Concentration and Dilution of Urine — MCQs
All of the following functions of vasopressin are mediated by V1 receptors, except
The site of action of vasopressin is
What happens to the concentration of inulin as fluid passes through the Proximal Convoluted Tubule (PCT)?
Which of the following is the primary mechanism that drives sodium reabsorption in the proximal tubule?
Which of the following is not true about syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
In a normally functioning kidney, which part of the nephron has the lowest permeability to water during antidiuresis?
A substance has a clearance similar to inulin clearance. How is this substance primarily excreted in urine?
Polyuria with low fixed specific gravity urine is seen in ?
A 10 year old boy is having polyuria, polydipsia, laboratory data showed (in mEq/lit) – Na+ 154, K+ 4.5, HCO3- 22, Serum osmolality – 295 mOsm/kg, Blood urea – 50 mg/dl, Urine specific gravity – 1.005. The likely diagnosis is –
Hormone primarily responsible for blood pressure regulation following acute blood loss is:
Concentration and Dilution of Urine Indian Medical PG Practice Questions and MCQs
Question 1: All of the following functions of vasopressin are mediated by V1 receptors, except
- A. Vasoconstriction
- B. Smooth muscle contraction
- C. Water reabsorption (Correct Answer)
- D. None of the options
Explanation: ***Water reabsorption*** - Vasopressin's effect on **water reabsorption** in the kidney collecting ducts is primarily mediated by **V2 receptors**. - **V2 receptors** activate a G protein-coupled signaling pathway leading to the insertion of **aquaporin-2 channels** into the apical membrane, increasing water permeability. *Vasoconstriction* - **Vasoconstriction** is a well-known function of vasopressin, mediated by its binding to **V1a receptors** (a subtype of V1 receptors) on vascular smooth muscle cells. - This activation leads to an increase in **intracellular calcium**, causing the muscle cells to contract and the blood vessels to narrow. *Smooth muscle contraction* - Vasopressin can induce **smooth muscle contraction** in various tissues, including the gastrointestinal tract and uterus, primarily through **V1 receptors**. - This effect is similar to its vasoconstrictor action, involving **calcium mobilization** and muscle fiber shortening. *None of the options* - This option is incorrect because **water reabsorption** is indeed mediated by V2 receptors, not V1 receptors. - The other functions listed (vasoconstriction and smooth muscle contraction) are correctly attributed to **V1 receptors**.
Question 2: The site of action of vasopressin is
- A. Descending limb of the loop of Henle
- B. Proximal tubule
- C. Distal tubule and collecting duct (Correct Answer)
- D. Ascending limb of the loop of Henle
Explanation: ***Distal tubule*** - Vasopressin, also known as **antidiuretic hormone (ADH)**, primarily acts on the collecting ducts and the late distal convoluted tubule. - Its main function is to increase the **reabsorption of water** by inserting **aquaporin-2 channels** into the apical membrane of principal cells. *Ascending limb of the loop of Henle* - This segment is largely **impermeable to water** regardless of hormonal influence, focusing on active reabsorption of solutes. - Its primary role is to dilute the tubular fluid and reabsorb ions like **Na+, K+, and Cl-**. *Descending limb of the loop of Henle* - This limb is freely permeable to water but largely impermeable to solutes, allowing water to exit the tubule due to the **medullary osmotic gradient**. - Vasopressin does not significantly influence water permeability in this segment. *Proximal tubule* - The proximal tubule reabsorbs a large percentage (about 65-70%) of filtered water and solutes in a relatively unregulated manner. - Its function is largely independent of vasopressin, which acts further down the nephron to fine-tune water reabsorption.
Question 3: What happens to the concentration of inulin as fluid passes through the Proximal Convoluted Tubule (PCT)?
