Renal Physiology — MCQs

Renal Physiology Indian Medical PG Practice Questions and MCQs

Question 51: What would tend to decrease GFR by more than 10% in a normal kidney?

A. Decrease in mean arterial pressure from 100 to 85 mm Hg
B. 50% decrease in afferent arteriolar resistance
C. 50% decrease in efferent arteriolar resistance (Correct Answer)
D. 50% increase in the glomerular capillary filtration coefficient

Explanation: **Explanation:** The Glomerular Filtration Rate (GFR) is determined by the balance of Starling forces, primarily the **Glomerular Capillary Hydrostatic Pressure ($P_{GC}$)**. **Why Option C is Correct:** The efferent arteriole provides the primary resistance to blood exiting the glomerular capillaries. A **50% decrease in efferent arteriolar resistance** allows blood to flow out of the glomerulus more easily. This leads to a significant drop in $P_{GC}$, which directly reduces the driving force for filtration. Because the efferent arteriole is a major site of resistance, such a drastic reduction causes a substantial fall in GFR (typically >10%). **Analysis of Incorrect Options:** * **Option A:** Due to **Renal Autoregulation** (via myogenic mechanism and tubuloglomerular feedback), GFR remains relatively constant when mean arterial pressure (MAP) is between **75 and 160 mm Hg**. A drop from 100 to 85 mm Hg is well within this range and will result in minimal change in GFR. * **Option B:** A decrease in afferent resistance increases blood flow into the glomerulus and increases $P_{GC}$, which would **increase** GFR, not decrease it. * **Option C:** The filtration coefficient ($K_f$) is a measure of permeability and surface area. Increasing $K_f$ would **increase** GFR. **High-Yield Clinical Pearls for NEET-PG:** 1. **Constriction vs. Dilation:** Afferent constriction decreases GFR; Efferent constriction (at moderate levels) increases GFR by "backing up" pressure. 2. **Biphasic Efferent Effect:** While moderate efferent constriction increases GFR, *severe* constriction can actually decrease GFR because it significantly reduces renal plasma flow (RPF), leading to a rapid rise in oncotic pressure. 3. **ACE Inhibitors:** These drugs dilate the efferent arteriole. This reduces $P_{GC}$, which is why they are "renoprotective" in diabetic nephropathy but can cause a dangerous drop in GFR in patients with bilateral renal artery stenosis.

Question 52: Which cells in the kidney produce 1,25-dihydroxycholecalciferol?

A. Granular cells
B. Proximal convoluted tubule cells (Correct Answer)
C. Mesangial cells
D. Peritubular cells

Explanation: The kidney plays a vital role in mineral homeostasis by performing the final step in the activation of Vitamin D. ### **Explanation of the Correct Answer** The correct answer is **B. Proximal convoluted tubule (PCT) cells**. The enzyme **1-alpha-hydroxylase** is primarily located in the mitochondria of the PCT cells. This enzyme converts 25-hydroxycholecalciferol (calcidiol) into **1,25-dihydroxycholecalciferol (calcitriol)**, which is the most active form of Vitamin D. This process is tightly regulated by Parathyroid Hormone (PTH), which stimulates the enzyme in response to low serum calcium or phosphate levels. ### **Analysis of Incorrect Options** * **A. Granular cells:** These are modified smooth muscle cells located in the afferent arterioles. Their primary function is the synthesis, storage, and release of **renin**, not Vitamin D activation. * **C. Mesangial cells:** These provide structural support to the glomerular capillaries and have contractile properties to regulate the glomerular filtration rate (GFR). * **D. Peritubular cells:** Specifically, the peritubular interstitial cells (fibroblasts) in the renal cortex are the primary site for the production of **Erythropoietin (EPO)** in response to hypoxia. ### **High-Yield Clinical Pearls for NEET-PG** * **Chronic Kidney Disease (CKD):** Loss of PCT mass leads to calcitriol deficiency, resulting in secondary hyperparathyroidism and renal osteodystrophy. * **Regulation:** 1-alpha-hydroxylase is **stimulated by PTH** and low phosphate, but **inhibited by FGF-23** and high calcitriol levels (negative feedback). * **Site of 25-hydroxylation:** Occurs in the **Liver** (via 25-hydroxylase), while 1-alpha-hydroxylation occurs in the **Kidney**.

