Tag: Uncategorized

Posted on

Aminoglycoside avoidance in enterococci endocarditis

One of the joys of being a clinical nephrologist is convincing the infectious disease consultant to treat enterococcus endocarditis without gentamicin. The Infectious Disease Society and the American Heart Association have this table regarding treatment:

From Baddour LM, et al. Circulation 111 e394-e434; 2005

The article states that enterococci are relatively resistant to penicillin, ampicillin and vancomycin compared to streptococci. The antibiotics are bacteriostatic rather than bactericidal in these species. Adding an aminoglycoside restores the lethal activity of the Beta-lactam antibiotics. Interestingly the cell walls of enterococci are highly impermeable to the aminoglycosides and would require plasma concentrations incompatible with human tolerance but the beta-lactams increase cell wall permeability so lower doses are biologically active.

The recommendations advise 4-6 weeks of therapy with the combination beta-lactam and aminoglycoside, however it references an observational study that showed effective therapy with as little as two weeks of aminoglycoside exposure. This was a report on 5-years worth of endocardititis from Sweden. They had 93 cases of enterococcal endocarditis

  • Native valve infections: 66 cases
    • 54 were cured 
    • median duration of beta-lactam therapy: 42 days
    • median duration of aminoglycoside exposure: 16 days
    • acute valvular surgery: 11
    • relapse 2
    • deaths 10
  • Prosthetic valve endocarditis: 27 cases
    • 21 were cured
    • median duration of beta-lactam therapy: 42 days
    • median duration of aminoglycoside exposure: 15 days
    • acute valvular surgery: 8
    • relapse 1
    • deaths 5
This looks good to my urine stained eyes, it appears that we can comfortably get away with a shorter exposure to gentamicin, but what really caught my eye was this paragraph:
Seven patients without any aminoglycosides, all with good outcomes.
What about avoiding gentamicin altogether?

In 2007 Gavalda published a case series in the Annals of Internal Medicine. He looked at 43 patients with high-level aminoglycoside resistance (HLAR) or renal failure/high risk for renal failure without HLAR. They were treated with ampicillin 2g q4 hours and ceftriaxone 2g q12 hours.

The data was broken down as HLAR and non-HILAR

  • HLAR 21 cases
    • 6 deaths during treatment
  • Non-HILAR 22 cases
    • 6 death during treatment
    • 2 relapse (one patient received the wrong dose of ceftriaxone)
    •  2 death during follow-up
The most recent data comes from the same Spanish group, now with lead author Hidalgo. Published last week they reported on 159 patients treated with ampicillin-ceftriaxone (AC) and compared them to 87 treated with ampicillin-gentamicin (AG). Here are their results from the abstract:

Between AC and AG-treated E. faecalis IE patients, there were no differences in mortality while on antimicrobial treatment (22% vs 21%, P=0.81) or at 3-month follow-up (8% vs 7%, P=0.72), in treatment failure requiring a change in antimicrobials (1% vs 2%, P=0.54), or in relapses (3% vs 4%, P=0.67). However, interruption of antibiotic treatment due to adverse events was much more frequent in AG-treated patients than in those receiving AC (25% vs 1%, P<.001) Conclusions. AC appears as effective as AG for treating EFIE patients and can be used with virtually no risk of renal failure and regardless of the high-level aminoglycoside resistance (HLAR) status of E. faecalis.

I’m going to try this.
Posted on

Dialysis for cast nephropathy

I love being a clinical nephrologist. One of the great things about the job has been the non-clinical activities that have burrowed their way into my schedule. In the last 12 months I have:

