Renal Physiology Practice Questions

Q: Which of the following results in increased ADH activity?

Hypovolemia. ***Hypovolemia*** - **Hypovolemia** (decreased blood volume) is a potent stimulus for antidiuretic hormone (ADH) release, as the body attempts to conserve water and increase blood volume. - Reduced **stretch receptor activity** in the atria and great vessels due to decreased blood volume signals the posterior pituitary to release ADH. *Hypervolemia* - **Hypervolemia** (increased blood volume) would lead to a *decrease* in ADH activity, as the body tries to excrete excess water to normalize blood volume. - Increased stretch receptor activity in the atria inhibits ADH release. *Hypertension* - **Hypertension** (high blood pressure) generally *reduces* ADH secretion because the increased stretch on baroreceptors signals to decrease fluid volume. - This typically promotes diuresis rather than water retention. *Decrease osmolarity* - A **decrease in plasma osmolarity** (more dilute blood) inhibits ADH release, as the body aims to excrete excess water to bring osmolarity back to normal. - **Osmoreceptors** in the hypothalamus are sensitive to changes in plasma osmolarity and are the primary regulators of ADH secretion.

Q: Calcitriol is formed in:

PCT. ***PCT*** - The final step in calcitriol (active vitamin D) synthesis, 1-alpha hydroxylation, primarily occurs in the **proximal convoluted tubule (PCT)** cells of the kidney. - This enzymatic step converts **25-hydroxyvitamin D** into the potent hormone **1,25-dihydroxyvitamin D (calcitriol)**, which regulates calcium and phosphate homeostasis. *Glomerulus* - The **glomerulus** is primarily responsible for **filtering blood** to form ultrafiltrate, not for hormone synthesis. - While vitamin D precursors are filtered, the enzymatic conversion to calcitriol does not occur here. *Bowman's capsule* - **Bowman's capsule** surrounds the glomerulus and collects the filtered fluid, acting as a passive receiver. - It plays no direct role in the synthesis or metabolism of vitamin D. *DCT* - The **distal convoluted tubule (DCT)** is involved in fine-tuning reabsorption of ions like calcium and sodium, responding to hormones. - It is not the primary site for the **1-alpha hydroxylation** required for calcitriol synthesis.

Q: Which of the following does not have a Tm value?

Creatinine. ***Creatinine*** - **Creatinine** is freely filtered at the glomerulus but is **not reabsorbed** by the renal tubules. - Since there is **no reabsorption mechanism** for creatinine, there is no tubular maximum (Tm) for reabsorption. - A small amount of creatinine is secreted in the proximal tubule, but secretion mechanisms are distinct from the Tm concept which applies to reabsorption. - This makes creatinine an excellent marker for **glomerular filtration rate (GFR)** assessment. *Glucose* - **Glucose** has a well-defined **tubular maximum (Tm)** of approximately **375 mg/min** in adults. - It is reabsorbed via specific carrier proteins (**SGLT2** in early proximal tubule, **SGLT1** in late proximal tubule). - When plasma glucose exceeds the renal threshold (~180 mg/dL), the carriers become saturated and glucose appears in urine (glucosuria). *Urea* - **Urea** undergoes passive reabsorption driven by concentration gradients, particularly in the proximal tubule (~50%) and collecting duct. - While primarily passive, urea transporters (UT-A1, UT-A3) facilitate its movement and can exhibit **saturation kinetics**. - Some sources consider urea to have a form of Tm, though it's less clearly defined than glucose. *Na+* - **Na+** reabsorption occurs via multiple carrier-mediated mechanisms including **Na-K-ATPase**, Na-H exchangers, and various cotransporters. - These carrier systems **do exhibit saturation kinetics** and can be considered to have Tm characteristics, particularly in the proximal tubule where ~65% of filtered Na+ is reabsorbed. - However, Na+ handling is also heavily regulated by hormones (aldosterone, ANP) and hemodynamic factors, making its Tm less clinically apparent than glucose.

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

Increases. ***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.

Q: Aldosterone mainly acts upon

Distal renal tubule. ***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.

Q: Deficiency of vasopressin results in:

Inability of the kidney to concentrate urine. ***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.

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

Increased secretion when plasma osmolality is low. ***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.

Q: What does aquaporin deficiency cause?

Nephrogenic diabetes insipidus. ***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.

Q: 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.

14 mm Hg. ***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.

Q: GFR is increased by all except?

Renal stone in ureter. ***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 1

Which of the following results in increased ADH activity?

Accepted Answer

Hypovolemia

Answer

Hypervolemia

Answer

Hypertension

Answer

Decrease osmolarity

Question 2

Calcitriol is formed in:

Accepted Answer

PCT

Answer

Glomerulus

Answer

Bowman's capsule

Answer

DCT

Question 3

Which of the following does not have a Tm value?

Accepted Answer

Creatinine

Answer

Urea

Answer

Glucose

Answer

Na+

Question 4

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

Accepted Answer

Increases

Answer

Level is independent of the donation

Answer

Decreases

Answer

Remains Same

Question 5

Aldosterone mainly acts upon

Accepted Answer

Distal renal tubule

Answer

Loop of Henle

Answer

PCT

Answer

Glomerulus

Question 6

Deficiency of vasopressin results in:

Accepted Answer

Inability of the kidney to concentrate urine

Answer

Increased water loss

Answer

Increased urine output

Answer

Hyponatremia

Question 7

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

Accepted Answer

Increased secretion when plasma osmolality is low

Answer

Acts on collecting ducts and increases water permeability

Answer

Secreted by neurosecretion from posterior pituitary

Answer

Post-operative increase in secretion

Question 8

What does aquaporin deficiency cause?

Accepted Answer

Nephrogenic diabetes insipidus

Answer

Liddle syndrome

Answer

Bartter syndrome

Answer

Gitelman syndrome

Question 9

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.

Accepted Answer

14 mm Hg

Answer

28 mm Hg

Answer

Data not sufficient

Answer

34 mm Hg

Question 10

GFR is increased by all except?

Accepted Answer

Renal stone in ureter

Answer

Efferent arteriole constriction

Answer

Increased renal blood flow

Answer

Decreased oncotic pressure

Renal Physiology — MCQs

Renal Physiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?