- A. Concentration of inulin increases (Correct Answer)
- B. Concentration of urea remains constant
- C. Concentration of HCO3- increases
- D. Concentration of Na+ decreases
Explanation: ***Concentration of inulin increases*** - Inulin is **freely filtered** at the glomerulus and is neither reabsorbed nor secreted along the renal tubule, making it an excellent marker for **glomerular filtration rate (GFR)**. - As water is reabsorbed from the PCT, the volume of tubular fluid decreases, causing the concentration of **unreabsorbed solutes**, like inulin, to increase. *Concentration of urea remains constant* - Urea is **reabsorbed** along the tubule, though passively; its concentration typically **increases** initially in the PCT due to water reabsorption, but then decreases as some is reabsorbed. - The statement is incorrect because urea concentration changes significantly throughout the nephron, particularly increasing as water is reabsorbed and then decreasing with some reabsorption. *Concentration of HCO3- increases* - The majority (approximately 80-90%) of **bicarbonate (HCO3-)** is reabsorbed in the PCT, primarily through its conversion to CO2 within the tubular lumen and then back to HCO3- intracellularly. - Therefore, the concentration of HCO3- in the tubular fluid actually **decreases** significantly as fluid passes through the PCT. *Concentration of Na+ decreases* - **Sodium (Na+)** is actively reabsorbed along the entire nephron, with about 65-70% reabsorbed in the PCT. - While Na+ is reabsorbed, water follows passively, so its concentration in the tubular fluid remains relatively **iso-osmotic** with plasma, meaning its concentration does not significantly decrease as fluid passes through the PCT, remaining fairly constant.
Question 4: Which of the following is the primary mechanism that drives sodium reabsorption in the proximal tubule?
- A. Sodium reabsorption through cotransport with amino acids at the luminal membrane.
- B. Sodium reabsorption through cotransport with glucose at the luminal membrane.
- C. Sodium reabsorption through countertransport with hydrogen ions at the luminal membrane.
- D. Active sodium transport via the Na+-K+-ATPase pump at the basolateral membrane. (Correct Answer)
Explanation: ***Active sodium transport via the Na+-K+-ATPase pump at the basolateral membrane.*** - This pump **actively transports sodium out of the cell** into the interstitial fluid, creating a low intracellular sodium concentration. - The **Na+-K+-ATPase** is the primary driver of sodium reabsorption throughout the nephron, creating the electrochemical gradient for other sodium transporters. *Sodium reabsorption through cotransport with amino acids at the luminal membrane.* - While **sodium-amino acid cotransport** does occur in the proximal tubule, it accounts for only a fraction of total sodium reabsorption. - The primary driving force for this cotransport is the **low intracellular sodium concentration** maintained by the Na+-K+-ATPase. *Sodium reabsorption through cotransport with glucose at the luminal membrane.* - **Sodium-glucose cotransporters (SGLTs)** are crucial for glucose reabsorption in the proximal tubule, moving glucose into the cell along with sodium. - However, glucose cotransport represents a specific mechanism for glucose handling, not the overarching mechanism for sodium reabsorption. *Sodium reabsorption through countertransport with hydrogen ions at the luminal membrane.* - The **Na+-H+ exchanger (NHE3)** is significant for exchanging sodium for hydrogen ions at the luminal membrane in the proximal tubule. - This mechanism is important for **acid-base balance** and some sodium reabsorption, but it is secondary to the Na+-K+-ATPase in driving the overall sodium gradient.
Question 5: Which of the following is not true about syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
- A. Patient can be clinically euvolemic to hypovolemic
- B. Urine osmolality >100 mOsm/kg
- C. Urinary sodium <20 mEq/L (Correct Answer)
- D. Serum sodium <135 mEq/L
Explanation: ***Urinary sodium <20 mEq/L*** - In **SIADH**, the inappropriate secretion of ADH leads to increased water reabsorption, causing **dilutional hyponatremia**. [1] - The kidneys respond by trying to excrete excess water and dilute the urine, leading to **increased urinary sodium concentration**, typically *greater than* 20 mEq/L. *Patient can be clinically euvolemic to hypovolemic* - Patients with **SIADH** are typically **euvolemic** because the excess water is retained intracellularly and extracellularly in balanced proportions, without significant edema or dehydration. [1] - While fluid retention occurs, it's not enough to cause significant clinical volume overload, and they are never truly hypovolemic. *Urine osmolality >100 mOsm/kg* - In **SIADH**, the continued action of **ADH** despite hypotonicity results in the reabsorption of water, leading to the production of **concentrated urine**. [1] - This elevated urine osmolality, typically **greater than 100 mOsm/kg**, indicates an inability to adequately excrete free water. [1] *Serum sodium <135 mEq/L* - **SIADH** is defined by **hyponatremia**, a serum sodium concentration **below 135 mEq/L**, due to the excessive retention of water. - This dilutes the extracellular fluid, leading to a reduction in the relative concentration of sodium.
