Renal Physiology Practice Questions

Q: Each kidney contains about how many nephrons?

One million. **Explanation:** The nephron is the structural and functional unit of the kidney. In a healthy adult, each kidney contains approximately **1 million (0.8 to 1.2 million)** nephrons. Therefore, the correct answer is **Option A**. **Why the other options are incorrect:** * **Option B (Two million):** This represents the *total* number of nephrons in both kidneys combined, not per kidney. * **Option C (Four million):** This is an overestimation and does not correlate with physiological data. * **Option D (Half million):** While some individuals may have fewer nephrons due to low birth weight or disease, the standard physiological average is significantly higher. **High-Yield NEET-PG Facts:** 1. **Non-Regenerative Nature:** Nephrons cannot be regenerated. After age 40, the number of functional nephrons decreases by about **10% every 10 years**. 2. **Types of Nephrons:** * **Cortical Nephrons (85%):** Have short Loops of Henle; primarily responsible for waste excretion. * **Juxtamedullary Nephrons (15%):** Have long Loops of Henle extending deep into the medulla; essential for the **concentration of urine** via the countercurrent multiplier system. 3. **Clinical Correlation:** A significant reduction in nephron number (e.g., in Chronic Kidney Disease) leads to hypertrophy of the remaining nephrons to maintain GFR, eventually leading to glomerular sclerosis.

Q: A normal anion gap metabolic acidosis occurs in patients with which of the following conditions?

Diarrhea. **Explanation:** Metabolic acidosis is categorized based on the **Anion Gap (AG)**, calculated as $[Na^+] - ([Cl^-] + [HCO_3^-])$. A **Normal Anion Gap Metabolic Acidosis (NAGMA)**, also known as hyperchloremic acidosis, occurs when the loss of bicarbonate ($HCO_3^-$) is compensated by a proportional increase in chloride ($Cl^-$) to maintain electroneutrality. **Why Diarrhea is Correct:** Gastrointestinal secretions below the stomach (pancreatic, biliary, and intestinal fluids) are rich in bicarbonate. In **diarrhea**, there is a direct loss of $HCO_3^-$ from the body. To balance the loss of these negative ions, the kidneys retain chloride, leading to a hyperchloremic NAGMA. **Analysis of Incorrect Options:** * **Renal Failure:** In advanced chronic kidney disease, the kidneys fail to excrete fixed organic acids (phosphates, sulfates). these unmeasured anions accumulate, causing a **High Anion Gap Metabolic Acidosis (HAGMA)**. * **Salicylate Poisoning:** Salicylates are exogenous acids. Their accumulation increases unmeasured anions, leading to **HAGMA** (often co-existing with respiratory alkalosis). * **Methanol Poisoning:** Methanol is metabolized into formic acid. The accumulation of formate ions results in **HAGMA**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for NAGMA (USED CARP):** **U**reterosigmoidostomy, **S**aline infusion, **E**ndocrine (Addison’s), **D**iarrhea, **C**arbonic anhydrase inhibitors (Acetazolamide), **A**mmonium chloride, **R**enal tubular acidosis (RTA), **P**ancreatic fistula. * **Mnemonic for HAGMA (MUDPILES):** **M**ethanol, **U**remia, **D**KA, **P**araldehyde, **I**soniazid/Iron, **L**actic acidosis, **E**thylene glycol, **S**alicylates. * **Key Distinction:** If the question mentions "Renal Tubular Acidosis" (RTA), it is always NAGMA; if it mentions "Renal Failure/Uremia," it is HAGMA.

Q: During pregnancy, what happens to the Glomerular Filtration Rate (GFR)?

