Yesterday, in Nephrology Morning Report, we reviewed the tried and true approach to acute kidney injury (AKI). All together now: pre-renal, intra-renal, and post-renal.
Moreover, we learned about the spectrum of injury caused by intravascular volume depletion (which can be either due to true hypovolemia or low effective circulating volume), namely:
- pre-renal AKI (the cardiac equivalent would be "stable angina")
- all the way to intra-renal AKI, in the form of ischemic acute tubular necrosis (ATN) (the cardiac equivalent would be "myocardial infarction")
ATN is largely caused by two broad categories of injury:
1) ischemic ATN (as described above)
2) nephrotoxic ATN (classic causes include aminoglycosides, CT contrast, and hemepigments, such as in rhabdomyolysis)
In order to distinguish pre-renal AKI from ischemic ATN, one can look at the urine sediment looking for heme granular casts, which are often described as "muddy brown" in appearance.
If a patient has sustained AKI in the form of ATN, then it is prudent to monitor for acute indications of dialysis. These include:
1) Hyperkalemia (refractory to medical management)
2) Volume overload (refractory to medical management)
3) Uremia, typically resulting in pericarditis (refractory to medical management)
4) Acidosis (refractory to medical management)
5) Removal of toxins, such as lithium or salicylates (refractory to medical management)
Let's end off today's post by paying homage to one of the greatest puppeteers of all time, Jim Henson, who we learned died from a Group A Streptococcus infection. Thank goodness for the Muppets.