Question 53: What is the principal site of sodium absorption in the nephron?

A. Proximal convoluted tubule (Correct Answer)
B. Distal convoluted tubule
C. Loop of Henle (thick portion)
D. Collecting duct

Explanation: **Explanation:** The **Proximal Convoluted Tubule (PCT)** is the "workhorse" of the nephron. It is the principal site for the reabsorption of the majority of the glomerular filtrate. Approximately **65-70% of filtered sodium (Na+)** is reabsorbed here, primarily through the Na+/H+ exchanger (NHE3) and co-transport with glucose, amino acids, and phosphate. This reabsorption is iso-osmotic, meaning water follows sodium passively to maintain osmotic balance. **Analysis of Incorrect Options:** * **Loop of Henle (Thick Ascending Limb):** This segment reabsorbs about **20-25%** of filtered sodium via the **Na+-K+-2Cl- cotransporter (NKCC2)**. It is the site of action for loop diuretics (e.g., Furosemide). * **Distal Convoluted Tubule (DCT):** This segment reabsorbs only about **5-8%** of sodium via the **Na+-Cl- symporter**. It is the site of action for Thiazide diuretics. * **Collecting Duct:** This is the final site for "fine-tuning" sodium balance, accounting for only **2-3%** of reabsorption. Sodium entry here occurs through **ENaC (Epithelial Sodium Channels)**, which are regulated by Aldosterone. **High-Yield Clinical Pearls for NEET-PG:** * **Obligatory Reabsorption:** Reabsorption in the PCT is "obligatory" and independent of hormonal control, unlike the distal segments. * **Glucose Reabsorption:** 100% of filtered glucose is reabsorbed in the PCT (via SGLT2/SGLT1) unless the renal threshold (180 mg/dL) is exceeded. * **Carbonic Anhydrase:** The PCT is the site of action for Acetazolamide, which inhibits sodium bicarbonate reabsorption. * **Smallest fraction of Na+ reabsorption:** Occurs in the medullary collecting ducts.

Question 54: Fractional excretion of sodium (FENa) is calculated as:

A. (Urine sodium x Serum potassium) / (Serum sodium x Urine potassium) x 100
B. (Urine potassium x Serum sodium) / (Serum potassium x Urine sodium) x 100
C. (Urine sodium x Urine potassium) / (Serum sodium x Serum potassium) x 100
D. (Urine sodium / Serum sodium) / (Urine potassium / Serum potassium) x 100 (Correct Answer)

Explanation: ### Explanation **Concept and Calculation** Fractional Excretion of Sodium (FENa) measures the percentage of sodium filtered by the kidney that is actually excreted in the urine. It is the ratio of the **Sodium Clearance** to the **Creatinine Clearance** (used as a proxy for GFR). The formula is derived as follows: $FENa = \frac{\text{Clearance of Na}^+}{\text{Clearance of Creatinine}} \times 100$ Since Clearance ($C$) = $\frac{U \times V}{P}$, the volume ($V$) terms cancel out, leaving: $FENa = \frac{(U_{Na} / P_{Na})}{(U_{Cr} / P_{Cr})} \times 100$ In the context of this question, **Creatinine** is substituted with **Potassium** (though clinically less common, the mathematical principle of the ratio remains the same for calculating fractional excretion of one solute relative to another). Thus, **Option D** correctly represents the ratio of the fractional clearances. **Analysis of Incorrect Options** * **Options A, B, and C:** These are mathematically incorrect arrangements of the variables. They do not represent the ratio of urinary-to-plasma concentration for sodium divided by the same ratio for the reference solute (Creatinine or Potassium). They result in units that do not represent a fractional percentage of clearance. **Clinical Pearls for NEET-PG** * **Prerenal Azotemia:** FENa is typically **< 1%**. The kidneys are intact and reabsorbing sodium aggressively to restore blood volume. * **Acute Tubular Necrosis (ATN):** FENa is typically **> 2%**. The tubules are damaged and cannot reabsorb sodium, leading to high sodium loss in urine. * **Exception:** FENa can be < 1% in certain intrinsic causes like Contrast-induced nephropathy or Myoglobinuria (Pigment nephropathy). * **Diuretics:** FENa is unreliable if the patient is on diuretics; in such cases, **Fractional Excretion of Urea (FEUrea)** is a more accurate marker (FEUrea < 35% suggests prerenal etiology).

