The nurse is caring for a client with a pulmonary embolism. Which of the following manifestations are most prominent in a client with a pulmonary embolism?

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.

Rationale:

A. Dark, cloudy urine and facial edema are hallmark features of post-streptococcal glomerulonephritis (PSGN). PSGN is an immune-mediated disorder that develops after infection with nephritogenic strains of Streptococcus pyogenes, typically following a throat or skin infection. Immune complexes deposit in the glomeruli, leading to inflammation and damage to the filtration barrier. This results in hematuria, causing dark or tea-colored urine, and proteinuria, which contributes to fluid retention. Sodium and water retention lead to edema, often first noticeable in the periorbital area, and hypertension may also develop due to volume expansion.

B. Elevated serum calcium is not associated with PSGN. Calcium levels in the blood are primarily regulated by parathyroid hormone, vitamin D, and renal excretion of calcium. PSGN primarily affects glomerular filtration and fluid balance, not calcium metabolism. Any abnormalities in calcium would likely be incidental or due to other conditions, not a direct consequence of post-streptococcal glomerulonephritis.

C. Sudden onset of severe flank pain is more typical of renal calculi (kidney stones) or acute pyelonephritis. Kidney stones can obstruct urine flow, causing sharp, colicky flank pain radiating to the groin. Pyelonephritis, an infection of the renal pelvis, may cause flank pain accompanied by fever and urinary symptoms. PSGN, however, does not usually produce acute pain; its manifestations are primarily related to glomerular inflammation and fluid retention rather than obstruction or infection.

D. Excessive concentrated urine output and low blood pressure is inconsistent with PSGN. In PSGN, the glomerular injury reduces filtration, often causing oliguria (reduced urine output). Retained sodium and water contribute to fluid overload and hypertension rather than hypotension. Excessively concentrated urine is more characteristic of conditions with high antidiuretic hormone activity or dehydration, not post-infectious glomerulonephritis.