Renal Physiology — MCQs

Renal Physiology Indian Medical PG Practice Questions and MCQs

Question 81: Efferent arteriole constriction causes which change in Glomerular Filtration Rate (GFR)?

A. Increased GFR
B. Decreased GFR
C. GFR to initially increase then decrease (Correct Answer)
D. GFR to initially decrease then increase

Explanation: ### Explanation The effect of efferent arteriole constriction on GFR is **biphasic**, depending on the degree of constriction. **1. Why Option C is Correct:** * **Initial Increase:** Mild to moderate constriction of the efferent arteriole increases resistance to outflow from the glomerulus. This raises the **Glomerular Capillary Hydrostatic Pressure ($P_{GC}$)**, which is the primary driving force for filtration, thereby increasing GFR. * **Subsequent Decrease:** With severe or prolonged constriction, the renal plasma flow (RPF) decreases significantly. As blood stays longer in the capillary and more fluid is filtered, the **Capillary Oncotic Pressure ($\pi_{GC}$)** rises sharply. Eventually, this oncotic pressure (which opposes filtration) increases enough to outweigh the hydrostatic pressure, causing the GFR to fall. **2. Why Other Options are Incorrect:** * **Option A:** This is only true for mild/moderate constriction. It ignores the effect of rising oncotic pressure and reduced plasma flow seen in severe constriction. * **Option B:** This only occurs during severe constriction or if the afferent arteriole were constricted. * **Option D:** This sequence is physiologically incorrect; the hydrostatic pressure rise always precedes the limiting effect of oncotic pressure. **3. High-Yield Clinical Pearls for NEET-PG:** * **Afferent Arteriole Constriction:** Always **decreases** both RPF and GFR. * **ACE Inhibitors/ARBs:** These drugs dilate the efferent arteriole. This reduces $P_{GC}$, which is why they are **renoprotective** in diabetic nephropathy (reducing hyperfiltration) but can cause a transient drop in GFR. * **Filtration Fraction (FF):** Since Efferent constriction increases GFR (initially) and decreases RPF, the **FF (GFR/RPF) always increases.**

Question 82: Renal medullary hyperosmolarity is due to which of the following?

A. Increased Na+ concentration (Correct Answer)
B. Increased Na+ content
C. Increased Glucose concentration
D. All of the above

Explanation: **Explanation:** The renal medullary interstitium maintains a high osmotic gradient (up to 1200–1400 mOsm/L) essential for urine concentration. This hyperosmolarity is primarily generated by the **Countercurrent Multiplier system** and is maintained by the **Countercurrent Exchanger (Vasa Recta)**. **Why Option A is Correct:** The hyperosmolarity of the medulla is specifically due to the high **concentration** of solutes, primarily **Sodium (Na+)**, Chloride (Cl-), and **Urea**. Sodium is actively reabsorbed from the Thick Ascending Limb (TAL) of the Loop of Henle into the interstitium via the NKCC2 transporter. Osmolarity is defined as the number of osmoles per liter of solution; therefore, an increase in the *concentration* of Na+ directly elevates the osmotic pressure of the medullary tissue. **Why Other Options are Incorrect:** * **Option B (Increased Na+ content):** "Content" refers to the total amount of sodium present, whereas "Concentration" refers to the amount relative to the volume of water. Hyperosmolarity is a function of concentration. If both Na+ and water increase proportionally, the content increases but the osmolarity remains unchanged. * **Option C (Increased Glucose concentration):** Under physiological conditions, glucose is entirely reabsorbed in the Proximal Convoluted Tubule (PCT) and does not reach the medulla. It does not contribute to the medullary osmotic gradient. **High-Yield Facts for NEET-PG:** 1. **Solute Contribution:** Approximately 50% of medullary hyperosmolarity is due to NaCl, and the remaining 50% is due to Urea. 2. **Urea Recycling:** ADH increases the permeability of the medullary collecting ducts to urea (via UT-A1 transporters), allowing urea to contribute to the gradient. 3. **Vasa Recta:** Acts as a countercurrent exchanger; its slow blood flow prevents the "washout" of these medullary solutes. 4. **NKCC2 Transporter:** This is the target of Loop Diuretics (e.g., Furosemide), which abolish the medullary gradient, leading to diuresis.