Question 6: In a normally functioning kidney, which part of the nephron has the lowest permeability to water during antidiuresis?
- A. Distal Convoluted Tubule
- B. Proximal Convoluted Tubule
- C. Thick Ascending Limb of Loop of Henle (Correct Answer)
- D. Collecting Duct
Explanation: ***Thick Ascending Limb of Loop of Henle*** - This segment is **completely impermeable to water** regardless of the presence of ADH, making it the segment with the lowest water permeability in the nephron. - Its primary function is to actively reabsorb solutes like **Na+, K+, and Cl-** via the Na-K-2Cl cotransporter, diluting the tubular fluid without water following. - This impermeability is critical for establishing and maintaining the **medullary osmotic gradient**. *Proximal Convoluted Tubule* - The **proximal convoluted tubule** is highly permeable to water, responsible for reabsorbing about **65% of filtered water** through constitutively expressed aquaporin-1 (AQP-1) channels. - Water reabsorption here is obligatory and **not regulated by ADH**. *Distal Convoluted Tubule* - The **distal convoluted tubule** has low water permeability in the absence of ADH but can be increased when ADH is present (though less responsive than the collecting duct). - Its primary role is in fine-tuning electrolyte reabsorption, particularly **sodium and calcium**. *Collecting Duct* - The **collecting duct** has variable water permeability that is highly **ADH-dependent**. - During antidiuresis (high ADH), aquaporin-2 channels are inserted into the apical membrane, making it highly permeable to water for final urine concentration. - Without ADH, it has low permeability, but it's never as impermeable as the thick ascending limb.
Question 7: A substance has a clearance similar to inulin clearance. How is this substance primarily excreted in urine?
- A. Tubular Secretion
- B. Glomerular filtration (Correct Answer)
- C. Vascular leakage
- D. Both tubular secretion and glomerular filtration
Explanation: ***Glomerular filtration*** - **Inulin** is a gold standard for measuring **glomerular filtration rate** (GFR) because it is freely filtered by the glomeruli and is neither reabsorbed nor secreted by the renal tubules. - Therefore, a substance with clearance similar to inulin is primarily excreted via **glomerular filtration**. *Tubular Secretion* - If a substance were primarily excreted by tubular secretion, its clearance would be **higher than the GFR**, as secretion adds more of the substance to the urine than filtration alone. - This mechanism is characteristic of substances like **para-aminohippurate (PAH)**, which is used to measure renal plasma flow. *Vascular leakage* - **Vascular leakage** is not a normal mechanism of substance excretion in the urine. - It refers to the abnormal passage of fluid and macromolecules from blood vessels into tissues, often seen in conditions like inflammation or sepsis, and does not directly contribute to renal clearance. *Both tubular secretion and glomerular filtration* - If a substance were excreted by both **tubular secretion and glomerular filtration**, its clearance would also be **higher than the GFR**, similar to substances that undergo significant tubular secretion. - The fact that its clearance is *similar* to inulin specifically points to filtration as the predominant and almost exclusive mechanism.
Question 8: Polyuria with low fixed specific gravity urine is seen in ?
- A. Diabetes mellitus
- B. Diabetes insipidus
- C. Chronic glomerulonephritis (Correct Answer)
- D. Potomania
Explanation: ***Chronic glomerulonephritis*** - Damage to the **renal tubules** in chronic glomerulonephritis impairs their ability to concentrate urine, leading to polyuria with a **low, fixed specific gravity**. [1] - This fixed specific gravity reflects the kidneys' inability to adjust urine concentration in response to hydration status, a hallmark of **chronic kidney disease**. [2] *Diabetes mellitus* - Polyuria in diabetes mellitus is caused by **osmotic diuresis** due to high glucose levels in the urine, leading to increased urinary volume. [2] - While there is polyuria, the specific gravity is not necessarily fixed and can vary, often being high due to the presence of glucose. *Diabetes insipidus* - Diabetes insipidus causes polyuria and dilute urine due to either a deficiency of **ADH (central DI)** or renal unresponsiveness to ADH **(nephrogenic DI)**. - While it causes polyuria with low specific gravity, it's typically *not* fixed; the urine specific gravity can still fluctuate to some extent depending on the patient's hydration, or in response to ADH if it's central DI. *Potomania* - Potomania, or **primary polydipsia**, is excessive water intake that leads to dilutional hyponatremia and polyuria. - The kidneys are otherwise healthy and can still concentrate urine to some extent if water intake is restricted, preventing a truly fixed low specific gravity.