  • Judged resident research day
  • Taught renal physiology to second year medical students (back to the class room for the first time in a decade)
  • Worked on the scientific advisory board for the National Kidney Foundation of Michigan
  • Attended the editorial board meeting of the American Journal Kidney of Kidney Disease
  • Participated in a mock FDA new drug approval meeting
  • Implemented an EMR and patient portal for my practice
These events, in addition to my regular teaching gigs and taking care of patients, keep my work interesting. 
Last week, I had another novel experience. One of my medical school colleagues, who is now a myeloma expert, asked me to review a case and write a letter in support of a request for “compassionate-use” exception for an unapproved dialyzer. He wanted to use the Gambro HCO 1100 dialyzer, the Nimbus 2000 of dialyzers.
What makes the HCO1100 unique is the exceptionally large pore size. Cast nephropathy is the predominant cause of acute renal failure in multiple myeloma. Removing the offending agent, serum free light chains should have an ameliorating effect on the kidney injury. Previously we have used plasmapheresis to treat this, however this is not beneficial. The HCO1100 is able to effectively remove particles with a molecular weight up to 45,000 daltons and Hutchison et al showed that it can actually dialyze free light chains from the serum. Look at the following clearance data from Hutchison:
The second from the last column on the right has the clearance data.
The Gambro CHO1100 is literally orders of magnitude better than the competition. Hutchison looked at clearance data by examining light chains in the discarded dialysate, this avoided confusion from light chains absorbed to the membrane. Absorption removes light chains from the serum but requires frequent replacing the dialyzer.
The same group followed that paper with an uncontrolled case series of patients, all with biopsy-proven, dialysis-dependent, cast nephropathy. Each was treated with the protocol established by the previous paper* and they had excellent results. Nineteen patients received the therapy. Fourteen of them were able to receive uninterrupted chemotherapy and all fourteen recovered renal function (became dialysis independent). The five who had interruptions to their chemo regimen all remained dialysis dependent. The interruptions were all due to infections and all of these patients died during follow up.
Renal recovery in green, renal non-recovery in red.
The most recent data (good coverage here) I’m aware of comes from Heyne et al. They also published on 19 patients with biopsy proven cast nephropathy. All of the patients were treated on the same chemotherapy regimen which was based on bortezo­mib (Velcade) rather than the various regimens used in the Hutchison series. They too, found a 75% renal recovery. I’m waiting for the PDF of the article because of the Springer paywall (grr).
Definitive information on how effective this therapy is should come from the EuLITE trial which is expected to have results this year. Ironic that some of the only RCT data in nephrology will come from the hematologists.
If you are interested in this you should take a look at Amyloid Planet’s excellent post on suffering from Theralite Envy.
* for those interested the dialysis protocol calls for daily 8 hour treatments. They used 2 HCO1100 placed in series to increase the surface are up to about 2 meters squared. They ran the blood flows at 250 ml/min and the dialysate at 500 ml/min. Dialysis was run daily for 5 days then every other day for 12 days then for 6 hours three days a week.
Update: above I mentioned my frustration with the Springer Paywall and four different readers sent me the PDF. Thank-you. Nice to live in a networked world.
Posted on

Come on ASN, respect your audience.

I am working on a review of electrolyte disorders in geriatric patients. As part of gathering data I found a resource at ASN Online. They have an entire geriatric nephrology textbook that is available as a PDF for members. That looks awesome. They also have the slide sets from the 2009 and 2008 Renal Week post graduate courses on Geriatric Nephrology, subtitled: An Epidemiologic and Clinical Challenge.

I was looking at those slides sets when I came across this clunker by Myron Miller from Johns Hopkins. Here are some of the low-lights:

I swear the camera on my phone does a better job of scanning image that the undergrad he enslaved to do this transfer.

Nothing says you care, like handwriting the reference.
What a hot mess. It’s hard to imagine you could make a 4×2 chart worse than this one. 

These are the worst slides I have seen in a long time. People who sign up for the post grad classes take an additional two-days off of work and stay in a hotel for what is supposed to be the highest quality nephrology education available. Dr. Miller expresses disdain for his audience with his all-caps, poor scanning and hand scrawled notes. ASN, I’d be happy to talk at any of your sessions. Call me. Maybe?

I tweeted about that last slide and got the following response.

@kidney_boy Take the one that you posted & repost after applying the @kidney_boy filter. Curious what you would do.
— Jim Smith (@jklm) January 31, 2013

I didn’t apply the Kidney_boy Filter™ but I did rework and bring up to date my hyponatremia lecture. Here it is in Keynote (25mb) and PDF (12mb). Feel free to download, comment, remix and rework at your discretion.

The lecture is about an hour long.
Credit (along with a link to pbfluids.com) is appreciated.

Update March 20, 2013: I recently received this e-mail

I am a big fan and review your posts frequently. I saw your recent post on Myron Miller’s slides and agree that they are “clunky” without the mastery that you provide in your lectures, pdf, and posts. I will tell you though that Myron (though an Endocrinologist and Gerontologist by trade) is in part responsible for me becoming a Nephrologist as he guided me through my Residency, exposing me to the wonders of renal physiology and fluid and electrolyte issues. His early work on fluid and electrolyte issues was done in the “low tech” days before IRBs, evidence based medicine, and sophisticated statistical analyses. I am fortunate to work with him as a colleague and continue to learn when he lectures. I have many of his original papers and share them with our fellows. Best.