Question 83: In the proximal convoluted tubule, H+ is exchanged for which ion?

A. Cl-
B. K+
C. Na+ (Correct Answer)
D. HCO3-

Explanation: **Explanation:** In the **Proximal Convoluted Tubule (PCT)**, the secretion of Hydrogen ions ($H^+$) is primarily mediated by the **Sodium-Hydrogen Exchanger 3 (NHE3)**. This is an example of **secondary active transport** (specifically, counter-transport or antiport). The process is driven by the low intracellular concentration of $Na^+$, maintained by the $Na^+/K^+$ ATPase pump on the basolateral membrane. This electrochemical gradient allows $Na^+$ to enter the cell from the tubular lumen, while simultaneously pumping $H^+$ out into the lumen. This secreted $H^+$ then combines with filtered bicarbonate ($HCO_3^-$) to facilitate its reabsorption, a crucial step in maintaining acid-base balance. **Analysis of Incorrect Options:** * **A. Cl-:** Chloride is primarily reabsorbed in the later parts of the PCT via paracellular pathways and $Cl^-/Base$ exchangers (like $Cl^-/Formate$), but it is not directly exchanged for $H^+$. * **B. K+:** Potassium is mostly reabsorbed in the PCT via paracellular solvent drag. $H^+/K^+$ exchange occurs in the **Alpha-Intercalated cells** of the collecting duct, not the PCT. * **D. HCO3-:** Bicarbonate is reabsorbed into the blood, not exchanged for $H^+$. In fact, $H^+$ secretion is the *mechanism* that allows $HCO_3^-$ to be reclaimed from the lumen. **High-Yield Clinical Pearls for NEET-PG:** * **Carbonic Anhydrase Inhibitors (Acetazolamide):** These drugs act in the PCT by inhibiting the enzyme required to process the $H^+$ secreted by the NHE3 pump, leading to alkaline urine and metabolic acidosis. * **Angiotensin II:** Stimulates the NHE3 exchanger in the PCT, increasing $Na^+$ reabsorption and $H^+$ secretion (contributing to contraction alkalosis). * **Site of Action:** Remember that **85% of filtered bicarbonate** is reabsorbed in the PCT through this $Na^+/H^+$ exchange mechanism.

Question 84: Which of the following statements about renal circulation is FALSE?

A. It accounts for about 25% of the cardiac output.
B. Glomerular capillary hydrostatic pressure is approximately 30 mmHg. (Correct Answer)
C. Renal cortical blood flow is greater than renal medullary blood flow.
D. Autoregulation of renal blood flow (RBF) is primarily mediated by the myogenic mechanism.

Explanation: ### Explanation **Why Option B is the Correct (False) Statement:** The glomerular capillary hydrostatic pressure ($P_{GC}$) is much higher than in other systemic capillaries. In a healthy adult, it is approximately **60 mmHg**, not 30 mmHg. This high pressure is essential to provide the driving force for ultrafiltration across the glomerular filtration barrier. It is maintained by the high-resistance efferent arteriole, which acts as a "dam," backing up blood into the glomerulus. **Analysis of Other Options:** * **Option A (True):** The kidneys receive a disproportionately large share of the cardiac output (approx. **20–25%** or 1.1–1.2 L/min) to ensure adequate filtration and waste clearance, rather than to meet metabolic demands. * **Option C (True):** Renal blood flow is heterogeneously distributed. The **cortex receives >90%** of the total RBF to facilitate filtration, while the medulla receives <10% (specifically the inner medulla receives ~1-2%). This low medullary flow is crucial to maintain the osmotic gradient required for urine concentration. * **Option D (True):** Autoregulation (maintaining constant RBF between 80–180 mmHg) is primarily mediated by two mechanisms: the **Myogenic mechanism** (fastest/primary) and **Tubuloglomerular feedback (TGF)**. **High-Yield NEET-PG Pearls:** * **Oxygen Consumption:** Despite high RBF, the kidney has a high arteriovenous oxygen difference; however, oxygen consumption is directly proportional to the **sodium reabsorption rate**. * **Vasa Recta:** These vessels use a countercurrent exchange mechanism and have extremely slow blood flow to prevent "washing out" the medullary interstitial gradient. * **Pressure Profile:** The largest drop in blood pressure within the renal circulation occurs in the **afferent and efferent arterioles**, which are the primary sites of resistance.

