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Question:

A 76-year-old man comes to the hospital due to acute, bright red blood from the rectum.  The patient had 3 large bloody bowel movements this morning, and he has felt light-headed and dizzy since.  He has a history of sigmoid diverticulosis and, 2 years ago, had a similar episode of bleeding that resolved spontaneously.  Temperature is 36.9 C (98.4 F), blood pressure is 90/50 mm Hg, and pulse is 110/min.  Examination shows mild lethargy and delayed capillary refill.  Abdominal examination shows no abnormalities.  Which of the following physiologic changes in kidney function would be most likely in this patient?

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Explanation:

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This patient has acute gastrointestinal hemorrhage resulting in hypovolemic shock.  Clinically significant hypovolemia can occur due to acute blood loss, third-spacing (eg, pancreatitis, vasodilation in sepsis), or renal or gastrointestinal losses (eg, excessive diuresis, diarrhea).  Signs of hypovolemia include dry skin with decreased turgor, dry mucous membranes, decreased urine output, and orthostatic hypotension.

Changes in blood volume or osmolality are detected by sensors in the carotid, hypothalamus, atria, and kidneys and result in activation of multiple compensatory mechanisms:

  • Activation of the renin-angiotensin-aldosterone system results in systemic vasoconstriction and increased aldosterone release.  Aldosterone increases sodium reabsorption and potassium excretion in the distal tubule and collecting duct.
  • The hypothalamus stimulates thirst and increases the secretion of antidiuretic hormone (via the posterior pituitary), which promotes water reabsorption in the collecting duct and increases systemic vasoconstriction.
  • Sympathetic activity increases renal tubular sodium reabsorption, cardiac output, and systemic vasoconstriction.

The net effect is a rapid increase in blood pressure that helps maintain tissue perfusion, while the kidney begins the slower process of restoring circulatory volume by increasing sodium, urea, and water reabsorption.  Increased urea reabsorption is mediated by antidiuretic hormone, which increases urea permeability in the inner medullary collecting ducts. The increase in urea reabsorption accentuates the medullary concentration gradient, promoting maximal free water retention.  These actions typically result in an elevated serum urea level and blood urea nitrogen/creatinine ratio (typically >20:1).  Urine parameters typically show low urine sodium concentration (<20 mEq/L), low fractional excretion of sodium, high urine osmolality (>450 mOsmol/kg), and elevated urine potassium.

(Choices A, B, and C)  Hypovolemia leads to increased renal salt reabsorption and elevated urine osmolality due to high serum levels of aldosterone and antidiuretic hormone.

(Choices D and E)  Renal blood flow and tubular hydrostatic pressure are decreased, not increased, in patients with hypovolemia.  Although activation of the renin-angiotensin-aldosterone system increases renal blood flow and tubular hydrostatic pressure in an attempt to maintain the glomerular filtration rate, these would still be lower in this patient than in a healthy patient.

Educational objective:
Compensatory mechanisms for hypovolemia include activation of the renin-angiotensin-aldosterone system and increased antidiuretic hormone release.  This results in increased renal sodium, chloride, water, and urea reabsorption with increased potassium excretion.