In prerenal acute kidney injury, why is the BUN-to-creatinine ratio often disproportionately elevated?

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Multiple Choice

In prerenal acute kidney injury, why is the BUN-to-creatinine ratio often disproportionately elevated?

Explanation:
When renal perfusion falls, the kidney conserves water and solutes. Urea is freely filtered and reabsorbed with water in the proximal tubule, so as blood flow decreases, more water is reabsorbed and carries urea back into the bloodstream. This increases the serum BUN disproportionately to creatinine, because creatinine is not significantly reabsorbed and its rise mainly reflects the lower GFR. The result is an elevated BUN-to-creatinine ratio, often greater than 20:1 in prerenal azotemia. The other ideas aren’t the driving mechanism here: creatinine secretion isn’t a major factor, BUN production isn’t the defining change in this scenario, and creatinine reabsorption is not increased.

When renal perfusion falls, the kidney conserves water and solutes. Urea is freely filtered and reabsorbed with water in the proximal tubule, so as blood flow decreases, more water is reabsorbed and carries urea back into the bloodstream. This increases the serum BUN disproportionately to creatinine, because creatinine is not significantly reabsorbed and its rise mainly reflects the lower GFR. The result is an elevated BUN-to-creatinine ratio, often greater than 20:1 in prerenal azotemia. The other ideas aren’t the driving mechanism here: creatinine secretion isn’t a major factor, BUN production isn’t the defining change in this scenario, and creatinine reabsorption is not increased.

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