Paul Segal
Assistant Professor of Medicine, Division of Nephrology,
Johns Hopkins, Clinical Nephrologist and Informatician

BTW…no nod to IS Edelman in your Sodium lecture?

In a follow up letter he elaborated on Edelman:

Getting back to Edelman, to me, the equation essentially describes everything you need to know about treatment by examining both the numerator and denominator. In addition, it reminds students that potassium is an important component of plasma sodium (as per T Berl and A Rastegar’s AJKD article 2010), and a component of EFWC.

Great stuff thanks.

Posted on

NSAID alert! or not.

The news wires lit up last week with the revelation that ibuprofen can cause acute renal failure and it even can happen in children. 
MD Mama
CBC News Health
Everyday Health
Counsel and Heal
MedPage Today
NewsMedical.Net
EmaxHealth
My favorite tweet on this came from pediatric nephrologist, Pascale Lane:

“@asnkidney: Could NSAIDs contribute to an increased risk for acute kidney injury in children? bit.ly/14hBifN” Yes. Next question
— Pascale Lane (@PHLane) January 26, 2013


The publicity department of Indiana University must be quite pleased with themselves with the wide coverage this study has produced but behind the curtain we really have very little data. The study was published in J Peds (Abstract | PDF). The authors did a retrospective chart review of 11.5 years of inpatient records from Riley Children’s Hospital in Indianapolis. They found 1,015 patients with acute renal failure by screening ICD-9 codes. This is a shockingly low frequency to me. Eighty-eight cases a year in a major children’s teaching hospital makes me think theire screening methodology was quite insensitive.
The authors did not comment on how accurate the ICD-9 screening methodology was. They said they examined all of the charts but didn’t mention if any of the cases were excluded after examination because of a lack of acute renal failure. This also seems unlikely, as many patients with chronic kidney disease are initially coded as acute renal failure. It would have been nice to get a sense of how specific the ICD9 screening methodology was, even if they couldn’t comment on the sensitivity. (Update, this article looking at AKI in adults states that ICD9 codes have a sensitivity of 28% and specificity of 99%)
Having amassed this trove of acute renal failure data the authors did not report on acute renal failure in general (hopefully a future paper will elaborate on this. I would love to see comprehensive data on the epidemiology of pediatric acute kidney injury, something like The Madrid Acute Renal Failure Project) and instead did a deep dive on NSAIDs. Here is the breakdown of etiologies of acute kidney injury in this study:
Co-morbid conditions were defined as: malignancy, complex congenital heart disease, sickle cell disease, etc.
Alternate diagnosis were defined as:obstruction, hemolytic uremic syndrome, pyelonephritis, sepsis, transplant rejection, or glomerulonephritis.
I have pulled out the two slivers which represent the NSAID associated renal failure. The ignored elephant in the room, is the absence of pre-renal azotemia in the lists of diagnosis. This has previously reported to be the most common cause of kidney failure in patients presenting with ARF and the second most common in hospital acquired ARF (Madrid ARF study | PDF). The authors had little to say about volume deficiency as it pertained to the etiologies of renal failure. This what I could find:

Although volume depletion is an independent risk factor for AKI, patients with a history of volume depletion in the absence of sepsis or multiorgan failure were not excluded from classification as having NSAID-associated AKI, as it is likely that volume depletion increases the risk of NSAID use leading to AKI.

The authors had this to say about the frequency of NSAID induced ARF:

Our study is the largest series to date demonstrating that NSAIDs are a common cause of AKI in children.

I read that statement and look at the pie chart and then look at results that show 27 cases of AKI over 12 years and I must say, I’m not impressed.
The authors try to pump up the frequency by expanding their definition of NSAID induced AKI:

However, it should be noted that in our population, many patients who were deemed to have developed multifactorial AKI (and thus were not included in the case definition of NSAID-associated AKI) did have NSAID exposure as one of their multiple risk factors for AKI.

This feels disingenuous. If you create the case definition, don’t try to spin your results by essentially saying, if we had a different, less specific, case definition we would have found more cases.

Of note: the authors found that 44% of the cases were above the 95% for height:weight or BMI. The authors tried to see if this was due to NSAID overdose because of parents dosing kids by actual rather than ideal weight. This was not the case. However this is consistent with the recent results about adiposity being related to AKI in trauma patients. Obesity, an independent risk factor for AKI. Neat.

