suppress renin secretion**, which would lead to decreased angiotensin II and aldosterone production. - Suppressed renin is a *consequence* of mineralocorticoid excess, not the mechanism for escape. *Mineralocorticoid-like action of cortisol* - While **cortisol** can exert mineralocorticoid effects, especially at high concentrations or in conditions like apparent mineralocorticoid excess, it would perpetuate rather than resolve the issues of sodium and water retention. - The escape phenomenon describes the body's adaptation *despite* the continued presence of mineralocorticoid activity.

Question 450: Which of the following rightly describes the mechanism of "Vasopressin Escape" in SIADH?

A. Characterized by sudden decrease in urine volume with increase in urine osmolality independent of circulating vasopressin levels.
B. Characterized by sudden increase in urine volume with decrease in urine osmolality independent of circulating vasopressin levels. (Correct Answer)
C. Characterized by sudden decrease in urine volume with increase in urine osmolality dependent on circulating vasopressin levels.
D. Characterized by sudden increase in urine volume with decrease in urine osmolality dependent on circulating vasopressin levels.

Explanation: ***Characterized by sudden increase in urine volume with decrease in urine osmolality independent of circulating vasopressin levels.*** - **Vasopressin escape** (or ADH escape) in SIADH refers to the kidney's ability to excrete excess water despite persistently high levels of **antidiuretic hormone (ADH/vasopressin)**, leading to increased urine volume. - This escape mechanism is due to the activation of local paracrine factors, such as **prostaglandins**, and downregulation of **aquaporin-2** channels, making the collecting duct less responsive to ADH. - This protective mechanism prevents severe, life-threatening hyponatremia in chronic SIADH. *Characterized by sudden decrease in urine volume with increase in urine osmolality independent of circulating vasopressin levels.* - A decrease in urine volume with increased osmolality would indicate a response to **ADH**, not an escape from its effects. - The "independent of circulating vasopressin levels" part is inconsistent with the expected renal response to sustained ADH. *Characterized by sudden decrease in urine volume with increase in urine osmolality dependent on circulating vasopressin levels.* - This scenario describes the normal physiological action of **ADH** (vasopressin), where high levels lead to water reabsorption, concentrating the urine and reducing its volume. - It does not represent an escape mechanism, which inherently means a deviation from the expected ADH-mediated response. *Characterized by sudden increase in urine volume with decrease in urine osmolality dependent on circulating vasopressin levels.* - While an increase in urine volume and decrease in osmolality are features of vasopressin escape, stating it is "dependent" on circulating vasopressin levels is incorrect. - The key aspect of vasopressin escape is that it occurs *despite* high vasopressin levels due to renal insensitivity rather than dependency on these levels for the change in urine parameters.

Practice by Chapter

Renal Blood Flow and Glomerular Filtration

Practice Questions

Tubular Reabsorption and Secretion

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Concentration and Dilution of Urine

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Acid-Base Regulation by the Kidneys

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Sodium and Water Balance

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Potassium Regulation

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Calcium and Phosphate Handling

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Micturition Physiology

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Renal Function Tests

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Integrative Responses to Fluid Challenges

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