New medical blog

Kamran Boka, a resident at St John's wrote an excellent on-call manual. It has been released under creative commons license.


This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License.

Free to share and free to make derivative versions, with attribution. The manual is nicely put together and you can find the PDF at his blog, Vagal Thoughts.

AASK: a cautionary tale for bardoxolone?

Robert Leversee had some questions regarding my presentation on diabetic nephropathy. You can see his concerns in the comments after the post. he was specifically concerned about this slide.

Robert felt it minimized the GFR gains found with bardoxolone. What is not clear from the deck is that 56 weeks, represents the GFR one month after stopping the drug. In the lecture, I pointed out that patients that were on bardoxolone all had a higher GFR than at baseline, while patients randomized to placebo had a lower GFR.

As a reminder, the primary end-point of the study was the change in GFR at 24 weeks and that was dramatic.

The reason I included the slide showing the 56 week data was my concern that bardoxolone may be pulling a creatinine slight of hand. My personal concern is that the changes in GFR are due to simple hemodynamic changes like were seen with amlodipine in AASK.

AASK was a trial of hypertension therapy in African Americans with a renal end-point rather than a cardiovascular end-point that are more common in hypertension trials. The trial is a two by three design with two blood pressure targets (MAP 102-107 vs <92) and three blood pressure medications (amlodipine, ramipril, metoprolol).

The data is difficult to interpret because the amlodipine caused an acute hemodynamic-related bump in the GFR, but after 12 months the loss of GFR in the amlodipine group was faster than with ramipril. The study designers designated co-primary end points, a total change in GFR and a chronic change in GFR that ignored the initial 3 months.

Ramipril was superior to amlodipine in the chronic phase but not in the total change in GFR. Though this ambiguity was not represented in the conclusions of the trial:

The fact that amlodipine improved renal function for one year makes me nervous about the one year duration of the bardoxolone study. Thankfully BEACON is in full swing enrolling patients so a definitive answer is just ahead.

Brilliant little video on exercise

My pithy little push for exercise is that it is the closest thing we have found to the fountain of youth. That it doesn't mater what disease you look at, increasing you exercise or fitness is associated with better outcomes.

Love this video.

Less medicine, better care

Thought provoking article at Zocalo Public Square by Ken Murray a family practice doctor who writes that he was so frustrated with futile end-of-life care he suspended his hospital practice.

Of course, doctors don’t want to die; they want to live. But they know enough about modern medicine to know its limits. And they know enough about death to know what all people fear most: dying in pain, and dying alone.

The essay feels right but relies on anecdote rather than data to support the central premise that doctors are more likely to to use hospice and palliative care to have gentler passing.

Diabetic nephropathy

I was invited to do grand-rounds at St John and was given no guidance on selecting my topic. I recently received a phone call from a long-time family friend, this man had literally changed my diapers, and he asked me to help a relative get bardoxolone. My group is participating in Beacon (the current phase II trial for bardoxolone) and though I am not one of the investigators I assured him that we would evaluate his friend. I couldn't guarantee he would get study drug rather than placebo or even qualify for the trial.

The whole event shocked me. I had no idea that the results of the Bardoxolone study had slipped beyond the geek fringes of nephrology. It reminded me of a story that Judah Folkman told. He came to Indiana University to collect an award and give a lecture, shortly after a NYTimes profile. In that front page story James Watson (yes that James Watson) said Folkman would cure cancer in two years.

Judah told the story that he was getting phone calls from strangers and friends asking for his miracle cure and was heart broken because he had nothing to offer them. At that stage his drug was only for mice.

That's Judah and me following the afore mentioned lecture in 1999.

Getting that call from my friend gave me the same sort of Folkman moment. I never thought people would be calling me trying to get experimental therpy. So I decided to talk about Bardoxolone.

As I started my research I became concerned that patients randomized to bardoxolone developed increased albumniuria.

Some patients tripled their albuminuria! The drug increased GFR, but the increased albuminuria could not be fully accounted for by the improved function.

ASN Kidney Week fell 10 days prior to my Grand Rounds so I planned on grabbing some good ideas at the meeting. On Friday I went to Kidney Disease in Type 2 Diabetes: New Insights. There were four lectures. The last two were homeruns.

Dr. Bruce Perkins was perfect for my talk. He spoke of how albuminuria is not a great surrogate end-point for diabteic nephropathy studies. Bad outcomes often follow a reduction in proteinuria.

I used my iPhone to record the audio and took pictures of each slide with my Nikon (this was before I learned that ASN did not want attendees taking pics of the lectures. WTF). When I got home I grabbed the best thoughts from his lecture and made it the cornerstone of my talk on diabetic nephropathy, bardoxolone, and a more modern view of albuminuria.

Thanks Dr. Perkins.

The lecture was a little light, I finished in 45 minutes and used some filler from my Diabetic Nephropathy 2009 lecture. Before I use the lecture again I would add some of the points from Andrew Bomback's excellent lecture, "RAAS Blockade: More is better? Yes. No. It depends."

Here is my PowerPoint (58mb) and PDF (51mb).

Note to self: the Helvetica Neue UltraLight, didn't project so well.

We've got one! Finding a functional adrenal adenoma

A year ago, a slender, 40 year old, white female presented to my clinic with new onset elevated blood pressure. The hypertension was discovered during a routine visit for a minor injury. The family practitioner refused to believe the vitals and kept having the patient return for follow-up visits before resigning himself to the diagnosis. Surprisingly, this otherwise healthy woman, was resistant to multiple medications. He began to suspect a more sinister diagnosis and initiated a work-up for secondary hypertension and referred her to me.

