Acute Tubular Obstruction – AKI

by Amy Sussman, MD

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    00:01 So moving again in our tubular interstitial disease process, we're gonna be talking and focusing on acute tubular obstruction When our patients have acute tubular obstruction, it's essentially precipitation of substances in the tubules and there's a couple of different categories that we really need to think about.

    00:18 We can have protein from immunoglobulins, this would be in the case of cast nephropathy which we'll talk about in a minute.

    00:25 This can be urate as in tumor lysis syndrome just like our patient had.

    00:30 We can have calcium phosphate precipitate in the tubules and that oftentimes can occur after receiving a phosphorous-containing enema or laxative And finally, giving medications can cause intratubular crystal precipitations.

    00:47 What's important is that when patient develops intertubular obstruction, it almost always occurs in the setting of volume depletion and acidic urine.

    00:56 So let's go over our first situation.

    00:59 Our patient might develop acute tubular obstruction from having cast nephropathy This is going to typically occur when patients have plasma cell dyscrasia or malignancies like multiple myeloma.

    01:10 Remember in multiple myeloma, our patients essentially have an overproduction of immunoglobulin light chains, that are monoclonally restricted and so they're produce in such a quantity that it burdens the kidney.

    01:22 The kidney normally can reabsorb those immunoglobulins in the proximal tubule but they're so much and there's such an incredible amount that it actually starts to glob up those tubules.

    01:32 And again, combining that with a Tamm-Horsfall protein, then causes that to essentially obstruct that outflow of urine.

    01:41 We can also see acute tubular obstruction with tumor lysis syndrome just like our patient had.

    01:47 So this can occur following chemotherapy where somebody has a very very high grade tumor, And we can also see in this situation that that tumor essentially liquefies, we see this intracellular release of uric acid, phosphate and potassium.

    02:03 And that's what is most indicative in our patient population.

    02:08 Phosphorous-containing enemas are also a problem and that actually wasn't discovered until really probably around the early part of the century around 2002.

    02:17 So this includes a bowel prep for colonoscopy.

    02:22 So where we used to see this scenario is that our patients will be undergoing potentially a sigmoidoscopy and our gastroenterology colleagues might be giving something like a sodium phosphorous enema or a laxative.

    02:34 And in that setting of volume depletion, they can precipitate calcium phosphorous in their tubules and interstitium.

    02:41 Again, you can see that when that deposits, it's associated with interstitial inflammation.

    02:47 The highest risk is in our patients with underlying chronic kidney disease.

    02:52 And this is a very significant situation, again you have to be a very good detective but we have transplanted patients over this situation.

    03:00 So it's very important to be cognizant of these phosphorous-containing enemas.

    03:05 Medications are also important.

    03:07 And then again, this is being a good detective in understanding what your patients are getting but we can see this with intravenous acyclovir.

    03:13 So a patient perhaps who's coming in with HSV encephalitis, with intravenous methotrexate which we use in our chemotherapy armamentarium, and things like sulfonamide antibiotics.

    03:27 So, how do we diagnose our patients and how do we work them up in order to clinch that diagnosis? Once again, as we've been talking about, we're gonna be good detectives and we're really going to scour that chart, and really take a very good history in our patients.

    03:40 Sometimes, it's relatively easier if we know that our patient perhaps has a history already of multiple myeloma.

    03:47 We might be thinking about precipitation of those immunoglobulin light chains causing cast nephropathy.

    03:52 If our patient has a known malignancy and they recently had chemotherapy administered, then we think about things like tumor-lysis syndrome Have our patients recently used a fleet enema or an oral sodium-phosphorous laxative? That's also very important and what I really want you to focus on as well is that that really does take good detective qualities.

    04:14 So remember patients who are coming in perhaps from a skilled nursing facility.

    04:18 It's not uncommon for nursing facilities to automatically place enemas on their patients in order to keep from constipation and having issues like that.