Question 85: Which of the following aquaporin water channels is located on the apical membrane of principal cells of the collecting duct?

A. Aquaporin 1
B. Aquaporin 2 (Correct Answer)
C. Aquaporin 3
D. Aquaporin 4

Explanation: **Explanation:** The correct answer is **Aquaporin 2 (AQP2)**. **1. Why Aquaporin 2 is correct:** Aquaporin 2 is the only water channel in the collecting duct that is **hormonally regulated**. It is located on the **apical (luminal) membrane** of the principal cells. When Antidiuretic Hormone (ADH/Vasopressin) binds to V2 receptors on the basolateral membrane, it triggers a cAMP-mediated signaling pathway that causes the insertion of AQP2-containing vesicles into the apical membrane. This increases the water permeability of the collecting duct, allowing for concentrated urine production. **2. Why other options are incorrect:** * **Aquaporin 1 (AQP1):** This is found in the **Proximal Convoluted Tubule (PCT)** and the descending limb of the Loop of Henle. It is responsible for constitutive (always active) water reabsorption and is not regulated by ADH. * **Aquaporin 3 & 4 (AQP3 & AQP4):** These are located on the **basolateral membrane** of the principal cells in the collecting duct. Unlike AQP2, they are constitutively expressed and provide the exit pathway for water to move from the cell into the medullary interstitium. **3. High-Yield Clinical Pearls for NEET-PG:** * **Nephrogenic Diabetes Insipidus:** Can be caused by mutations in the AQP2 gene or the V2 receptor, rendering the kidney unable to concentrate urine despite high ADH levels. * **Lithium Toxicity:** A common cause of acquired nephrogenic diabetes insipidus because lithium downregulates the expression of AQP2. * **Location Summary:** Apical = AQP2; Basolateral = AQP3, AQP4; PCT = AQP1.

Question 86: How does glomerular capillary pressure differ from other capillaries of the body?

A. Higher filtration pressure (Correct Answer)
B. Lower filtration pressure
C. Both of the above
D. None of the above

Explanation: **Explanation:** The glomerular capillary pressure is significantly higher than that of other systemic capillaries, a feature essential for the kidney's primary function of ultrafiltration. **Why Option A is Correct:** In most systemic capillaries, the hydrostatic pressure is approximately **15–30 mmHg**. In contrast, the glomerular capillary hydrostatic pressure ($P_{GC}$) is maintained at a much higher level, roughly **60 mmHg**. This high pressure is achieved due to two unique anatomical features: 1. **The "High-Resistance" Arrangement:** The glomerular capillaries are situated between two arterioles—the **afferent** and the **efferent**. The high resistance of the efferent arteriole acts as a "dam," backing up blood and elevating the pressure within the glomerular tuft. 2. **Short, Wide Afferent Arteriole:** The afferent arteriole is relatively short and wide, offering low resistance to incoming blood flow directly from the renal artery. **Why Options B, C, and D are Incorrect:** * **Option B:** Lower filtration pressure would result in a failure to overcome the opposing oncotic pressure, leading to a cessation of glomerular filtration and subsequent renal failure. * **Options C & D:** These are logically excluded as the physiological mechanism is unidirectional and specific to high-pressure filtration. **High-Yield Clinical Pearls for NEET-PG:** * **Starling Forces:** Net Filtration Pressure (NFP) = $(P_{GC} + \pi_{BS}) - (P_{BS} + \pi_{GC})$. In the glomerulus, $\pi_{BS}$ (oncotic pressure in Bowman's space) is effectively zero. * **Autoregulation:** The Myogenic mechanism and Tubuloglomerular Feedback (TGF) work to keep $P_{GC}$ constant despite fluctuations in systemic blood pressure. * **Effect of Drugs:** **ACE Inhibitors** dilate the efferent arteriole more than the afferent, thereby *decreasing* glomerular capillary pressure—a key mechanism in their nephroprotective effect in diabetic patients.