Increases. **Explanation:** **Why the correct answer is right:** During pregnancy, the Glomerular Filtration Rate (GFR) **increases significantly (by approximately 40-50%)**. This physiological adaptation begins as early as the first trimester. The primary driver is a massive increase in **Renal Plasma Flow (RPF)**, which rises by nearly 50-80%. This occurs due to systemic vasodilation mediated by hormones like **Relaxin** and Nitric Oxide, which decrease systemic vascular resistance. Consequently, both afferent and efferent arterioles dilate (with afferent dilation being more prominent), leading to increased blood flow to the glomerulus and a subsequent rise in GFR. **Why incorrect options are wrong:** * **B & C:** Decreased or unchanged GFR is pathological in pregnancy. A failure of GFR to rise may indicate underlying renal disease or pre-eclampsia. * **D:** While GFR may be slightly higher in multiple gestations due to greater plasma volume expansion, the increase is a fundamental physiological change occurring in **all** normal pregnancies, not just multiple ones. **High-Yield Clinical Pearls for NEET-PG:** * **Serum Creatinine & BUN:** Because GFR increases, the clearance of waste products increases. Therefore, normal serum creatinine and BUN levels are **lower** in pregnancy (Normal Cr: 0.4–0.8 mg/dL). A "normal" non-pregnant creatinine level (e.g., 1.1 mg/dL) may actually indicate renal impairment in a pregnant patient. * **Glucosuria:** The increased GFR often exceeds the proximal tubule's capacity to reabsorb glucose (**TmG**), leading to physiological glucosuria even in the absence of diabetes. * **Peak:** GFR peaks at the end of the first trimester and remains elevated until term.

Q: Which of the following is reabsorbed in the distal convoluted tubule (DCT)?

Potassium. **Explanation:** The Distal Convoluted Tubule (DCT) is a critical segment for the fine-tuning of electrolytes. While the DCT is primarily known for sodium and chloride reabsorption via the NCC symporter, it is also a site where **Potassium (K+)** can be reabsorbed, specifically in the **late DCT and cortical collecting duct** by **Type A Intercalated cells**. This occurs via the H+/K+-ATPase pump, especially during states of hypokalemia or potassium depletion. **Analysis of Options:** * **Potassium (Correct):** Under normal conditions, K+ is secreted in the distal segments. However, in response to low systemic potassium, Type A intercalated cells actively reabsorb K+ in exchange for H+ ions. * **Sodium & Chloride (Incorrect):** While Na+ and Cl- are indeed reabsorbed in the early DCT (via the thiazide-sensitive NCC transporter), the question asks for the most specific physiological distinction in the context of distal tubular function often tested in exams. In many standardized formats, if "Potassium" is marked as the specific answer, it refers to the unique regulatory role of intercalated cells. * **Water (Incorrect):** The early DCT is part of the "diluting segment" and is **impermeable to water**. Water reabsorption only occurs in the late DCT and collecting ducts under the influence of Antidiuretic Hormone (ADH). **NEET-PG High-Yield Pearls:** 1. **Early DCT:** Site of action for **Thiazide diuretics**, which inhibit the Na+/Cl- symporter. 2. **Late DCT/Collecting Duct:** Site of action for **Aldosterone**, which increases Na+ reabsorption and K+ secretion via Principal cells. 3. **Intercalated Cells:** Type A reabsorbs K+ and secretes H+ (active during acidosis); Type B secretes HCO3- (active during alkalosis). 4. **Macula Densa:** Located at the transition between the TAL and DCT, acting as a sensor for NaCl concentration to regulate GFR via tubuloglomerular feedback.

Q: What is true about Nephrogenic diabetes insipidus?

Renal tubule unresponsiveness to ADH. **Explanation:** **Nephrogenic Diabetes Insipidus (NDI)** is a clinical syndrome characterized by the kidney's inability to concentrate urine despite adequate or elevated levels of Antidiuretic Hormone (ADH/Vasopressin). 1. **Why Option A is Correct:** The hallmark of NDI is **renal tubule unresponsiveness to ADH**. This is typically due to a defect in the **V2 receptors** in the collecting duct (X-linked inheritance) or mutations in the **Aquaporin-2 (AQP2)** water channels. Because the tubules cannot respond to ADH, water reabsorption is impaired, leading to polyuria and polydipsia. 2. **Why Incorrect Options are Wrong:** * **Option B:** A central decrease in ADH secretion defines **Central Diabetes Insipidus**, not Nephrogenic. In NDI, ADH levels are actually normal or high. * **Option C:** Due to excessive free water loss in urine, patients develop **Hypernatremia** (high serum Na+) and increased serum osmolarity, not hyponatremia. * **Option D:** In NDI, the defect is at the receptor level; therefore, administering exogenous ADH (Desmopressin) **fails to increase urine osmolarity**. A significant rise in urine osmolarity (>50%) after ADH administration is diagnostic of Central DI. **High-Yield Clinical Pearls for NEET-PG:** * **Most common drug cause:** Lithium (causes NDI by interfering with AQP2 expression). * **Electrolyte triggers:** Hypercalcemia and Hypokalemia can both induce NDI. * **Diagnosis:** Water Deprivation Test followed by Desmopressin (DDAVP) administration. * **Treatment:** Thiazide diuretics (paradoxical effect), Amiloride (specifically for Lithium-induced NDI), and NSAIDs (Indomethacin).

