A patient presents after prolonged vomiting with dehydration. Labs show BUN 42 mg/dL, creatinine 1.8 mg/dL (BUN/Cr ratio ≈ 23:1). Which diagnosis best fits, and why?
AAcute tubular necrosis, because high BUN indicates tubular damage from volume depletion
BPrerenal AKI, because the elevated BUN/Cr ratio reflects intact tubules avidly reabsorbing urea to conserve volume
CPostrenal AKI, because dehydration causes downstream obstruction
DIntrinsic renal AKI, because dehydration directly injures glomeruli
In prerenal AKI, kidney tissue is structurally intact but hypoperfused. The tubules continue reabsorbing urea (BUN) efficiently in an attempt to conserve fluid, so BUN rises disproportionately to creatinine — producing a BUN/Cr ratio >20:1. In ATN, tubular reabsorption is impaired, so BUN does not accumulate disproportionately and the ratio is typically <20:1. The ratio is thus a first-pass tool for distinguishing functional (prerenal) from structural (intrinsic) injury.
Question 2 Multiple Choice
Patient A has creatinine rising from 1.0 to 2.2 mg/dL over 36 hours. Patient B has a stable creatinine of 3.5 mg/dL (their baseline for months). Which patient more likely has acute kidney injury?
APatient B, because their absolute creatinine level is higher and indicates worse kidney function
BPatient A, because the rapid rate of rise reflects acute GFR decline even though the absolute value is lower
CBoth are equivalent — creatinine level directly mirrors GFR regardless of trajectory
DNeither qualifies as AKI without urine output data
AKI is defined by rate of change, not absolute value. Creatinine must accumulate in a large volume of distribution, so the absolute level lags behind actual GFR decline. A rapidly rising creatinine (1.0→2.2 in 36 hours) meets KDIGO Stage 2 criteria and signals acute injury, while a stable creatinine of 3.5 in a patient with chronic kidney disease reflects a new steady state. This is the key clinical nuance: a modest but rising creatinine can represent more acute danger than a higher but stable level.
Question 3 True / False
Oliguria (urine output <0.5 mL/kg/hr) is a required criterion for diagnosing acute kidney injury.
TTrue
FFalse
Answer: False
Non-oliguric AKI is well recognized and actually carries a better prognosis than oliguric AKI. KDIGO criteria allow diagnosis based on either a creatinine rise ≥0.3 mg/dL within 48 hours or ≥1.5× baseline within 7 days, OR urine output <0.5 mL/kg/hr for ≥6 hours. Either criterion suffices; neither is required. Clinicians who anchor on oliguria may miss non-oliguric AKI until it progresses.
Question 4 True / False
In prerenal AKI, the structural integrity of kidney tissue is preserved; the primary defect is inadequate renal perfusion pressure to drive glomerular filtration.
TTrue
FFalse
Answer: True
This is the defining feature of prerenal AKI and is what makes it potentially reversible with volume resuscitation or treatment of the underlying cause (e.g., heart failure, sepsis, hemorrhage). Because tubular cells are not injured, the kidney still concentrates urine appropriately and reabsorbs urea avidly — hence the BUN/Cr >20:1. If hypoperfusion is prolonged or severe, it can progress to intrinsic ATN, at which point tubular cells are damaged and the prognosis worsens.
Question 5 Short Answer
Why does the BUN-to-creatinine ratio differ between prerenal AKI and acute tubular necrosis, and what is the diagnostic significance of this difference?
Think about your answer, then reveal below.
Model answer: Both BUN and creatinine rise when GFR falls. But BUN is also regulated by tubular reabsorption: in prerenal AKI, intact tubules avidly reabsorb urea as part of volume-conservation reflexes, so BUN rises disproportionately to creatinine, giving a ratio >20:1. In ATN, tubular cells are damaged and cannot reabsorb urea normally, so the BUN/Cr ratio stays closer to 10-15:1. The ratio therefore reveals not just that GFR is reduced but whether the tubules themselves are functioning — distinguishing a perfusion problem (treat with fluids or addressing the cause) from a structural injury (supportive care, avoid nephrotoxins, consider renal replacement therapy).
Creatinine is freely filtered and neither significantly secreted nor reabsorbed in the tubule, making it a reliable GFR marker. BUN is filtered but subject to significant tubular reabsorption. This difference in tubular handling is what makes the ratio clinically informative.