Question 87: The ability of the kidney to form concentrated urine will decrease if:

A. The permeability of the collecting duct to water decreases
B. Rate of blood flow through the medulla increases (Correct Answer)
C. Activity of Na+/K+-pump in the loop of Henle decreases
D. Aquaporin insertion is suppressed

Explanation: ### Explanation The ability of the kidney to concentrate urine depends on the maintenance of a **hypertonic medullary interstitium**, which provides the osmotic gradient necessary for water reabsorption. **Why Option B is Correct:** The medullary blood flow occurs via the **Vasa Recta**, which acts as a **countercurrent exchanger**. To preserve the medullary gradient, blood flow must be slow. If the rate of blood flow through the medulla increases (termed "medullary washout"), the solutes (Na+ and Urea) are carried away from the interstitium faster than they can be replaced. This dissipates the osmotic gradient, making it impossible to reabsorb water from the collecting duct, thereby decreasing the kidney's ability to concentrate urine. **Analysis of Other Options:** * **Option A & D:** Both decreased water permeability and suppressed aquaporin insertion (typically due to lack of ADH) prevent water from leaving the tubule. While this results in **dilute urine**, these are *mechanisms* of diuresis rather than the physiological *limitation* of the kidney's concentrating capacity itself. * **Option C:** The Na+/K+/2Cl- co-transporter (driven by the Na+/K+ pump) in the Thick Ascending Limb is the "Single Effect" that *creates* the gradient. While its decrease would impair concentration, the question specifically highlights medullary blood flow as a primary physiological regulator of gradient maintenance. **High-Yield Pearls for NEET-PG:** * **Countercurrent Multiplier:** Loop of Henle (creates the gradient). * **Countercurrent Exchanger:** Vasa Recta (maintains the gradient). * **ADH (Vasopressin):** Acts on V2 receptors to insert **Aquaporin-2** in the collecting ducts. * **Urea Recycling:** Contributes nearly 50% of the medullary hypertonicity; protein-malnourished individuals have a decreased ability to concentrate urine due to low urea levels.

Question 88: In a healthy individual on a normal diet, which of the following is significantly reabsorbed in the renal tubules, except?

A. Sodium (Na+)
B. Potassium (K+)
C. Chloride (Cl-)
D. Urea (Correct Answer)

Explanation: **Explanation:** The renal tubules are highly efficient at conserving essential electrolytes and water while selectively excreting metabolic waste. The distinction lies in the **percentage of the filtered load** that is reabsorbed. **Why Urea is the Correct Answer:** In a healthy individual, urea is a metabolic end-product of protein metabolism. While it is partially reabsorbed (approximately **40-50%**) to maintain the medullary osmotic gradient, a significant portion (about 50%) is **excreted** in the urine. Compared to the other options, urea has the lowest fractional reabsorption rate. It is considered a waste product that the kidney is designed to eliminate, rather than conserve. **Why the other options are incorrect:** * **Sodium (Na+):** Over **99%** of filtered sodium is reabsorbed (65% in the PCT) to maintain extracellular fluid volume and blood pressure. * **Chloride (Cl-):** Follows sodium passively and actively; approximately **99%** is reabsorbed to maintain electrical neutrality. * **Potassium (K+):** Under normal conditions, about **85-95%** of filtered potassium is reabsorbed before reaching the distal tubule. While the distal tubule can secrete K+ based on aldosterone levels, the bulk of the filtered load is recovered. **High-Yield NEET-PG Pearls:** 1. **PCT Reabsorption:** 100% of Glucose and Amino Acids are reabsorbed in the Proximal Convoluted Tubule (PCT) via secondary active transport. 2. **Urea Recycling:** Urea reabsorption occurs mainly in the PCT and the Medullary Collecting Ducts (via UT-A1/A3 transporters), contributing to the **corticopapillary osmotic gradient**. 3. **ADH Influence:** Antidiuretic Hormone (ADH) increases urea reabsorption in the medullary collecting ducts, further concentrating the medullary interstitium.

Question 89: Formation of a small volume of concentrated urine in dehydration is associated with which of the following?