Question 55: In which region of the nephron are P cells (principal cells) located?

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

Explanation: **Explanation:** The correct answer is **D. Collecting duct.** **1. Why the Collecting Duct is Correct:** Principal cells (P cells) are the predominant cell type found in the **late distal tubule** and throughout the **collecting duct**. Their primary physiological role is the regulation of water and electrolyte balance under hormonal control: * **Sodium (Na+) Reabsorption:** They reabsorb Na+ via Epithelial Sodium Channels (ENaC). * **Potassium (K+) Secretion:** They are the main site for K+ secretion into the tubular lumen. * **Water Reabsorption:** They express Aquaporin-2 (AQP2) receptors, which are regulated by **Antidiuretic Hormone (ADH/Vasopressin)**. * **Aldosterone Action:** Aldosterone acts primarily on P cells to increase Na+ reabsorption and K+ secretion. **2. Why Other Options are Incorrect:** * **A. PCT:** This region is lined by cells with a prominent brush border (microvilli) for bulk reabsorption of glucose, amino acids, and ions. It does not contain P cells. * **B. Loop of Henle:** The thin segments consist of simple squamous epithelium, while the Thick Ascending Limb (TAL) contains cuboidal cells specialized for the Na+-K+-2Cl- cotransporter (NKCC2). * **C. DCT:** The early DCT contains "DCT cells" specialized for the Na+-Cl- symporter (NCC). While P cells begin to appear in the late (connecting) tubule, the collecting duct is their definitive and most characteristic location. **3. High-Yield Clinical Pearls for NEET-PG:** * **Intercalated Cells (I cells):** Also found in the collecting duct, these are responsible for acid-base balance (**Type A** secretes H+; **Type B** secretes HCO3-). * **Liddle’s Syndrome:** Caused by overactivity of ENaC channels in P cells, leading to hypertension and hypokalemia. * **Potassium-Sparing Diuretics:** Amiloride and Triamterene work by blocking ENaC channels in the P cells, while Spironolactone antagonizes the aldosterone receptor within these same cells.

Question 56: What is the exact number of solutes transported in the thick ascending limb of the Loop of Henle per carrier pump?

A. Transports one Na+, one K+, and two Cl-. (Correct Answer)
B. Transports two Na+, two K+, and two Cl-.
C. Transports two Na+, one K+, and two Cl-.
D. Transports three Na+, two K+, and two Cl-.

Explanation: ### Explanation The correct answer is **A: Transports one Na+, one K+, and two Cl-**. **Underlying Concept:** The thick ascending limb (TAL) of the Loop of Henle is known as the "diluting segment" of the nephron. The primary transport mechanism on the apical (luminal) membrane is the **NKCC2 symporter** (Sodium-Potassium-2-Chloride co-transporter). This carrier protein moves four ions simultaneously into the cell: **one sodium (Na+), one potassium (K+), and two chloride (Cl-) ions**. This process is **electroneutral**, meaning the net charge moved across the membrane by the pump itself is zero (1+ + 1+ - 2 = 0). This transporter utilizes the sodium gradient created by the basolateral Na+/K+ ATPase to drive the secondary active transport of these solutes. **Analysis of Incorrect Options:** * **Options B, C, and D:** These are incorrect because they misstate the stoichiometry of the NKCC2 pump. Any ratio other than 1:1:2 would violate the electroneutrality of this specific symporter and does not align with the physiological structure of the SLC12A1 protein (the gene encoding NKCC2). **High-Yield Clinical Pearls for NEET-PG:** * **Loop Diuretics:** Drugs like **Furosemide** and Torsemide act by specifically inhibiting the NKCC2 symporter. * **Bartter Syndrome:** A genetic defect in the NKCC2 transporter (Type 1) or the ROMK channel (Type 2) mimics the effect of chronic loop diuretic use, leading to hypokalemia, metabolic alkalosis, and hypercalciuria. * **Lumen-Positive Potential:** While the pump is electroneutral, some K+ leaks back into the lumen via **ROMK channels**, creating a +10 to +20 mV potential. This "lumen-positive" charge is the driving force for the **paracellular reabsorption** of divalent cations like **Calcium (Ca2+) and Magnesium (Mg2+)**.

