Prescribing Safety Assessment (PSA) Practice Exam 2025 - Free Prescribing Safety Practice Questions and Study Guide

In intrinsic renal acute kidney injury (AKI), it is common for the rise in urea to be less pronounced compared to the rise in creatinine. This is primarily due to the different physiological processes involved in the metabolism and excretion of these two substances.

Urea is a byproduct of protein metabolism and is produced in the liver, while creatinine is produced at a relatively constant rate from muscle metabolism and is primarily eliminated by the kidneys. In intrinsic AKI, which often results from damage to the kidney tubules and complications in glomerular function, creatinine levels can rise significantly as the kidneys’ filtering ability declines. Since urea is subject to reabsorption in the nephron, its rise may be influenced by factors like hydration status and dietary protein intake, which can vary more than creatinine levels.

Therefore, in intrinsic renal AKI, while both urea and creatinine levels can rise, creatinine typically rises more sharply than urea. This forms the basis of understanding renal function during AKI and interpreting laboratory results.