Posted on

What does renal denervation mean for the future?

Symplicity HTN-2 just published its one-year results. The results are just as impressive as the 6-months results. Symplicity 2 is the first randomized controlled trial of radiofrequency denervation. The technique (described here) uses a catheter to deliver radiofrequency energy to the renal arteries. This denervates the kidneys and decreases sympathetic inflow. The lack of sympathetic stimulation reduces renin and peripheral norepinephrine levels which serve to decrease the blood pressure. The study enrolled patients with resistant hypertension, i.e. uncontrolled blood pressure despite compliance with three anti-hypertensive medications including a diuretic.

The primary end-point was change in office blood pressure at 6 months. An average of 30 mmHg drop in patients with resistant hypertension is incredible!

After the primary end-point, patients randomized to the control group had the option of receiving the procedure and their data is also presented in this update.

In addition to the average drops in blood pressure, the benefits were widespread with 83.7% having a lower systolic BP at 6 months and 78.7% at 12 months.

There was not a statistical difference in number of blood pressure medications used at the end of the trial (see table 5 below) but the results are tantalizing and I believe represent a Type II error. This should be an interesting outcome to keep an eye in the forthcoming Symplicity HTN-3 trial.


The procedure appeared safe with 1 episode of renal artery dissection in the cross-over group and one episode of hypotension following procedure that responded to conventional treatment. There was 1 dissection in the 153 patients in Symplicity HTN-1.

The procedure was without complication in 97% of patients (149 of 153 patients). One patient experienced the renal artery dissection on placement of the treatment catheter before RF energy delivery was delivered in that artery. The dissection was treated with renal artery stenting without any subsequent complication or delay in hospital discharge. Three other patients developed a pseudoaneurysm/ hematoma in the femoral access site; all had had an 8F guide and were treated without any subsequent complication.

This data is consistent with the Symplicity-1 results which, though non-randomized, showed a durable anti-hypertensive effect through 3 years.

Symplicity-3 is currently recruiting. It is also a randomized controlled trial but it is twice the size of Symplicity HTN-2. Additionally it uses 24-hour ambulatory blood pressures rather than office pressures to measure efficacy.
This looks like an effective therapy and of course we will have to wait until it is approved for wider use but it is hard to look at this technique and see anything but a game-changer. We are looking at a non-pharmacologic therapy for hypertension that does not require medical compliance. Imagine cardiologists, instead of boxing the kidneys with drive-by renal angiograms, actually helping the patient by lowering their blood pressure. Cardiologists helping the kidney, difficult to wrap my brain around that. Brave new world indeed.
Posted on

Kidney International, you may want to look at your podcasts.

I spend half an hour commuting to work everyday and usually listen to podcasts. My tastes mostly satisfy my unnatural Apple cravings. I listen to a lot of 5×5, TWiT and Slate podcasts, but recently I subscribed to a handful of Kidney podcasts.

I was listening to the Kidney International Podcast and they start interviewing (iTunes Link) Barry Freedman of Wake Forrest. He starts talking about the MYH9 gene. This tweaks my interest and I start paying attention, thinking to myself, “Is this gene making a comeback?” And then he starts talking about the the Nature Genetics papers from 2008. No mention of APOL1. I glance down at my iPhone, the podcast is from 2009. I was relieved that I hadn’t missed a major U-turn. Listenning to the remainder on the podcast I can’t help but smirk at the hyperbole.

His paper was on hypertension associated end-stage renal disease and its tight association with MYH9. He waxes on about how it is one of the most strongly associated genes in any common disease. He states that if you could remove the MYH9 risk variants from the African American population, 70% of the non-diabetic kidney disease would disappear. He states that MYH9 is responsible for initiating most kidney disease in African Americans and that hypertension is very unlikely to be an initiating factor in kidney disease.