Question 57: The glomerular filtration barrier does not permit which of the following molecular sizes?

A. 4000 daltons
B. 400 daltons
C. 40000 daltons (Correct Answer)
D. 40 daltons

Explanation: ### Explanation The glomerular filtration barrier (GFB) is a highly selective semipermeable membrane that filters blood based on two primary criteria: **molecular size** and **electrical charge**. **The Underlying Concept:** The GFB consists of the fenestrated endothelium, the glomerular basement membrane (GBM), and the podocyte slit diaphragms. The effective pore size of the slit diaphragm is approximately **4 to 8 nm**. * Molecules with a molecular weight (MW) **less than 7,000 Daltons** (like water, glucose, and urea) are filtered freely. * As MW increases, filterability decreases. The "threshold" for significant restriction begins around **40,000 Daltons**. * Molecules larger than **69,000 Daltons** (the size of Albumin) are almost completely excluded under normal physiological conditions. Therefore, **40,000 Daltons** represents a size that is significantly restricted compared to smaller solutes. **Analysis of Options:** * **B & D (40 and 400 Daltons):** These are very small molecules (e.g., electrolytes, glucose, amino acids). They pass through the GFB as easily as water (filtration ratio of 1.0). * **A (4,000 Daltons):** This is below the 7,000-Dalton limit for free filtration. Molecules like Inulin (5,200 Da) fall into this category and are filtered freely. * **C (40,000 Daltons - Correct):** At this size, the filtration fraction drops significantly. While not zero, it is the only option provided that faces substantial resistance from the filtration barrier. **High-Yield Clinical Pearls for NEET-PG:** * **Charge Selectivity:** The GFB is lined with **heparan sulfate** (polyanionic), which repels negatively charged proteins (like Albumin). In **Minimal Change Disease**, the loss of this negative charge leads to massive proteinuria despite no visible structural change on light microscopy. * **Albumin (69,000 Da):** It is the "gold standard" for size exclusion. Its presence in urine (Albuminuria) indicates a breakdown of the GFB. * **Neutral vs. Cationic:** For the same size, cationic (positive) molecules are filtered more easily than neutral ones, which are filtered more easily than anionic (negative) ones.

Question 58: Which of the following statements is true regarding calcium reabsorption in the kidney?

A. Most of the calcium reabsorption occurs in the distal convoluted tubule (DCT).
B. The major regulating factor for calcium reabsorption is parathormone. (Correct Answer)
C. Parathormone decreases calcium reabsorption.
D. Increased plasma phosphate decreases calcium reabsorption.

Explanation: **Explanation:** **1. Why Option B is Correct:** Parathyroid hormone (PTH) is the primary physiological regulator of renal calcium handling. It acts specifically on the **Distal Convoluted Tubule (DCT)** and the thick ascending limb of Henle to increase calcium reabsorption by upregulating apical calcium channels (TRPV5). This ensures that plasma calcium levels are maintained within a narrow homeostatic range. **2. Why the Other Options are Incorrect:** * **Option A:** While the DCT is the site of hormonal regulation, it is **not** where the "most" reabsorption occurs. Approximately **65%** of filtered calcium is reabsorbed in the **Proximal Convoluted Tubule (PCT)**, primarily via passive, paracellular pathways. * **Option C:** This is the opposite of the physiological effect. PTH **increases** calcium reabsorption (to raise blood calcium) while simultaneously decreasing phosphate reabsorption in the PCT (phosphaturic effect). * **Option D:** Increased plasma phosphate actually **stimulates** the release of PTH. This, in turn, **increases** renal calcium reabsorption. High phosphate levels also lead to the formation of calcium-phosphate complexes, lowering ionized calcium and further triggering PTH secretion. **3. High-Yield Clinical Pearls for NEET-PG:** * **Segmental Reabsorption:** PCT (65%) > Thick Ascending Limb (25%) > DCT (8%). * **Diuretic Effects:** **Thiazides** increase calcium reabsorption in the DCT (useful in hypercalciuria/stones), whereas **Loop Diuretics** (Furosemide) inhibit calcium reabsorption by abolishing the lumen-positive potential (used in acute hypercalcemia). * **PTH Action:** "Phosphate Trashing Hormone"—it saves Calcium but loses Phosphate in the urine.

