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agreed "granular deposits" rules out MCD (the only other nephrotic syndrome) because MCD is IF (-)
could someone explain why the other choices are ruled out by biopsy?
@cooldudeboy1 PSGN does have a granular immunofluorescence, but there is no previous illness or hematuria mentioned so you can rule that out. Goodpasture is classically linear IF since they're antibodies against the GBM. IgA nephropathy is mesangial IF so it would deposit more in the middle. Minimal change wouldn't show anything on IF
Totally agree w/ you Qball... I thought MPGN too, but I think Penicillamine makes it Membranous Nephropathy
i like the way to remember acd but there is no bacterial etiology in Rheumatoid arthritis is there?
The body recognises chronic inflammatory states as infections
Ferritin is not the "iron delivery trucks", that's actually TRANSFERRIN (transfers iron to liver and bone marrow). Ferritin is the STORAGE form of iron in the liver and bone marrow. In anemia of chronic disease, there usually is an inflammatory process going (whether infectious, auto-immune [as in this case of Rheumatoid Arthritis], or cancer). During inflammation, the body releases IL-6, which releases hepcidin. Hepcidin downregulates ferroportin channels in the gut and on macrophages; therefore you absorb less iron from the GI and iron is trapped in macrophages (ferritin) and cannot be used for RBC production. All this causes INCREASED FERRITIN, decreased TIBC (if ferritin goes up, TIBC goes down and vice versa), and decreased serum iron levels and TIBC saturation (the bone marrow will suck up all the serum iron to make RBCs because it cannot make use of the iron stored as ferritin).
crackles are heard bilaterally so there is pulm patho which leads to increased pulm vascular resistance, since systemic blood flows into the lungs.
any block in the flow ahead (lungs) will increase resistance in flow behind ( systemic )
This patient is hypoxic increased diffusion distance. This causes pulmonary vasoconstriction. Ordinarily this response is designed to shunt blood to parts of the lungs that are well ventilated, but the response is maladaptive in global hypoxia
I dont believe decreased venous oxygen tension would lead to pulmonary vasoconstriction (this is typically in the setting of low PAO2 you see this; shunting blood away from poorly oxygenated alveoli). You can get to increased pulmonary vascular resistance due to pulm edema from Left heart failing leading to fluid overload in pulm vasculature).