Elevated BUN: creatinine ratio favors UPPER over lower GI bleed.
Why?
1) Hb in stomach --> amino acids (aa). 2) aa absorbed by small intestine. 3) aa transported and taken up by liver. 4) In the liver, aa undergo deamination, leading to release of NH3.
2/4
5) NH3 (aka ammonia) is converted to urea by the urea cycle, leading to elevated blood urea levels. 6) Meantime, creatinine is not influenced by the protein/aa bolus. 7) Thus, BUN/creatinine ratio is increased.
3/4
So why does blood cause this bump in urea and increase in BUN/creatinine ratio, whereas a steak dinner does not?
Because blood has poor BIOLOGICAL VALIUE (the protein is poorly utilized by the body).
The LOWER the biological value of a protein, the HIGHER the urea.
Patients with SLE can present with a staggering array of hematologic abnormalities. Virtually no component of the blood is spared. Everything is fair game:
Have you ever wondered why plasma exchange saves lives in TTP but does nothing in ITP? Both are IgG-mediated. So why the difference?
2/4
In ITP, antibodies opsonize platelets. Even if you remove some by exchange, IgG quickly re-equilibrates from the extravascular pool and continues to be produced. With no missing factor to replace, there’s no lasting benefit.
3/4
In TTP, antibodies inhibit ADAMTS13. Plasma exchange not only removes antibody but also replaces the missing enzyme (and helps clear ULVWF multimers). That dual action is why it works.