Renal Physiology — MCQs

Renal Physiology Indian Medical PG Practice Questions and MCQs

Question 461: Immediately after kidney donation what happens to the creatinine level in the donors?

A. Level is independent of the donation
B. Decreases
C. Increases (Correct Answer)
D. Remains Same

Explanation: ***Increases*** - Following the donation of one kidney, the remaining kidney experiences a temporary **reduction in overall renal mass** and a subsequent **transient decrease in glomerular filtration rate (GFR)**. - This immediate post-operative decrease in GFR leads to a **temporary rise in serum creatinine** as the body adjusts to the function of a single kidney. *Level is independent of the donation* - This statement is incorrect because the GFR is directly related to the total functional renal mass, which changes significantly after **nephrectomy**. - Renal function, as measured by creatinine, is undeniably affected by the **loss of a kidney**. *Decreases* - Creatinine levels would decrease if the **GFR of the remaining kidney improved significantly** or if there was an underlying condition causing an already elevated creatinine to normalize post-donation, neither of which is the immediate physiological response. - A decrease in creatinine after donation would imply improved kidney function or reduced burden, which is not what occurs acutely. *Remains Same* - This is unlikely because the removal of one kidney immediately **reduces the total filtration capacity** of the body by approximately half, even if there's rapid compensatory hypertrophy. - While the remaining kidney will undergo **compensatory hypertrophy and hyperfiltration** in the long term, the immediate effect is a reduction in overall GFR.

Question 462: Aldosterone mainly acts upon

A. Loop of Henle
B. Distal renal tubule (Correct Answer)
C. PCT
D. Glomerulus

Explanation: ***Distal renal tubule*** - Aldosterone primarily acts on the **principal cells** of the **distal convoluted tubule** and collecting duct. - Its main function is to promote **sodium reabsorption** and **potassium excretion** in these segments. *Loop of Henle* - The Loop of Henle is primarily involved in establishing the **medullary osmotic gradient** and reabsorbing water and solutes, but it is **not the primary site** of aldosterone action. - While some sodium is reabsorbed here, this process is largely independent of aldosterone's direct influence. *PCT* - The **proximal convoluted tubule (PCT)** is responsible for the bulk reabsorption of filtered substances, including about 65% of sodium and water. - Aldosterone has **minimal to no direct effect** on the reabsorptive processes occurring in the PCT. *Glomerulus* - The **glomerulus** is the site of **ultrafiltration**, where blood is filtered to form a protein-free filtrate. - Aldosterone has no direct action on the filtration barrier or the cells of the glomerulus.

Question 463: Deficiency of vasopressin results in:

A. Increased water loss
B. Increased urine output
C. Hyponatremia
D. Inability of the kidney to concentrate urine (Correct Answer)

Explanation: ***Inability of the kidney to concentrate urine*** - Vasopressin, also known as **Antidiuretic Hormone (ADH)**, acts on the renal collecting ducts to increase water reabsorption. - A deficiency in vasopressin means the kidneys cannot reabsorb water effectively, leading to the production of large volumes of dilute urine, which is an inability to concentrate urine. *Increased water loss* - While there is **increased water loss** from the body due to a lack of reabsorption, this is a consequence of the primary physiological defect, which is the kidney's inability to concentrate urine. - The direct effect of vasopressin deficiency is on the kidney's concentrating mechanism. *Increased urine output* - **Increased urine output**, or polyuria, is a clinical manifestation of the kidney's inability to concentrate urine due to vasopressin deficiency. - It describes the symptom rather than the underlying physiological impairment at the renal tubules. *Hyponatremia* - **Hyponatremia** (low sodium) typically occurs with an excess of ADH (like in SIADH), leading to water retention and dilutional hyponatremia. - In vasopressin deficiency (diabetes insipidus), patients are more prone to **hypernatremia** due to excessive water loss.

Question 464: All of the following are true about the action of ADH, except:

A. Acts on collecting ducts and increases water permeability
B. Secreted by neurosecretion from posterior pituitary
C. Post-operative increase in secretion
D. Increased secretion when plasma osmolality is low (Correct Answer)

Explanation: ***Increased secretion when plasma osmolality is low*** - **Antidiuretic hormone (ADH)** secretion is *inhibited* when plasma osmolality is low. - ADH is secreted to conserve water and *increase* plasma osmolality when it is too high, or plasma volume is too low. - Normal osmolality range is 280-290 mOsm/kg; ADH secretion increases above this threshold. *Acts on collecting ducts and increases water permeability* - This statement is true; ADH binds to **V2 receptors** on the principal cells of the collecting ducts. - This binding leads to the insertion of **aquaporin-2 channels** into the apical membrane, increasing water reabsorption. *Secreted by neurosecretion from posterior pituitary* - This statement is true; ADH is synthesized in the **hypothalamus** (supraoptic and paraventricular nuclei) and transported down nerve axons. - It is then stored in and released from the **posterior pituitary gland**, a process known as neurosecretion. *Post-operative increase in secretion* - This statement is true; surgical stress, pain, and common postoperative medications (e.g., narcotics) can stimulate ADH release. - This can lead to **hyponatremia** and fluid retention in the postoperative period due to excessive free water reabsorption.

