A 28-year-old man is hospitalized following a motor vehicle collision complicated by severe hemorrhage. Over the next 8 hours his urine output is markedly decreased. Laboratory results reveal elevated blood urea nitrogen. The patient is given aggressive intravenous fluid hydration. After 24 hours of therapy, urine output is increased and blood urea nitrogen declines toward normal. Which of the following additional laboratory abnormalities suggests that this patient's initial oliguria is a compensation for volume contraction?
Acute kidney injury | ||
Prerenal | Acute tubular necrosis | |
Mechanism | Decreased renal perfusion (eg, hypovolemia, CHF) | Renal ischemia (eg, hemorrhage, sepsis) or nephrotoxins (eg, aminoglycosides, radiocontrast) |
BUN/creatinine ratio | Typically >20 | Typically ~10-15 |
Fractional excretion of sodium | <1% | >2% |
Urine osmolality | >500 mOsm/kg | ~300 mOsm/kg |
Microscopy | Hyaline casts | Muddy brown casts |
BUN = blood urea nitrogen; CHF = congestive heart failure. | ||
This patient developed symptoms of acute renal failure (ARF) (eg, low urine output, high blood urea nitrogen) after a massive hemorrhage. ARF can be classified according to 1 of 3 etiologies:
Prerenal: Caused by decreased renal perfusion; the nephrons remain intact and tubular function is preserved. Etiologies include volume loss (eg, hemorrhage), low-output states (eg, myocardial infarction, congestive heart failure), or systemic vasodilation (eg, sepsis).
Intrinsic: Caused by tubular epithelial or glomerular damage; resorptive capacity is lost. Etiologies include acute tubular necrosis (due to renal ischemia or nephrotoxins) or glomerular diseases (eg, glomerulonephritis, nephrotic syndrome).
Postrenal: Caused by urinary tract obstruction with normal nephron capacity. Etiologies include bilateral calculi, enlarged prostate, or a renal tumor in an individual with a sole functional kidney.
This patient with severe blood loss was at risk for prerenal and intrinsic renal failure; however, his rapid improvement with hydration suggests a prerenal (hypovolemic) etiology. His laboratory results reflect intact renal tubular function, with compensatory mechanisms to restore blood volume. Increased tubular sodium reabsorption results in low urine sodium (<20 mEq/L) and low fractional excretion of sodium (FENa), whereas increased water reabsorption leads to high urine osmolarity. Urea reabsorption also increases to help concentrate the urine, resulting in increased serum levels of urea; creatinine continues to be excreted, resulting in the characteristic BUN/creatinine ratio >20.
In contrast, intrinsic ARF reflects tubular epithelium damage and loss of renal reabsorptive capacity. Water, sodium, and urea are excreted in the urine, leading to lower urine osmolarity, higher urinary sodium, higher urinary FENa, and a normal serum BUN/creatinine ratio.
(Choice A) Dark, granular, "muddy brown" casts seen on urinalysis are composed of degenerating tubular epithelial cells. This finding is associated with acute tubular necrosis, which is a common cause of intrinsic ARF.
(Choices B, C, and D) A serum BUN/creatinine ratio <15, urine FENa >2%, and urine osmolarity <350 mOsm/kg are characteristic of intrinsic ARF. These alterations in the laboratory indices of renal function represent the diminished ability of tubular epithelial cells to reabsorb urea, sodium, and water, respectively.
Educational objective:
Blood volume loss can cause prerenal or intrinsic acute renal failure (ARF). Prerenal ARF is associated with normal nephron function (eg, low urine sodium level, low fractionated sodium excretion, high urine osmolarity, and a high BUN/creatinine ratio), whereas intrinsic ARF features diminished renal reabsorptive capacity (eg, lower urine osmolarity, higher urinary sodium, normal serum BUN/creatinine ratio).