If you are not familiar with the history of this wrong-turn, here is a brief overview:

  • In October 2008, Jeff Kopp, using a new technology known as admixture-mapping linkage-disequilibrium genome scan found an association with FSGS and a variant in the a gene called MYH9. The same gene variant was also associated with HIVAN. This was hailed as a major break-through explaining the excess kidney disease burden found in African Americans.
  • MYH9 had already been associated with a cohort of genetic conditions that all had glomerular pathology so the link seemed pathophysiologically sound.
  • The nephrology research world became fascinated with this gene and for about a year tremendous resources were focussed on this gene.
  • In July 2010, Science published data that showing that a different gene, APOL1, located close to MYH9 on the chromosome, was actually responsible for the high association of disease. Of note Barry Freedman is also an author of this paper.
  • Being heterozygous for APOL1 is protective against the Trypanosoma parasites that cause African Sleeping sickness
    • Trypanosoma brucei brucei infects many mammals but is unable to infect humans because human serum contains a complex, trypanosome lytic factor (TLF)
    • Trypanosoma brucei rhodesiense and Trypanosoma gambiense evolved a defense against TLF and were able to infect humans.
    • A single copy of APOL1 restores TLF and makes the carrier immune to sleeping sickness
    • Two copies of the APOL1 predisposes the carrier to proteinuric kidney disease and HIVAN
    • Balanced polymorphism
    • APOL1 mutation is about 10,000 years old, but humans migrated to Europe 70,000 years ago, so Europeans, never shared in the mutation.
A more thorough rehash can be seen in my Dialysis for the Internist lecture (Keynote, PDF).
While it is hilarious to listen to the certainty of Dr. Freedman’s proclamations, the incident also has a lesson for dealing with social media. Publishers, including bloggers, are constantly publishing information that expires. Facts become falsehoods and time reveals truths. However, what we have published remains. Leaving these mistakes, without editorial comment is a disservice to our readers. Even though what we wrote may be buried under dozens of posts, Google still indexes it and still sends readers to this material. Kidney International unfortunately never did another podcast, so when one subscribes to their podcast, this story is what is downloaded as “most recent.” 
Search and the permanence of internet means that we need to take responsibility for old content, in a way that wasn’t necessary in the past.
Posted on

Grand Rounds: Social and Health Care

On Tuesday December 4, I will be presenting grand rounds for St John Hospital and Medical Center. This page has the references, lecture notes and a copy of the slides.

PDF of the slide deck (17.3 MB)

One of the gimmicks of the talk was that a scheduled tweets to drop during the presentation. I also peppered my tweet stream with my talk’s hashtag in the 2 days leading up to the talk. This resulted in a nice little buzz of social activity. Looking over the hashtag (#SJHMCsmhc) a day later I found 20 retweets, 14 replies, 11 favorites. This was spread-out over 17 different tweets All way above normal activity for @kidney_boy.

This only captures activity with the hashtag #SJHMCsmhc

I used HootSuite to schedule the tweets.

Notes and References

Picture of Me and Bud
    1. Shame on You… Facebook page
    2. Preemie Primer post by Dr. Jen Gunter the queen of OB/GYN on Twitter
    3. Forbes blog post, Is KV Pharma Evil?
    4. Eli Reschef, OB/GYN leading charge agains Makena pricing
    5. Academic OB/GYN on the Makena Controversy

Posted on

Weight loss and CKD, one patient’s experience.

I just discharged a patient from my CKD clinic. I first saw her in the CKD clinic in 2008. When she presented she had CKD stage 3/4 (eGFR of 30 mL/min) with a creatinine of 1.8. I was very concerned about her risk of progression to ESRD due to three elements from her history:

  1. Recent episode of ARF following a UTI. We know now that AKI is a risk factor CKD progression, especially in diabetics, but even 5 years ago I used it as a personal bias flagging patients with scant renal reserve and fragile kidneys.
  2. She had previously had a nephrectomy for renal cell carcinoma. I always worry about these patients getting hyperfiltration injury, though in my experience this is rare and they generally do much better than their peers with equally diminished GFRs.
  3. She had a BMI of 45, which also increasing her risk of hyperfiltration injury.
Image via Methodist Hospital

On her first visit, she asked if losing weight would help her kidney disease. I told her that I felt it would. She had already tried a variety of diet and exercise programs and had repeatedly failed. Over the ensuing year we discussed weight loss options and ultimately she consulted with a bariatric surgeon. In February 2009 she went for a laproscopic gastric band procedure.

Since that procedure she has lost 132 pounds. Her hemoglobin A1c has gone down from 9.9 to 5.7 in the face of stopping insulin and her three oral hypoglycemics. But the most remarkable thing for me has been the way her creatinine has melted away from 1.8 to 0.7. Her microalbuminuria went from 139 to 3 mg/g creatinine. She went from CKD 3/4 to CKD 1.

