Which structure is responsible for filtering blood in the kidney?

Rationale:

A. Very low-density lipoprotein (VLDL) is incorrect. VLDL is considered a “bad” lipoprotein because it carries triglycerides from the liver to peripheral tissues and can contribute to plaque formation in arteries. Elevated VLDL levels increase the risk of atherosclerosis and cardiovascular disease.

B. High-density lipoproteins (HDL) is correct. HDL is referred to as “good cholesterol” because it transports excess cholesterol from peripheral tissues back to the liver for excretion or recycling. High levels of HDL are associated with reduced risk of atherosclerosis and cardiovascular events. HDL also has anti-inflammatory and antioxidant properties, providing additional protection to blood vessels.

C. Intermediate-density lipoproteins (IDL) is incorrect. IDL is a transitional lipoprotein formed during the metabolism of VLDL to LDL. It is considered atherogenic, meaning it can contribute to plaque buildup, and is not classified as “good cholesterol.”

D. Low-density lipoproteins (LDL) is incorrect. LDL is commonly referred to as “bad cholesterol” because it transports cholesterol from the liver to peripheral tissues, where it can deposit in the arterial walls and lead to atherosclerosis, heart attacks, and strokes.

Rationale:

A. Calcitonin is a hormone produced by the parafollicular cells of the thyroid gland. Its primary role is to reduce elevated blood calcium levels by inhibiting osteoclast activity and increasing calcium excretion by the kidneys. While calcitonin influences calcium and phosphate balance, it has no significant function in regulating water reabsorption in the kidneys. Disorders affecting calcitonin levels do not cause abnormalities in fluid balance or urine concentration, which makes it unrelated to the physiologic mechanism of water conservation.

B. Aldosterone is a mineralocorticoid hormone released by the adrenal cortex. It acts on the distal tubules and collecting ducts of the kidney to increase sodium reabsorption and potassium excretion. Because water follows sodium osmotically, aldosterone can indirectly contribute to water retention. However, aldosterone does not directly change the kidney’s permeability to water. Water reabsorption in the presence of aldosterone still depends on antidiuretic hormone (ADH) to insert aquaporin channels into the renal tubules. Therefore, aldosterone cannot be considered the hormone responsible for water reabsorption itself; it influences sodium handling rather than direct water movement.

C. Atrial natriuretic peptide (ANP) is a hormone released by the atria of the heart when they are stretched due to increased blood volume. ANP has the opposite effect of hormones that promote fluid retention. It increases sodium and water excretion by dilating the afferent arteriole, increasing glomerular filtration rate, and inhibiting sodium reabsorption in the collecting ducts. It also antagonizes aldosterone and renin, promoting further loss of sodium and water. Because ANP enhances diuresis rather than water conservation, it does not play a physiological role in promoting water reabsorption. Instead, it helps reduce blood volume and blood pressure.

D. Antidiuretic hormone (ADH), also called vasopressin, is the hormone directly responsible for regulating water reabsorption from the kidney tubules. ADH is synthesized in the hypothalamus and stored in the posterior pituitary, where it is released in response to increased plasma osmolality or decreased circulating blood volume. Once released, ADH binds to V2 receptors in the distal tubules and collecting ducts of the kidneys, triggering the insertion of aquaporin-2 water channels into the tubular membrane. This action increases the kidney’s permeability to water, allowing water to be reabsorbed back into the bloodstream independently of sodium. As a result, urine becomes more concentrated and plasma osmolality decreases. Clinically, ADH is essential for maintaining proper fluid balance, and abnormalities in its production or response, such as in diabetes insipidus or SIADH, lead to serious disturbances in hydration and serum sodium levels. ADH is therefore the primary and direct regulator of renal water reabsorption.