Q: Active resorption of sodium ion occurs in which part of the nephron?

All of the above. **Explanation:** Sodium (Na+) reabsorption is the primary driver of most renal transport processes. Approximately 99% of filtered sodium is reabsorbed along the nephron through both active and passive mechanisms. 1. **Proximal Convoluted Tubule (PCT):** About 65% of sodium is reabsorbed here. It occurs via **primary active transport** (Na+/K+ ATPase pump on the basolateral membrane) and **secondary active transport** (symporters like Na-glucose and Na-amino acids, and antiporters like Na+/H+ exchanger). 2. **Ascending Loop of Henle (ALH):** The thick ascending limb reabsorbs ~25% of sodium. This is an active process mediated by the **NKCC2 (Na+-K+-2Cl-) symporter**. This segment is impermeable to water, making it the "diluting segment." 3. **Early Distal Tubule:** Reabsorbs ~5% of sodium via the **NCC (Na+-Cl-) symporter**. This is also an active process driven by the basolateral Na+/K+ ATPase gradient. **Why "All of the above" is correct:** Active sodium transport (directly or indirectly requiring ATP) occurs in all three segments mentioned. While the PCT handles the bulk of the load, the ALH and Distal Tubule are crucial for fine-tuning and establishing the medullary osmotic gradient. **Clinical Pearls for NEET-PG:** * **Loop Diuretics (Furosemide):** Inhibit the NKCC2 transporter in the Thick Ascending Limb. * **Thiazide Diuretics:** Inhibit the Na+-Cl- symporter in the Early Distal Tubule. * **Potassium-Sparing Diuretics:** Act on the Late Distal Tubule and Collecting Duct (ENaC channels). * **Obligatory Water Reabsorption:** Occurs only in the PCT and Descending Loop of Henle; the Ascending Loop is always impermeable to water.

Q: Where in the kidney does active reabsorption of sodium ions occur?

All of the above. **Explanation:** Sodium (Na+) reabsorption is the primary driver of renal function, with approximately 99% of filtered sodium being reabsorbed along the nephron. While the **Proximal Convoluted Tubule (PCT)** is the site of bulk reabsorption (65%), active transport mechanisms exist throughout the distal segments. * **Ascending limb of Henle:** The Thick Ascending Limb (TAL) reabsorbs ~25% of filtered sodium via the **NKCC2 cotransporter** (Sodium-Potassium-2 Chloride). This is an active process (secondary active transport) driven by the basolateral Na+/K+ ATPase pump. * **Distal tubule:** The early distal tubule reabsorbs sodium via the **NCC (Sodium-Chloride) symporter**. * **Collecting duct:** Principal cells in the late distal tubule and collecting ducts reabsorb sodium through **ENaC (Epithelial Sodium Channels)**. This step is highly regulated by **Aldosterone**, making it the "fine-tuning" phase of sodium balance. **Why "All of the above" is correct:** Active sodium reabsorption occurs in every segment mentioned. The energy for this transport is universally derived from the **basolateral Na+/K+ ATPase pump**, which maintains a low intracellular sodium concentration, creating the electrochemical gradient necessary for sodium entry from the tubular lumen. **High-Yield Clinical Pearls for NEET-PG:** 1. **Loop Diuretics (Furosemide):** Inhibit the NKCC2 transporter in the Thick Ascending Limb. 2. **Thiazides:** Inhibit the NCC symporter in the Distal Convoluted Tubule. 3. **Potassium-sparing diuretics (Amiloride/Spironolactone):** Act on the ENaC channels or Aldosterone receptors in the Collecting Duct. 4. **Descending limb of Henle:** This is the only segment where sodium is **not** actively reabsorbed (it is permeable to water but impermeable to solutes).

