Holy crap - busiest month ever. I srsly don't know where the last month went. It just disappeared. :S
USMLE studying has basically gone out the window lately. :( But I am trying to get back into it with renal! Renal physiology is kind of meh but the pathology is amazingly cool.
Acute tubular necrosis is the commonest intra-renal cause of acute renal failure. It can be caused by toxins or ischaemia. At first this seemed straightforward to me, but then I realized that pre-renal acute renal failure is ischaemic. This caused me to question, how in the &$%! do you tell the difference between intra-renal ischaemic acute renal failure and pre-renal ischaemic acute renal failure??
Apparently it goes like this:
Pre-renal: renal cells are hypoperfused, but tubular function remains intact! Tubule cells increase reabsorption of sodium, and urea is retained in the medulla. This is an attempt to create concentrated urine and maintain plasma volume (...and thereby maintain perfusion).
-BUN/Creatinine ratio (quick and dirty, but not specific): Elevated >20:1
-Fractional excretion of Na+ (more specific measure .. basically the clearance of sodium weighted by creatinine clearance): Reduced <1%
Intra-renal: renal tubule cell function is impaired! Sodium and urea cannot be reabsorbed.
-BUN/Creatinine ratio: Reduced <10:1
-FENa+: Elevated >2%
Also, toxins which can cause ATN:
"Color, contrast, and chemo"
= Heme pigments (Hb and Mb)
= Radiography contrast media
= Chemotherapeutic agents: cisplatin, aminoglycoside A/Bs, & Amphotericin B