A randomized clinical trial assessing the effect of automated medication-targeted alerts on acute kidney injury outcomes. F Perry Wilson, et al. Nature Communications 2023.
Diagnostic Performance of Fractional Excretion of Sodium for the Differential Diagnosis of Acute Kidney Injury. Abdelhafez, Mohammad Et al. CJASN 2022.
And the editorial by Seethapathy H, and Fenves AZ CJASN 2022
Weekend Hospital Admission, Acute Kidney Injury, and Mortality James et al JASN 2010
Timing of Renal-Replacement Therapy in Patients with Acute Kidney Injury and Sepsis Barbar S, NEJM 2018
Timing of Initiation of Renal-Replacement Therapy in Acute Kidney Injury STARRT-AKI Investigators NEJM 2020
Intensity of Renal Support in Critically Ill Patients with Acute Kidney Injury The VA/NIH Acute Renal Failure Trial Network NEJM 2008
Early versus standard initiation of renal replacement therapy in furosemide stress test non-responsive acute kidney injury patients (the FST trial) Nuttha Lumlertgul et al. Critical Care 2018
Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial. Samir Jaber The Lancet 2018.
Sometimes you listen to a podcast and wonder if the producers listen to their own podcast?
This week JASN dropped a podcast, Absolute CKD Progression Risk, that was poorly produced. This is a shame since the content was great. The host, Manjula Tamura, did a wonderful job interviewing Maria Clarissa Tio and Tariq Shafi on their fascinating study about the utility of absolute versus relative CKD risk. I loved the content. But the producers botched one of the steps in editing. Towards the end of editing, the producer needs to compress and normalize each track so that each speaker has roughly the same volume, and that volume is fairly loud. In this instance, Tamura was quiet, Tio was really quiet, and as I cranked up the volume to hear them, Shafi would blow out my eardrums. I spent the whole podcasts repeatedly turning volume up and down. Here is what it looks like:
I normalized the audio. It is not great, because I do not have the edited tracks in lossless audio, but I was able to improve the audio using Auphonic so that it looks like this:
Look at how the average volume is brought up quite a bit so that the difference between the quiet parts and loud parts is minimized. You can hear the result here:
For the last half year or so, I have been writing a newsletter for MashUpMD. I grab some interesting lingos from around the web, string them together with some of my thoughts and they send it out packaged with a handful of ads. And I get paid.
All and all it feels like blogging. Having someone give me a deadline and a small check apparently is what it took to bring me back to blogging.
I am going to try to bring these posts to PBFluids, but what you should really do is subscribe to me through MashUpMD.
Here is the most recent newsletter…
Hello and welcome to the NKF Spring Clinical Meetings. Follow @Neph_Times on X for updates. I will be live-tweeting the meeting on that account. Also, come to the Westin hotel bar tonight (Wednesday) to say “hi” and clink glasses with the “NephJC” posse.
Today’s email does a deep dive into an unfortunate case of osmotic demyelinating syndrome. We should try to learn all we can from these bad outcomes to protect future patients.
The next group of links concerns a new study in JAMA that aims to improve our basic cardiovascular (CV) risk models by adding contemporary CV blood tests. It does not go well and is a cautionary tale for all of those business plans built around high-margin executive physicals.
I close out with the latest results of the USMLE part 1. This is the second set of scores since the test went pass-fail in 2022, and the pass rate is down… again. But don’t jump to any conclusions before reading the thread in the link.
Thanks, and see you at the NKF Spring Clinical Meetings.
Terrible case of a patient who was admitted with hyponatremia, sodium 118 mmol/L. Using 3% saline, the team brought the sodium up to 125 but it then drifted back down to 121. This prompted a nephrology consult who recommended salt tablets, fluid restriction and tolvaptan 15mg. The next day the sodium was up to 125 and the then nephrologist bumped the tolvaptan to 30 mg. The next day the sodium riose 133 and the patient was discharged on 30 mg of tolvaptan daily. The following day the patient was confused and had sodium is 152! The patient presented to the ER the next day with a sodium of 170! I don’t use tolvaptan often, but when I do, I don’t pair it with another therapy for hyponatremia (no fluid restriction, no salt tablets, no urea).
This article by Rastogi and Velez looked at both tolvaptan’s efficacy and the risk of sodium over correction at two different doses. They found that the standard 15 mg dose regularly over corrects the sodium, using 8 mEq/L per day as their target, in SIADH. This is important. This study was practice changing for me. When the patient has SIADH, and I want to use tolvaptan, I use 7.5 mg. If there was a lower dose I would use that, but since tolvaptan is a triangular, crumbly pill, it is had to get a reliable dose less than 7.5 mg.
Tolvaptan’s effectiveness is highly dependent on the diagnosis. The risk of rapid correction with 15 mg was 84% less likely with heart failure as compared to SIADH. The authors found a low BUN (consistent with SIADH) and a low sodium to be the best predictors of rapid correction. The low sodium is consistently a risk factor for rapid correction. As sodium’s fall below 120 be more and more careful about overcorrection. I don’t use tolvaptan in those patients, and prefer 3% saline because I can turn it off if things go sideways.