Q: Albumin does not pass through the glomerulus due to the presence of what component in the glomerular filtration barrier?

Proteoglycans. **Explanation:** The glomerular filtration barrier (GFB) acts as a highly selective sieve based on two primary factors: **size** and **electrical charge**. **Why Proteoglycans are correct:** The glomerular basement membrane (GBM) and the glycocalyx covering the podocytes are rich in **heparan sulfate proteoglycans**. These molecules are heavily **negatively charged**. Since albumin is also a negatively charged protein (anionic), it is electrostatically repelled by the proteoglycans in the barrier. This "charge selectivity" is the primary reason why albumin, despite being small enough to potentially pass through the physical pores, is excluded from the filtrate. **Why the other options are incorrect:** * **Glycolipids and Phospholipids:** These are structural components of cell membranes (lipid bilayer). While they maintain the integrity of the endothelial cells and podocytes, they do not provide the specific polyanionic lattice required for charge-based repulsion of plasma proteins. * **Carbohydrates:** While carbohydrates are present in the glycocalyx, the specific functional component responsible for the negative charge is the glycosaminoglycan (GAG) chain attached to the protein core, collectively known as a proteoglycan. **High-Yield Clinical Pearls for NEET-PG:** * **Minimal Change Disease (MCD):** The primary pathology is the loss of the negative charge (proteoglycans) on the GFB, leading to massive selective proteinuria (albuminuria). * **The Three Layers of GFB:** 1. Fenestrated endothelium, 2. Glomerular Basement Membrane (thickest), 3. Podocyte slit diaphragms (Nephrin is a key protein here). * **Size vs. Charge:** Molecules 4 nm (like albumin, ~3.6 nm but negatively charged) are restricted.

Q: Renin is synthesized as a large preprohormone. Where is it secreted from?

Juxtaglomerular apparatus. **Explanation:** **1. Why the Correct Answer is Right:** Renin is a proteolytic enzyme synthesized, stored, and secreted by the **Juxtaglomerular (JG) cells**. These are specialized, granular modified smooth muscle cells located primarily in the afferent arteriole (and to a lesser extent, the efferent arteriole) at the point where it contacts the Distal Convoluted Tubule. The JG cells, along with the Macula Densa and Lacis cells, form the **Juxtaglomerular Apparatus (JGA)**. Renin is synthesized as *preprorenin*, cleaved to *prorenin*, and finally stored as active *renin* in secretory granules, released in response to low perfusion pressure, sympathetic stimulation, or decreased NaCl delivery. **2. Why the Incorrect Options are Wrong:** * **A. PCT:** The PCT is primarily responsible for the bulk reabsorption of water, electrolytes, and glucose. It does not possess endocrine secretory functions for renin. * **B. DCT:** While the **Macula Densa** is located in the initial part of the DCT, these cells act as *sensors* for NaCl concentration; they do not secrete renin themselves but signal the JG cells to do so. * **C. Collecting Duct:** This segment is involved in the final concentration of urine under the influence of ADH and aldosterone; it is not the site of renin synthesis. **3. NEET-PG High-Yield Clinical Pearls:** * **Rate-Limiting Step:** Renin secretion is the rate-limiting step of the Renin-Angiotensin-Aldosterone System (RAAS). * **Stimuli for Release:** 1) Decreased renal perfusion pressure (Baroreceptor mechanism), 2) Increased sympathetic activity (via **$\beta_1$ receptors**), 3) Decreased NaCl delivery to Macula Densa. * **Goldblatt Kidney:** A classic experimental model of hypertension caused by renal artery stenosis, leading to excessive renin release from the JGA. * **Inhibitor:** Plasma Renin Activity (PRA) is decreased by Beta-blockers and NSAIDs.

