A client with nephrotic syndrome is admitted with swelling and foamy urine. Which finding does the nurse expect?

Rationale:

A. Purulent fluid is thick, opaque, and often yellow, green, or brown in color. It contains leukocytes, cellular debris, and bacteria, and is typically associated with infection. Because purulent fluid is not clear, it does not match the description provided by the client.

B. Hemorrhagic fluid contains blood. It appears red or dark red due to the presence of red blood cells and indicates bleeding into a wound or blister. Hemorrhagic fluid is not clear, so it does not correspond to the fluid described.

C. Serosanguineous fluid is a mixture of clear (serous) fluid and small amounts of blood, giving it a pale pink or light red appearance. While it is partially clear, the presence of blood changes its color, making it different from completely clear fluid.

D. Serous fluid is a clear, watery fluid that is typically seen in blisters caused by friction or minor burns. It is composed mainly of plasma and electrolytes and functions to cushion and protect underlying tissues. The fluid described by the client as “clear” corresponds to serous fluid, making it the correct classification.

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.