Muddy brown casts are diagnostic for ATN, or acute tubular necrosis, which is an intrinsic form of AKI. But if you don’t see muddy brown casts, can ATN be ruled out? The literature on this is surprisingly light. There is one study of 267 patients with AKI who were classified as low or high pretest probability for ATN and had urine samples analyzed. The study concludes: “In patients with a low pretest probability of ATN (initial diagnosis of prerenal AKI), lack of casts or RTEC on urinary sediment examination had a sensitivity of 0.73 and specificity of 0.75 for a final diagnosis of prerenal AKI. The negative predictive value of lack of casts or RTEC in patients with low pretest probability of disease was 91%.” One important point to take away is that your pretest probability matters a lot for how confident you should be about making a diagnosis.
This review, by the same group, has a nice discussion section about making the diagnosis of ATN through a combination of methods, including microscopy, and use of FeNa and FeUrea.
Here’s something you may see sometimes: a patient presents with a (non-hemolyzed ) potassium of 7.0. Scary! But you check a potassium on VBG, and it returns 5.5. Which is the right value? What’s going on here?
Serum potassium, generally speaking, is more accurate. Serum samples contains potassium released by platelets (which are separated out in the phlebotomy tube) so is usually 0.1-0.7 mmol/L higher than plasma samples. Whole blood potassium is usually accurate enough, especially when you need a potassium level quickly in a critical care/emergency setting.
This question came up when one of my co-residents stated during our discussion of a case that the patient, who had HIV, should not be considered immunosuppressed because his CD4 count was in the 300s.
Patients who are HIV-positive with a CD4 count <200-250 or who have had an AIDS-defining illness are immunocompromised. Patients with a CD4 count above this level may not necessarily count as immunocompromised.
As a reminder, CD4 counts dictate what patients should be prophylaxed against:
CD4 <250: IgG and IgM serologic screening for coccidiomycosis in endemic regions, administer fluconazole if positive.
CD4 <200: administer Bactrim/dapsone/atovaquone for PJP prophylaxis
CD4 <100: administer Bactrim or alternative for toxoplasmosis prevention. Patients are at risk for cryptococcus.
CD4 <50: patients are at risk for MAC, and if not on antiretrovirals, should be prophylaxed with azithromycin (if on ART, do not need prophylaxis)
A list of AIDS-defining illnesses from the CDC (see website for more details on the asterisks/caveats):
Bacterial infections, multiple or recurrent*
Candidiasis of bronchi, trachea, or lungs
Candidiasis of esophagus†
Cervical cancer, invasive§
Coccidioidomycosis, disseminated or extrapulmonary
Let’s say a patient presents to the medical floor with hypotension and hyperkalemia, and generalized fatigue and weakness. Adrenal insufficiency might be on your differential. What’s the most accurate way to test for it? Can you get away with using doing a random cortisol level?
A random serum cortisol level must always be in the context of what time of day it was taken. There are different laboratory cutoffs depending on what time of day the sample was taken. Typically, a morning cortisol level is most helpful. An AM cortisol level >15 mcg/dL is very reassuring that someone doesn’t have adrenal insufficiency. But any level <15 does not exclude adrenal insufficiency! As this case report shows.
A cort stim test (also called ACTH/cosyntropin stim test) involves measuring an AM serum cortisol, injecting 250 mcg of ACTH or cosyntropin, waiting 30 minutes, and then measuring serum cortisol again. An “adequate response” ruling out adrenal insufficiency is ≥18 to 20 mcg/dL before or after ACTH injection. If there is an inadequate response, you may consider directly measuring ACTH levels or doing other tests to further evaluate for primary vs. secondary adrenal insufficiency.
Note 1: patients with higher levels of cortisol-binding globulin (like cirrhotics or those with nephrotic syndrome) may have lower levels of cortisol, and may be incorrectly diagnosed with adrenal insufficiency using normal cut-off ranges.
Our belief is that adrenal insufficiency appears to be unlikely when a random cortisol measurement is greater than 34 μg per deciliter. Conversely, adrenal insufficiency is likely if the serum cortisol level is below 15 μg per deciliter during acute severe illness. For persons with cortisol levels between these two values, a poor response on a corticotropin test would indicate the possibility of adrenal insufficiency and a need for supplemental corticosteroids.
All too frequently, patients are started on antibiotics for a UTI because of a “positive UA” alone. This should not be! Sometimes, especially if a patient is unstable or really sick, it may be wise to empirically treat for a UTI, but in an otherwise stable patient, please think carefully about whether they truly have a UTI.
Technically, a UTI is defined in part by a positive urine culture that has >10,000 organisms, of no more than two species. (“Mixed genital flora” does not count!) However, often we let this slide if a patient has a “positive UA” and one of the following criteria:
fever >38.0 C
suprapubic tenderness or CVA tenderness
If a patient has a Foley in place, they will not be able to reliably tell you about urgency, dysuria, or frequency because the Foley catheter itself can cause these symptoms.
This is intended to provide a quick list for diagnosis of HRS, since HRS is a diagnosis of exclusion and should only be made once other conditions are “ruled out.” HRS is a clinical diagnosis, and there is no one perfectly sensitive or specific test. But if your patient meets these criteria, you should be worried.
Ascites is present
There is an AKI (creatinine >1.5)
Rule out infection: there is no UTI or pyelonephritis
Rule out prerenal injury: there is no improvement in serum Cr after resuscitation with 2 days of 1 mg/kg albumin, 100 g max
Rule out intrinsic disease: there is no hematuria (>50 RBCs) or proteinuria (>0.5 g) to suggest renal disease
Rule out meds: no nephrotoxic meds recently given
Rule out hypotension/ATN: no signs of ATN in the urine, no shock or profound hypotension
In the past, there were minor criteria including oliguria (<0.5 L urine output/day), low urine sodium (<20), and low serum sodium. These were found to have poor specificity and were dropped in 2007.
There are two types of HRS: Type 1 is rapid (develops in <2 weeks) and severe, with a 10% survival rate over 3 months. Type 2 is more gradual and on a spectrum with diuretic-resistant ascites.
You should also ask yourself: what triggered this episode of HRS? Common precipitants include infection (check a chest x-ray for pneumonia, urine studies for UTI, blood cultures, and rule out SBP), prerenal causes (not giving enough albumin after large-volume paracentesis, diuretics), post-TIPS, and nephrotoxic drugs.