Acute Tubular Necrosis, ATN, is an extremely important topic to know not only for the USMLE Exam,
but also when you are rotating on the wards.
Now ATN occurs when you have injury to the kidneys from toxins or ischemia
resulting in sloughing off of tubular cells into the urine.
Now ATN is the most common cause of acute renal failure in the hospital
and this is why it’s so important on USMLE.
It’s a common cause that you will see when rotating on the wards and also when you practice medicine.
Now ATN is self-reversible but it can be fatal if left untreated.
Now very high yield for you to know is that ATN causes granular muddy brown casts into the urine,
very important phrase, and this occurs due to detachment of the renal tubular epithelial cells.
Now the causes of ATN are very important to know
and we break them up into different categories: toxins and drug, renal ischemia and crush injury.
Now for toxins and drugs, these are really important that you know
because these are common causes of ATN and you can definitely see it on the wards.
Aminoglycosides, amphotericin B, cisplatin, foscarnet, radiocontrast dye and statins.
Now radiocontrast dye is extremely important that you understand.
Whenever you send a patient down for a contrast study, say it’s a CT scan with contrast,
you’re always going to be told, check the BUN and creatinine or check the renal function to see are they impaired,
at base line or not, because if they are, giving radiocontrast dye will only push them into more renal impairment,
so this goes to tell you how much of a potent a flick to radiocontrast dye is to cause ATN.
And also statins, people mainly think of statins as affecting liver functions but they can absolutely cause ATN as well.
Now renal ischemia, this makes sense.
In settings of sepsis and shock you’re gonna have hypoperfusion to the kidney and acute tubular necrosis will commonly occur.
In crush injury, when you have crush injury to really any major part of the body,
you’re gonna have myoglobulinuria in which myoglobin is released from the crush injury
and it naturally causes ATN within the kidney.
Now like I said, very high yield to know is that in ATN you will see granular muddy brown casts.
Now these muddy brown cast in ATN are due to renal tubular epithelial cells actually detaching
and they can cause occlusion of the renal tubules due to this cast formation
which will then increase tubular pressure which will then decrease glomerular filtration rate or GFR and then lead to oliguria.
Now the clinical course of ATN occurs in three stages and this is really important
that you understand in your mind to be able to better understand the path of physiology of the disease.
The three stages are one, an initiation or inciting event.
The second is maintenance or what’s called an oliguric phase and the third is the recovery.
So for step one of this three stage course, initiation or an inciting event.
You will have renal tubular cell damage begin due to some type of toxin exposure or ischemia.
Then the GFR starts to fall and urine output starts to decrease.
Then you will enter into stage two which is the maintenance stage or also called the oliguric phase.
Here, renal tubular injury and death is actually established, then GFR is below normal and urine output
will be low or even absent and this second stage will last roughly one to two weeks
and when you do light microscopy you will see granular casts
and you’ll have flattening of tubular epithelial cells and tubular epithelial necrosis.
And then the third phase is recovery.
You will have reepithelization of the renal tubes and they will regain their renal function
then you’ll have polyuria and gradual normalization of GFR.
Now people may think, why do we have polyuria?
It’s a response to the initial injury, you're making up renal function and this recovery phase takes roughly two to three weeks.
Now in ATN, the renal tubules become necrotic, very important to know,
renal tubules are actually dying and when they sloughed pink epithelial cells and debris
and you’ll have loss of nuclear detail.
Now this can also be the result of rhabdomyolysis by statin use.
Now myoglobin is released by the muscles when you take statins or from a crush injury
and this can cause an increase in CPK levels and these CPK, very important,
are toxic to the renal tubular cells especially the proximal tubule.