A. Increased reabsorption in the proximal convoluted tubule
B. Increased concentration in the loop of Henle
C. Increased reabsorption in the distal convoluted tubule and collecting ducts
D. All of the above (Correct Answer)

Explanation: **Explanation:** The formation of concentrated urine during dehydration is a coordinated physiological response aimed at conserving body water and maintaining hemodynamic stability. 1. **Proximal Convoluted Tubule (PCT):** In dehydration, decreased effective circulating volume triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**. Angiotensin II directly stimulates the Na⁺/H⁺ exchanger in the PCT, increasing the reabsorption of sodium, water, and bicarbonate. This "contraction alkalosis" mechanism ensures maximal fluid retention early in the nephron. 2. **Loop of Henle:** Dehydration leads to increased sympathetic activity and the action of **ADH (Vasopressin)**, which enhances the activity of the Na-K-2Cl cotransporter in the Thick Ascending Limb. This strengthens the medullary osmotic gradient, allowing for a higher concentration of tubular fluid as it passes through the descending limb. 3. **Distal Tubule and Collecting Ducts:** This is the most critical site for final urine concentration. High levels of ADH cause the insertion of **Aquaporin-2 channels** into the apical membrane of the principal cells. This allows water to be reabsorbed down its osmotic gradient into the hypertonic medullary interstitium, resulting in a small volume of highly concentrated urine. **Why "All of the above" is correct:** The renal response to dehydration is not localized to one segment; it involves an integrated increase in reabsorptive capacity across the entire nephron to minimize water loss. **High-Yield Clinical Pearls for NEET-PG:** * **Maximum Urine Osmolality:** Human kidneys can concentrate urine up to **1200–1400 mOsm/L**. * **Obligatory Urine Volume:** To excrete the daily solute load (~600 mOsm), a minimum of **0.5 L/day** of urine must be produced. * **V2 Receptors:** ADH acts on V2 receptors (Gs-coupled) in the collecting ducts to increase cAMP and insert Aquaporins. * **Urea Recycling:** ADH also increases urea transporters (UT-A1) in the medullary collecting duct, further strengthening the osmotic gradient.

Question 90: Absorption of glucose by the kidney occurs via which mechanism?

A. Secondary active transport (Correct Answer)
B. Facilitated diffusion
C. Primary active transport
D. Endocytosis

Explanation: **Explanation:** Glucose reabsorption in the kidney occurs almost exclusively in the **Proximal Convoluted Tubule (PCT)**. This process is a classic example of **Secondary Active Transport**. 1. **Mechanism (Why A is correct):** Glucose is transported across the apical membrane (from tubular lumen into the cell) against its concentration gradient. This is powered by the **Sodium-Glucose Co-transporters (SGLT-2 and SGLT-1)**. These symporters utilize the energy stored in the electrochemical gradient of Sodium ($Na^+$), which is established by the $Na^+/K^+$ ATPase pump on the basolateral membrane. Because the energy is derived indirectly from ATP (via the $Na^+$ gradient), it is termed "Secondary" active transport. 2. **Why other options are incorrect:** * **B. Facilitated Diffusion:** While glucose *leaves* the cell across the basolateral membrane via **GLUT-2/GLUT-1** through facilitated diffusion, the initial *absorption* from the lumen is active. * **C. Primary Active Transport:** This involves direct ATP hydrolysis by the carrier itself (e.g., $Na^+/K^+$ ATPase). Glucose transporters do not hydrolyze ATP directly. * **D. Endocytosis:** This mechanism is used for the reabsorption of larger molecules like small proteins and peptides, not simple sugars like glucose. **High-Yield Clinical Pearls for NEET-PG:** * **SGLT-2** is located in the early PCT (S1 segment) and accounts for **90%** of glucose reabsorption. * **SGLT-1** is located in the late PCT (S3 segment) and reabsorbs the remaining 10%. * **Renal Threshold for Glucose:** Glucosuria typically begins when plasma glucose exceeds **180 mg/dL**. * **Transport Maximum ($T_m$):** The point where all SGLT transporters are saturated (approx. **375 mg/min** in men). * **SGLT-2 Inhibitors (e.g., Dapagliflozin):** A class of drugs used in Diabetes Mellitus that block this secondary active transport to promote glucose excretion.

Practice by Chapter

Renal Blood Flow and Glomerular Filtration

Practice Questions

Tubular Reabsorption and Secretion

Practice Questions

Concentration and Dilution of Urine

Practice Questions

Acid-Base Regulation by the Kidneys

Practice Questions

Sodium and Water Balance

Practice Questions

Potassium Regulation

Practice Questions

Calcium and Phosphate Handling

Practice Questions

Micturition Physiology

Practice Questions

Renal Function Tests

Practice Questions

Integrative Responses to Fluid Challenges

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free