Question 9: A 10 year old boy is having polyuria, polydipsia, laboratory data showed (in mEq/lit) – Na+ 154, K+ 4.5, HCO3- 22, Serum osmolality – 295 mOsm/kg, Blood urea – 50 mg/dl, Urine specific gravity – 1.005. The likely diagnosis is –
- A. Barter's syndrome
- B. Recurrent UTI
- C. Diabetes insipidus (Correct Answer)
- D. Renal tubular acidosis
Explanation: ***Diabetes insipidus*** - The classic presentation of **polyuria and polydipsia** with **hypernatremia (Na+ 154 mEq/L)** and **low urine specific gravity (1.005)** indicates inability to concentrate urine. - The **serum osmolality of 295 mOsm/kg** (upper limit of normal) in the context of hypernatremia suggests inadequate water reabsorption, consistent with **diabetes insipidus (either central or nephrogenic)**. - The dilute urine despite elevated serum sodium is pathognomonic for DI. *Barter's syndrome* - Characterized by **hypokalemic metabolic alkalosis**, increased renin and aldosterone, and normal to low blood pressure. - The given laboratory values show **normal potassium (4.5 mEq/L)** and **normal bicarbonate (22 mEq/L)**, ruling out Barter's syndrome. - Results from defects in the **Na-K-2Cl cotransporter** in the thick ascending limb of loop of Henle. *Recurrent UTI* - While UTIs may cause polyuria and polydipsia, they typically present with **dysuria, fever, urgency, and pyuria/bacteriuria**. - UTIs do not cause **hypernatremia** or the specific pattern of dilute urine with elevated serum sodium. - The clinical picture does not suggest infectious etiology. *Renal tubular acidosis* - RTA presents with **metabolic acidosis** (low bicarbonate, typically <15-18 mEq/L) with normal anion gap. - The **normal bicarbonate level (22 mEq/L)** excludes RTA. - Often associated with hypokalemia, growth retardation, and nephrocalcinosis in children.
Question 10: Hormone primarily responsible for blood pressure regulation following acute blood loss is:
- A. Aldosterone
- B. ANP
- C. Epinephrine
- D. ADH (Correct Answer)
Explanation: ***ADH*** - **Antidiuretic hormone (ADH)**, also known as **vasopressin**, is released in response to decreased blood volume and pressure detected by **baroreceptors**. - Its primary role is to increase water reabsorption in the **renal collecting ducts** and cause **vasoconstriction**, both of which help restore blood volume and pressure. - This makes ADH the key **hormonal mechanism** for BP regulation following acute blood loss. *Aldosterone* - **Aldosterone** is crucial for long-term **blood pressure regulation** by increasing sodium and water reabsorption in the kidneys. - While important for volume restoration, its effects are **slower** (hours) and more focused on electrolyte balance rather than immediate BP stabilization after acute blood loss. *ANP* - **Atrial natriuretic peptide (ANP)** is released in response to **atrial stretch** due to increased blood volume and acts to lower blood pressure. - It promotes **vasodilation** and **sodium/water excretion**, counteracting the body's efforts to raise blood pressure after blood loss. - ANP levels are **suppressed** during hypovolemia. *Epinephrine* - **Epinephrine** increases heart rate and cardiac contractility, and causes vasoconstriction, providing an immediate increase in blood pressure. - However, it's primarily a **catecholamine** (not a classic hormone) part of the **sympathetic nervous system** response, and while it acts immediately, ADH provides the sustained hormonal BP regulation.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free