Question 465: What does aquaporin deficiency cause?

A. Liddle syndrome
B. Bartter syndrome
C. Gitelman syndrome
D. Nephrogenic diabetes insipidus (Correct Answer)

Explanation: ***Nephrogenic diabetes insipidus*** - Aquaporins, specifically **aquaporin-2**, are crucial for **water reabsorption** in the renal collecting ducts in response to ADH. - A deficiency or dysfunction of aquaporins leads to the kidneys being unable to concentrate urine, resulting in **excessive dilute urine production** and **polydipsia**, characteristic of nephrogenic diabetes insipidus. *Liddle syndrome* - This is an **autosomal dominant** disorder caused by a **gain-of-function mutation** in the **epithelial sodium channel (ENaC)**, leading to increased sodium reabsorption and hypertension. - It does not involve aquaporin deficiency but rather an overactive sodium channel. *Bartter syndrome* - Characterized by mutations in the **Na-K-2Cl cotransporter (NKCC2)** in the thick ascending limb of the loop of Henle, leading to impaired reabsorption of sodium, potassium, and chloride. - It results in **hypokalemia**, **metabolic alkalosis**, and **hypotension**, and is not directly caused by aquaporin deficiency. *Gitelman syndrome* - Caused by mutations in the **thiazide-sensitive Na–Cl cotransporter (NCC)** in the distal convoluted tubule, impairing sodium and chloride reabsorption. - It presents with symptoms similar to thiazide diuretic use, including **hypokalemia**, **hypomagnesemia**, and **metabolic alkalosis**, and is distinct from aquaporin-related disorders.

Question 466: Calculate net filtration pressure with the following data: PGC = 42 mm Hg, πGC = 12 mm Hg, PBC = 16 mm Hg. Assume that no proteins were filtered.

A. 14 mm Hg (Correct Answer)
B. 28 mm Hg
C. Data not sufficient
D. 34 mm Hg

Explanation: ***14 mm Hg*** - The **net filtration pressure (NFP)** is calculated using the formula: **NFP = (PGC - PBC) - πGC**. - Plugging in the given values: (42 mmHg - 16 mmHg) - 12 mmHg = 26 mmHg - 12 mmHg = **14 mmHg**. *28 mm Hg* - This answer likely results from an incorrect application of the NFP formula, such as adding the oncotic pressure instead of subtracting it, or miscalculating the difference between hydrostatic pressures. - For example, if both hydrostatic and oncotic pressures were added (42 + 12 + 16), it would yield a much higher number, or if the subtraction was done incorrectly. *Data not sufficient* - All necessary variables for calculating the NFP are provided: **glomerular hydrostatic pressure (PGC)**, **glomerular oncotic pressure (πGC)**, and **Bowman's capsule hydrostatic pressure (PBC)**. - The assumption that "no proteins were filtered" simplifies the calculation, confirming that sufficient data is available. *34 mm Hg* - This result would occur if the oncotic pressure in Bowman's capsule (πBC) was incorrectly considered, or if a different formulation of the NFP calculation was used. - Given that **πBC is assumed to be zero** (as no proteins are filtered into Bowman's capsule), any calculation that leads to 34 mmHg is likely based on an error in applying the formula, such as adding **πGC** instead of subtracting it from the hydrostatic pressure difference.

Question 467: GFR is increased by all except?

A. Renal stone in ureter (Correct Answer)
B. Efferent arteriole constriction
C. Increased renal blood flow
D. Decreased oncotic pressure

Explanation: ***Renal stone in ureter*** - A renal stone in the ureter causes **post-renal obstruction**, leading to a buildup of pressure in the Bowman's capsule, which in turn **reduces GFR**. - **Obstruction** impedes urine outflow, thereby increasing **hydrostatic pressure** in the tubular system and opposing filtration. *Efferent arteriole constriction* - **Constriction of the efferent arteriole** increases the **hydrostatic pressure** within the glomerulus, which promotes an increase in GFR. - This constriction retains blood in the glomerulus, thereby increasing the **filtration pressure**. *Increased renal blood flow* - An **increase in renal blood flow** elevates the **glomerular hydrostatic pressure** and increases the amount of plasma available for filtration, leading to an **increased GFR**. - A higher flow rate also helps to maintain a more constant **glomerular capillary oncotic pressure**, preventing early filtration equilibrium. *Decreased oncotic pressure* - **Decreased oncotic pressure** in the glomerular capillaries (e.g., due to hypoproteinemia) reduces the osmotic force opposing filtration. - This reduction in opposing force allows for a net increase in the **filtration pressure**, thereby **increasing GFR**.