JASN recently published a report by Turgeon, showing increasing complications with bariatric weight loss procedures in patients with chronic kidney disease.

In a 2009 meta-analysis, Navaneethan found that bariatric surgery reduced proteinuria, blood pressure and GFR. The reduction in GFR was not in CKD patients and really relfected a normalization of hyper-filtration from a GFR of 140 to 117 mL/min.

Risks occur with bariatric surgery, as shown in Turgeon’s study. In addition to the short term surgical complications, AKI, rhabdomyolysis, hyperoxaluria and kidney stones all can occur after weight loss surgery. An additional wild card in assessing how CKD patients do after surgery is the fact that using the MDRD in the morbidly obese is uncertain. Perhaps my patient’s improvement is due simply to increased accuracy of the MDRD equation as her BMI approached a more typical level. That said, given the reduction in her albuminuria, the apparent curing of her type two diabetes and her remarkable fall in creatinine I feel she has truly benefitted from the surgery.
Posted on

FENa and FEUrea revisited

At Renal Week I went to Mark Perazella’s talk on “Urine Microscopy for Diagnosis and Prognosis in Hospital-acquired AKI.” Perazella published the interesting paper in CJASN in 2008 on using urinalysis microscopy for prognosis. His talk focused on the same subject. The gist is that a trained observer of urine microscopy is not only more accurate at diagnosing the etiology than FENa and FEurea but can provide prognostic information. Additionally, urine microscopy performs as well as the novel biomarkers: KIM-1, NGAL and IL-18.

As part of his talk Perazella threw-up some slides with some surprising statistics on the diagnostic utility of FEUrea and FENa:

From Pepin AJKD 2007: 50:566-573

A sensitivity of 48% without diuretics? A specificity of 33% with diuretics? Terrible. A second study showed similarly terrible numbers:

From Darmon et al. Critical Care 2011: 15 R178.

Only a bit better than a coin toss.

I felt shamed. I had been teaching and using urinary acute renal failure indices for 20 years and to see that they sucked sucked, kinda hurt. But then as I thought about it, I remembered seeing primary data that was quite a bit more compelling. So I went back to the primary literature.

The fractional excretion of sodium was invented in 1976 by Carlos Hugo Espinel. His initial series was published in JAMA. In that study he found 100% sensitivity and specificity in 17 oliguric patients.

Holy shit! Shrier is a member of the
Indiana Basketball Hall of Fame!

The study that is usually referenced as the mother of the fractional excretion of sodium comes from Mr. Sodium himself, Robert Schrier (fun fact: the founding member of my practice, Joseph Beals, was college roomates with Robert Schrier). This group found excellent performance of FENa in 85 patients:

Dr. Kohn is in the middle

FEUrea was invented by Kaplan and Kohn in 1992 (Fun fact: Dr. Kohn was one of my professors at University of Chicago) but the technique was not validated until 2002 when Cavounis et al prospectively looked at 102 patients with AKI. I remember reviewing the Cavounis article in journal club with Dr. Kohn in the room.

Results for using FENa to diagnose pre-renal disease (<1%)

  • 92% sensitivity without diuretics
  • 48% sensitivity with diuretics
  • 76% sensitivity for the entire cohort

Results for FEUrea to diagnose pre-renal disease (<35%)

  • 90% sensitivity without diuretics
  • 88% sensitivity with diuretics
  • 89% sensitivity for the entire cohort

Kim et al looked at 107 patients with acute kidney injury. Instead of pre-renal versus ATN they used transient versus persistent. They also looked at the performance of the AKI indices in the context of diuretics. (disclosure, I just read the abstract)

Results for using FENa to diagnose pre-renal disease (<1%)

  • 96% sensitivity 100% specificity without diuretics
  • 63% sensitivity 98% specificity with diuretics

Results for FEUrea to diagnose pre-renal disease (<30%)

  • 92% sensitivity 87% specificity without diuretics
  • 96% sensitivity 83% specificity with diuretics

Diskin et al looked at 100 oliguric patients and evaluated FENa and FEUrea. They used 40% for the line with FEUrea and 1% for FENa.

  • FENa 54% sensitivity
  • FEUrea 95% sensitivity
This was all the data I could find on trials that look at FENa and FEUrea. Overall, it performed quite well in most studies. In fact the two trials that Perazella quoted were the only two with the indices embarrassing themselves.
Jonathon Gotfried’s article in the Cleveland Clinic Journal was a great resource for this article.