These investigators looked at over 160,000 people from 28 cohorts in 12 countries to try to improve the traditional CV risk assessment. Surely adding high sensitivity troponin-I, nt-ProBNP, and hsCRP to the traditional risk factors (age, gender, race, systolic blood pressure, HDL and total cholesterol, smoking, and diabetes status) would provide greater accuracy, and they do! But the headline is how little they move the needle. The area under the curve (or C-statistic) moved from 0.812 with traditional risk factors to 0.8194 with the addition of all 4 blood tests!
Bryan Carmody does his usual amazing job at dissecting this data without the typical sky-is-falling mentality found on X. Do not miss the expanded Y graph and the reminder of what the test scores means for individual test takers and their reproducibility.
Follow MashupMD @MdMashup to stay up to date on the latest topics your peers are discussing.
PowerPointWhat’s New in Nephron Town (16.9 MB) Note: I create, rehearse and deliver the presentation in Keynote. The PowerPoint version is a simple export of the Keynote presentation and often looks like garbage. If you want to see the presentation as it was meant to be, use Keynote.
PDFWhat’s New in Nephron Town (9.8 MB) Note: The PDF shows only the final build of the slides and often that is not very illustrative of the point that the slide was trying to make. If you want to see the presentation as it was meant to be, use Keynote.
Outline of the talk. I originally outlined a section on aldosterone synthase inhibitors and IgA nephropathy, but ran out of time preparing for the lectures (aldosterone synthase) and thought it was not a great topic for general medicine audience (IgA nephroathy).
This summer I was really optimistic. I was riding a #Flozin high that was being further buoyed by the successes of finerenone. Long dormant fields were yielding fresh life. How long has it been since we’ve had this much investigation into glomerulonephritis? So many trials. So many agents.
This is how I started a letter of rec I wrote this summer:
Can you feel it? Can you smell it? Yup, the winds of change have reached nephrology. Just as the most optimistic and sanguine nephrologists predicted, the new diagnostics, new therapies, and new hopes have blown in fresh enthusiasm for nephrology as a career. I am seeing more interns express interest in nephrology, more seniors asking for letters of recommendation, and more general interest for our specialty than I have seen in a score of years. Yes, the gains in the match results have been meager but change is coming and Dr. XXXXXX is a flag bearer for this renewed renal enthusiasm.
Well I was wrong. The winds of change were blowing us backward. After a good year for 2023’s starting class, this year’s match was a dud.
All those unfilled positions often make the training harder for the fellows that do match. And residents see how hard the training is. And they see the long and unpredictable hours. And hospitalist looks better and better.
I love nephrology. I want nephrology to be a vibrant, attractive specialty, but what we are doing, isn’t working.
We have added training capacity like mad without building the demand for the positions. Look at the number of people matching every year (yellow). It is pretty flat since 2014. But the number of positions, and unfilled positions has grown steadily (blue).
This graph from Brian Carmody is interesting. Look where rheumatology and endocrinology are. Two specialties that are not lucrative. But they fill. Reliably and competitively. Lifestyle is important. This has been neglected in nephrology. We work hard, long, hours for sick patients. This should be an area we work on to remodel the specialty around new visions of work. Do we need to train nephro-hospitalists? Consider a one year fellowship with a focus on ICU and inpatient nephrology. Less clinic. Less GN. Less chronic dialysis. And this could be paired with an outpatient nephrology fellowship. Also one year. Modeled after endo or rheumatology with a clinic based schedule. Time dedicated to learning the skills and procedures to create and maintain dialysis access. If we removed the burden of inpatient rounding, fellows could master outpatient nephro and outpatient dialysis in a single year.
Splitting the roles would make the job easier and less chaotic.
Now look at ID the other end of the graph. ID and nephrology. Two specialties that can’t draw fellows. We need to fix this. This is an existential moment for the field.
I tend to agree with Joel. [this is the most important part] The discussion around compensation is valid but doesn’t explain the strong demand for lower-paying specialties. Besides, as an entrepreneurial nephrologist in private practice a 500-600k salary is not unusual. Money is not everything. Nephrology in the way we currently practice it is not attractive. And trainees see that. Let me explain:
Nephrologists remain proud generalists in an era of ever more complex diagnostic and treatment options. Other than dialysis, for the most part, we don’t own anything that our patients need. We need to beg other specialties to help us with fistula, catheter, biopsy, imaging, infusions, pheresis, and invasive volume assessment. Had we shown some pride, ownership, and support for clinical research as cardiology did, we would have now branched into several subspecialties and be more attractive, given the diverse opportunities catering to different preferences. Still, we also would have likely been more inventive in driving progress. Again, using cardiology as an example, cardiac imaging has advanced because cardiologists understand the clinical problems and have content expertise in finding technical solutions. Cardiac MR or CT wouldn’t be where it was if it were for the radiologists who are busy with 60 different body parts and would remain unaware of questions that would have never been asked.
But rather than creating a subspecialty track, nephrology dwells in the nostalgia of being a generalist. In 2023 still talking about the same electrolyte and acid base problems from 60 years ago with formulas validated in 10 med students.