Question 468: Which of the following is not an effect of efferent arteriole constriction:

A. Increased glomerular hydrostatic pressure
B. Decreased blood flow in peritubular vessels
C. Decreased GFR (Correct Answer)
D. Increased oncotic pressure in peritubular vessels

Explanation: ***Decreased GFR*** - **Efferent arteriole constriction** typically *increases* GFR, not decreases it - Constriction raises **glomerular hydrostatic pressure** (PGC) by increasing resistance to outflow, which *enhances* the driving force for filtration - The initial and predominant effect is an **increase in GFR**, making "Decreased GFR" NOT a typical effect - Only with *severe* prolonged constriction might GFR eventually fall due to markedly reduced renal blood flow and extreme protein concentration *Increased glomerular hydrostatic pressure* - This IS an effect of efferent arteriole constriction - Constriction increases resistance to blood leaving the glomerulus, causing blood to "back up" and **raising hydrostatic pressure** in glomerular capillaries - This elevated pressure directly increases the filtration force *Decreased blood flow in peritubular vessels* - This IS an effect of efferent arteriole constriction - Blood exits the glomerulus through the efferent arteriole to reach peritubular capillaries - Constriction restricts this outflow, resulting in **reduced blood flow** to downstream peritubular vessels *Increased oncotic pressure in peritubular vessels* - This IS an effect of efferent arteriole constriction - As filtration increases due to higher glomerular pressure, plasma proteins (which cannot be filtered) become more concentrated in the blood - This concentrated blood flows into peritubular capillaries, resulting in **elevated oncotic pressure** that favors reabsorption

Question 469: Which of the following is the diluting segment of kidney?

A. Collecting duct
B. Descending loop of Henle
C. PCT
D. Ascending thick loop of Henle (Correct Answer)

Explanation: ***Ascending thick loop of Henle*** - The **thick ascending limb of the loop of Henle** is known as the *diluting segment* because it actively reabsorbs **solutes (Na+, K+, Cl-)** but is impermeable to **water**. - This action leads to a decrease in the osmolality of the tubular fluid, effectively *diluting* it entering the distal tubule. *Collecting duct* - The collecting duct is primarily involved in **water reabsorption** under the influence of **ADH**, which can concentrate the urine. - While it can reabsorb some solutes, its main role is to regulate **final urine concentration**. *Descending loop of Henle* - The descending loop of Henle is highly permeable to **water** but relatively impermeable to **solutes**. - As water leaves this segment, the tubular fluid becomes more **concentrated**, not diluted. *PCT* - The **proximal convoluted tubule (PCT)** reabsorbs a large percentage of both **water and solutes** in an isotonic manner. - Although it reduces the volume of filtrate, it does not significantly change its **osmolality** (i.e., it doesn't dilute the fluid).

Question 470: True about countercurrent multiplier system in the kidney except:

A. Involves collecting duct (Correct Answer)
B. Occurs in Loop of Henle
C. Requires NaCl transport
D. Creates hyperosmotic medulla

Explanation: ***Involves collecting duct*** - The **collecting duct** is *not* part of the countercurrent *multiplier* system but rather the countercurrent *exchange* system, - The collecting duct is the target of **ADH** where fine-tuning of water reabsorption occurs, influenced by the medullary osmotic gradient generated by the multiplier. *Occurs in Loop of Henle* - The **Loop of Henle**, specifically the ascending and descending limbs, is the anatomical site where the **countercurrent multiplier** system operates. - This structure's unique hairpin turn and differing permeabilities are crucial for establishing the osmotic gradient. *Requires NaCl transport* - Active transport of **NaCl** in the thick ascending limb of the Loop of Henle is the *driving force* for the countercurrent multiplication process. - This reabsorption of solutes without water permeability creates the initial osmotic gradient. *Creates hyperosmotic medulla* - The primary function of the **countercurrent multiplier** system is to establish and maintain a **hyperosmotic medullary interstitium**. - This high osmolarity is essential for subsequent water reabsorption from the collecting ducts, allowing for the concentration of urine.

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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