    04:29 And in that situation, those patients absolutely can be administered a fleet enema or a sodium-phosphorous enema or laxative that can precipitate this phenomena.

    04:39 So not just looking at their current medications that they're receiving in the hospital but really being that good detective in talking to their nursing facility or other sources where the patient may receive this type of medication.

    04:52 And then you want to do a thorough medication review.

    04:55 So looking at that medication administration record - the AMR, Have our patients received IV acyclovir? Again, coming in with HSV encephalitis, that would be a common scenario where we see this happen.

    05:08 Do they have IV methotrexate for a malignancy, or a sulfonamide antibiotics? Laboratory evaluation can also be very helpful in our diagnostic workup in clinching that diagnosis.

    05:23 So for cast nephropathy, what we're really looking for are those elevated free immunoglobulin light chains in the serum.

    05:29 So specifically, we may want to order a serum protein electrophoresis or SPEP with serum immunofixation.

    05:37 We also can look at serum free light chains and if these are elevated, this can really lead us to the diagnosis that perhaps cast nephropathy is what's causing this acute tubular obstruction.

    05:48 For tumor lysis syndrome, we're going to see things like high uric acid, high phosphorous, high potassium levels just as in the case of our patient at the beginning.

    05:58 For phosphate nephropathy, we tend to see very high phosphorouses and very low calciums.

    06:03 Why is that? Because remember what's happening, you have acute calcium phosphate deposition in those tubules.

    06:13 So for medications, what we oftentimes can do is we can look at the urinary sediments and we may see crystals from our precipitated medications that can really lead us to that diagnosis.

    06:27 So, what can we do to treat our patients who have acute tubular obstruction? So in cast nephropathy, remember what's happening and we have those immunoglobulin light chains that are precipitating.

    06:37 So we can actually administer chemotherapeutic agents like dexamethasone, proteasomal inhibitor-based regimens that are aimed at actually shutting down that immunoglobulin production.

    06:48 In cases of tumor lysis syndrome, we are really going to aim at preventing that from happening.

    06:54 So that means we are going to administer our chemotherapy with high amounts of isotonic fluids like saline.

    07:01 And uric acid lowering agents like allopurinol and rasburicase to prevent or shutdown production of uric acid so that doesn't obstruct the tubules.

    07:10 Acute phosphorous-nephropathy, unfortunately when we give those phosphate-containing enemas or laxatives, there's nothing we can do after that situation other than offer supportive care.

    07:20 But certainly there's something that we can do at preventing that and that's really just ensuring that our patients never receive these types of medications particularly our patients who have underlying chronic kidney disease because they are the ones that are so vulnerable to developing acute phosphate nephropathy And finally, for medication induced crystalline nephropathies, it's most important at the time that it's occurring to remove the offending drug.

    07:44 Now let's go back to that case again of that HSV encephalitis patient.

    07:48 A drug like acyclovir is critical for them in order to get better.

    07:53 So I can't keep that drug off completely, but what I can do is I can administer a lot of volume in the form of isotonic saline and then again retry that drug once that patient's volume status is optimized.

    About the Lecture

    The lecture Acute Tubular Obstruction – AKI by Amy Sussman, MD is from the course Acute Kidney Injury (AKI).

    Included Quiz Questions

    1. Cellular debris from hyperkalemia
    2. Urate crystals
    3. Protein
    4. Excessive immunoglobulin light chains
    1. Bowel prep for colonoscopy
    2. Methotrexate use
    3. Excessive intake of acetic acid
    4. Recurrent gout
    1. Elevated immunoglobulin light chains
    2. Elevated white blood cell count
    3. Elevated serum calcium
    4. Elevated serum phosphorous
    1. Saline with allopurinol
    2. Phosphorous binders
    3. Dexamethasone
    4. Kayexalate

    Author of lecture Acute Tubular Obstruction – AKI

     Amy Sussman, MD

    Amy Sussman, MD

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