S. Cr Case Study

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inverse relationship to GFR. Thus, a rise in S.Cr is associated with a corresponding decrease in GFR and generally implies a reduction in kidney function and vice versa.
There are limitations, however, with the use of S.Cr as a marker for AKI. First, S.Cr values may not show significant increases until approximately 50% of kidney function is lost. Second, several drugs can impair creatinine secretion and so could potentially cause a transient and reversible increase in S.Cr (i.e. trimethoprim, cimetidine). Third, a variety of non-renal factors influence creatinine production rate so that creatinine production is variable not merely from one patient to another, but also within the same patient placed under different conditions. Particularly, age, gender, muscular mass, diet (particularly protein intake), and nutritional status are major determinants of creatinine
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First, the rate of urea production is just not constant. Urea can be grossly modified by a high protein intake, critical illness (i.e. sepsis, burns, and trauma), gastrointestinal hemorrhage, or drug therapy such as the use of corticosteroids or tetracycline. On the other hand, patients with chronic liver disease and low protein intake can have lower urea levels without noticeable changes in GFR. Second, the rate of renal clearance of urea is not constant. Approximately 40–50% of filtered urea is passively reabsorbed by proximal renal tubular cells. Moreover, in states of decreased effective circulating volume (i.e. volume depletion, low cardiac output), there is certainly enhanced reabsorption of sodium and water in the proximal renal tubular cells along with a corresponding increase in urea reabsorption. As a result, the concentration of serum urea may increase out of proportion with changes in S.Cr and be under representative of
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