We are risking to become a profession of mediocre generalists. The average rheumatologist is better at treating lupus nephritis than the average nephrologist. Not because they are the better doctors but because the nephrologist also has to master peritoneal dialysis, CRRT in ICU, post-transplant renal care, hypoNa with seizure, and on and on. How do we expect trainees observing us (jacks of all trades and master of none) and getting inspired??
Nephrology as a specialty needs to have either a radical makeover or will diminish and perish, with endo taking over electrolyte management, rheum autoimmune disorders, cardiology volume and BP, critical care CRRT, and so on. Some say that would be good so. Because it would be better for the patients.
And though this was not in response to this essay it is a good thought
I, too, think about the #nephrology match, not that I can do much about it.
Crazy question: What changed in 2011, that might have precipitated a trend that would fully manifest a few years later?
I have a long-time patient who came in yesterday and we were reviewing their labs together and noted a tremendous success. The patient’s albuminuria has fallen 90% since 2018. This is due to adding and then maximizing losartan, adding dapagliflozin, and most recently starting finerenone.
Here is the albuminuria over time:
Over that time their eGFR looks like this:
How should we square the recent drop in eGFR with the reduction proteinuria? We typically switch to a risk based model, here are their Tangri KFRE scores over time:
I was quite surprised to see the KFRE rise over time despite the 90% reduction in albuminuria. I am not changing therapy. The eGFR is nearly intact and I am not going to tiny changes in creatinine (the most recent jump was less than 0.2 mg/dL) guide therapy decisions. I am going to continue to ride these medications which have repeatedly been shown to protect kidneys (and hearts).
It saddens me that #MedTwitter is dissolving but sometimes the old #MedTwitter shines through. A few weeks ago I published a Tweetorial on Gadolinium. Great comments. Great engagement.
I create all of my presentations in Keynote. In the past I was able to present them in Keynote but due to construction and having to give lectures in 156 of North Foundation I had to convert the presentations to PowerPoint. And then hope that PowerPoint on the PC was mostly like PowerPoint on the one true computer, the Mac. It works surprisingly well, but this slide is an outlier.
Here is what it looks like in PowerPoint on my iMac
This is better, but how does this slide fit into the lecture? It is a summary slide after I have discussed two of the causes of the maintenance of metabolic alkalosis. Here is the slide that introduces the four mechanisms for maintaining metabolic alkalosis
Then the lecture describes kidney failure (the easiest to unsderstand)
After that I cover the mechanisms by which hypokalemia maintains metabolic alkalosis in 7 slides as seen here:
The I do the same for chloride (volume) deficiency in 7 slides:
After going through that I noted similarities between the mechanisms of hypokalemia and chloride deficiency, the summary slide is designed to highlight those. Looking at that slide now, it doesn’t do such a good job of that. Does this pair of slides work better?
Here is the revised powerpoint for you to download
This is a frequent cause of confusion. I know that I was confused by this when I was a young learner. And I believe the source of this confusion was garbled teaching from a resident that was still struggling with the concept.
Take this ABG:
pH: 7.26
PaCO2: 80
HCO3: 39
The Henderson-Hasselbalch variables are moving in discordant directions (pH down, pCO2 and HCO3 going up) so it is a respiratory disorder. The pH is decreased so this is a respiratory acidosis.
Now look at the compensation to see if there is a second primary disorder affecting compensation.
In acute respiratory acidosis the HCO3 rises 1 mEq/L for every 10 mmHg the CO2 rises.
In chronic respiratory acidosis the HCO3 rises 3 mEq/L for every 10 mmHg the CO2 rises.
This patient’s CO2 is 80, an increase of 40, so the HCO3 should rise 4 (4×1) if the respiratory acidosis is acute, yielding a bicarb of 28 (24+4). The actual bicarbonate is 39, too high, so there is an additional metabolic alkalosis if the respiratory acidosis is acute.
If the respiratory acidosis is chronic, to increase in CO2 of 40 should increase the bicarbonate by 12 (4×3), so a bicarb of 36 (24+12). The actual bicarbonate is 39, which is just outside of our ±2 so we’ll call it nearly appropriate with just a touch of metabolic acidosis.
The ABG can be “solved” with either acute or chronic respiratory acidosis. Patients cannot be diagnosed with Occam’s razor so the simpler explanation (chronic respiratory acidosis without the need for additional acid-base disorders) may not be the right one. In medicine we need to assume Hickam’s Dictum “A patient can have as many diseases as he damn well pleases.”
The ABG does not determine whether a patient has acute or chronic respiratory disorder, the physician must do that.
So what’s my beef with the two Bruces? Take a look at this question from chapter 8…
The simple acid-base disorders are:
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Respiratory acidosis
Respiratory alkalosis
But this is answers the authors expect…
Since the question stipulates that these are simple acid-base disorders, one can extrapolate the acuity of the respiratory disorder by the degree the bicarb has adjusted, a large adjustment is chronic, and a smaller change is acute. But since patients don’t tell you if they have simple or complex acid-base disorders when the blood is drawn, this trains students to expect the ABG to provide information that it cannot provide.