Question 59: Glucose is absorbed through the apical membrane of the proximal convoluted tubule by which transporter?

A. SGLT-1
B. SGLT-2 (Correct Answer)
C. GLUT-1
D. GLUT-2

Explanation: **Explanation:** The reabsorption of glucose in the kidney occurs almost entirely in the **Proximal Convoluted Tubule (PCT)**. This process involves two distinct steps: transport across the apical (luminal) membrane and transport across the basolateral membrane. **Why SGLT-2 is correct:** Glucose is transported across the **apical membrane** against its concentration gradient via **Secondary Active Transport**. This is mediated by **SGLT-2** (Sodium-Glucose Co-transporter 2), which couples the movement of one sodium ion with one glucose molecule. SGLT-2 is a high-capacity, low-affinity transporter located in the early part (S1 segment) of the PCT, responsible for reabsorbing approximately **90%** of filtered glucose. **Analysis of Incorrect Options:** * **SGLT-1:** This is a low-capacity, high-affinity transporter located in the late PCT (S3 segment). It reabsorbs the remaining 10% of glucose. It is also the primary transporter for glucose absorption in the small intestine. * **GLUT-2:** This is a **Facilitated Diffusion** transporter located on the **basolateral membrane** of the early PCT. It moves glucose out of the cell into the interstitium. * **GLUT-1:** This transporter is located on the basolateral membrane of the late PCT (S3 segment), working in conjunction with SGLT-1. **High-Yield Clinical Pearls for NEET-PG:** 1. **Renal Threshold for Glucose:** Glucose begins to appear in the urine (glycosuria) when blood glucose levels exceed **180 mg/dL**. 2. **Tubular Transport Maximum ($T_m$):** The transport system becomes fully saturated at a plasma glucose level of approximately **375 mg/min** in men. 3. **SGLT-2 Inhibitors (Gliflozins):** Drugs like Dapagliflozin inhibit SGLT-2 and are used in treating Type 2 Diabetes to promote glucose excretion in urine.

Question 60: A 20-year-old male patient presents with a decrease in urinary output to about 400ml/day. Both renal blood flow (RBF) and glomerular filtration rate (GFR) were decreased. Which of the following causes a decrease in both RBF and GFR?

A. Dilation of the efferent arteriole
B. Dilation of the afferent arteriole
C. Constriction of the afferent arteriole (Correct Answer)
D. Constriction of the efferent arteriole

Explanation: **Explanation:** The Glomerular Filtration Rate (GFR) and Renal Blood Flow (RBF) are primarily regulated by the resistance of the afferent and efferent arterioles. **Why Option C is Correct:** **Constriction of the afferent arteriole** increases resistance *before* the blood reaches the glomerulus. This leads to: 1. **Decreased RBF:** Increased total renal vascular resistance reduces blood flow into the kidney. 2. **Decreased GFR:** Reduced flow into the glomerular capillaries lowers the glomerular hydrostatic pressure ($P_{GC}$), which is the primary driving force for filtration. **Analysis of Incorrect Options:** * **Option A (Dilation of efferent arteriole):** Decreases resistance to outflow. This **increases RBF** (less resistance) but **decreases GFR** because the "back pressure" in the glomerulus drops. * **Option B (Dilation of afferent arteriole):** Decreases resistance to inflow. This **increases both RBF and GFR** (due to increased $P_{GC}$). * **Option D (Constriction of efferent arteriole):** Increases resistance to outflow. This **decreases RBF** but **increases GFR** (up to a point) because it increases the hydrostatic pressure ($P_{GC}$) within the glomerular capillaries. **High-Yield Clinical Pearls for NEET-PG:** * **NSAIDs** inhibit prostaglandins (which normally dilate the afferent arteriole), leading to **afferent constriction** and a drop in GFR. * **ACE Inhibitors** prevent the action of Angiotensin II (which preferentially constricts the efferent arteriole), leading to **efferent dilation** and a drop in GFR. * **Key Rule:** If both RBF and GFR move in the **same** direction, the primary change is at the **afferent** arteriole. If they move in **opposite** directions, the primary change is at the **efferent** arteriole.

Practice by Chapter

Renal Blood Flow and Glomerular Filtration

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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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