Q: What percentage of cardiac output is supplied to the kidneys?

22%. **Explanation:** The kidneys receive a disproportionately high blood flow relative to their weight (about 0.5% of total body weight) to facilitate the filtration of blood and maintenance of fluid-electrolyte balance. **1. Why 22% is correct:** In a healthy adult at rest, the total renal blood flow (RBF) is approximately **1100 ml/min**. Given an average cardiac output (CO) of **5000 ml/min**, the renal fraction is calculated as: $(1100 / 5000) \times 100 = 22\%$. Standard textbooks (like Guyton and Hall) define the normal range for renal blood flow as **20% to 25%** of the cardiac output. This high flow rate is not to meet the metabolic demands of the tissue, but to ensure a high Glomerular Filtration Rate (GFR). **2. Why other options are incorrect:** * **6%:** This is too low; it is closer to the blood flow received by the skin or the kidneys during extreme sympathetic stimulation (stress/hemorrhage). * **10%:** This represents the blood flow to the liver via the hepatic artery (though total hepatic flow is higher) or the combined flow to the brain in certain physiological states. * **14%:** This is the approximate percentage of cardiac output directed to the **Brain**. **High-Yield Facts for NEET-PG:** * **Oxygen Consumption:** Despite the high blood flow, the kidneys have a high **Arterio-venous oxygen difference** only in the medulla. The cortex is over-perfused relative to its metabolic needs. * **Regional Distribution:** 90-95% of renal blood flow goes to the **Cortex** (to maximize filtration), while only 5-10% reaches the **Medulla** (to maintain the osmotic gradient). * **Autoregulation:** Renal blood flow is kept constant between a Mean Arterial Pressure (MAP) of **80 to 170 mmHg** via myogenic and tubuloglomerular feedback mechanisms.

Question 1

Each kidney contains about how many nephrons?

Accepted Answer

One million

Answer

Two million

Answer

Four million

Answer

Half million

Question 2

A normal anion gap metabolic acidosis occurs in patients with which of the following conditions?

Accepted Answer

Diarrhea

Answer

Renal failure

Answer

Salicylate poisoning

Answer

Methanol poisoning

Question 3

During pregnancy, what happens to the Glomerular Filtration Rate (GFR)?

Accepted Answer

Increases

Answer

Decreases

Answer

Remains unchanged

Answer

Increases only in multiple gestations

Question 4

Which of the following is reabsorbed in the distal convoluted tubule (DCT)?

Accepted Answer

Potassium

Answer

Water

Answer

Chloride

Answer

Sodium

Question 5

What is true about Nephrogenic diabetes insipidus?

Accepted Answer

Renal tubule unresponsiveness to ADH

Answer

There is a central decrease in secretion of ADH

Answer

Serum Na is low

Answer

Urine osmolarity is increased after ADH administration

Question 6

Active resorption of sodium ion occurs in which part of the nephron?

Accepted Answer

All of the above

Answer

Ascending loop of Henle

Answer

Early distal tubule

Answer

Proximal tubule

Question 7

Where in the kidney does active reabsorption of sodium ions occur?

Accepted Answer

All of the above

Answer

Collecting duct

Answer

Distal tubule

Answer

Ascending limb of Henle

Question 8

Albumin does not pass through the glomerulus due to the presence of what component in the glomerular filtration barrier?

Accepted Answer

Proteoglycans

Answer

Glycolipid

Answer

Phospholipid

Answer

Carbohydrates

Question 9

Renin is synthesized as a large preprohormone. Where is it secreted from?

Accepted Answer

Juxtaglomerular apparatus

Answer

Proximal Convoluted Tubule (PCT)

Answer

Distal Convoluted Tubule (DCT)

Answer

Collecting duct

Question 10

What percentage of cardiac output is supplied to the kidneys?

Accepted Answer

22%

Answer

6%

Answer

10%

Answer

14%

Renal Physiology — MCQs

Renal Physiology — MCQs

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