The initial work-up showed a aldosterone of 16 but the renin was not done. She also had modestly elevated metanephrines, but not high enough to suggest a pheochromacytoma. Her blood pressure typically ran 140-160/100 with labetalol 100 mg bid, but she admitted to being forgetful regarding her medications.

One of the findings that stood out for me was the hypokalemia on the initial labs

We repeated the renin-aldo ratio and did a EKG. Unfortunately she had LVH. For me, this ruled out white coat syndrome. The demonstration of end-organ damage also helped the patient see that this condition was "real" and after that she was compliant with the medical therapy.

The repeat Aldo was only 3 with a fully suppressed renin at 0.15. This is an aldosterone-renin ratio (ARR) of 20, however, I was taught a low total aldosterone ruled this diagnosis out. In other words, one needs an elevated aldosterone, not just a suppressed renin to make the diagnosis of primary hyperaldosteonism. This always made sense to me but the Endocrine Society states that this is not always true and questions the requirement for a high aldosterone:

Against a formal cutoff level for aldosterone are the findings of several studies. In one study, seated plasma aldosterone levels were less than 15 ng/dl in 36% of 74 patients diagnosed with PA after screening positive by ARR defined as more than 30 and showing failure of aldosterone to suppress during fludrocortisone suppression testing (FST), and in four of 21 patients found by AVS to have unilateral, surgically correctable PA.

Her potassium remained low at 3.1 despite potassium supplementation. She was breast feeding at the time so we did not use an ACEi or ARB and were successfully treating her blood pressure with a combination of nifedipine XL and labetalol.

The low aldosterone appeared to rule-out primary hyperaldo but with the unexplained hypokalemia I ordered a third ARR and hit pay-dirt

An ARR of close to 300 with a sky-high aldosterone of 29. Remember, when you calculate the aldosterone-renin ratio make sure the units are correct:

• aldosterone in nanograms per deciliter
• renin measured as plasma renin activity (PRA) in nanograms per milliliter per hour

With a positive ARR, the endocrine society recommends a confirmatory test. There are four recommended tests, all of which are variations on attempts to suppress endogenous aldosterone via sodium loading or fludrocortisone suppression. I did not do this. I feel that the critical diagnosis to make is the functional adenoma that is surgically curative. Whether the patient has bilateral hyperplasia or simply aldosterone driven hypertension that doesn't meet the criteria for primary aldosterone is not important to me because I'm going to treat both of those conditions identically, with spironolactone or eplerenone.

So we proceeded with the work-up for a functional adenoma and sent her for a CT scan. We found a 1 x 2 cm left adrenal mass.

Here is where it gets tricky. This sounds like a functional adenoma, however functional adrenal adenomas are rare diagnosis, and even in the presence of documented hyperaldosteronism, non-functional incidentalomas are too common (0.35-5%) to assure that a CT finding of an adrenal mass represents a functional adenoma. Following a CT scan, you can neither rule-out nor rule-in the diagnosis of a surgically correctible functional adenoma. Patients still need to get adrenal vein sampling. Here is the experience from University of Texas Southwestern:

Twenty patients had unilateral CT abnormalities, and 14 (70%) of them lateralized to the same side (concordant). Of the remaining 6 patients with unilateral CT abnormalities (3 left and 3 right), 1 patient each lateralized to the opposite side and 2 patients each had bilateral hypersecretion. Only 5 of 15 patients (33%) with bilateral CT abnormalities showed concordant bilateral aldosterone hypersecretion. The other 10 patients (67%) demonstrated unilateral hypersecretion. Of the 5 patients with normal-appearing adrenal glands on CT, 1 patient each lateralized to 1 side, and the other 3 patients had bilateral hypersecretion.

The authors did not provide a 2x2 table to determine sensitivity or specificity (insert rant regarding surgical literature here) so I put one together. This is how I interpreted the data above:

• Positive test: 20 with unilateral findings, 14 true positives and 6 false positives (I considered the CT scan identifying the wrong affected adrenal as being a fail)
• Negative test: 15 patients with bilateral findings, 5 were true negatives and 10 were false negatives
• Negative test: 5 patients with normal adrenals, 2 lateralized, false negatives and 3 true negatives

The two-way table looks like this:

What? You're still using Epocrates' medical
calculator? Don't be a tool, get a tool, MedCalc

It should be apparent that a CT scan looks truly terrible at diagnosing a functional adenoma. A negative predictive value of only 40%. Ughh! Note: these numbers assume the adrenal vein sampling is a valid gold-standard.

We sent her for adrenal vein sampling to see if the aldosterone secretion lateralizes. It did with a 20-fold increase in aldosterone on the left side. Because aldosterone levels can be unreliable due to dilution and technique, it is recommended that an adjusted aldosterone (aldo/cotisol) exceed the contralateral adrenal by three fold. In our case, it was 10-fold.

She went for an laparoscopic left adrenalectomy and is now normotensive off all medications.

The endocrine society had published consensus recommendations on screening, diagnosis and treatment of primary hyperaldosteronism. I love it when important articles are available in PDF for free.

Water humor.

Inorganic chemistry jokes: rare and rarely funny.

And the data keeps rolling in...

I am a believer in Richard Johnson's theory regarding fructose uric acid and hypertension/CKD. So I love it when I see another study adding to the foundation. This from Diabetes Care. The investigators looked at 1500 patients with diabetes and normal renal function and no proteinuria. Over 5 years they tracked who developed CKD (either GFR<60 or proteinuria):

During a 5-year follow-up period, 194 (13.4%) patients developed incident CKD. The cumulative incidence of CKD was significantly greater in patients with hyperuricemia than in those without hyperuricemia (29.5 vs. 11.4%, P < 0.001). In univariate logistic regression analysis, the presence of hyperuricemia roughly doubled the risk of developing CKD.

the iPhone as tricorder

Looks like bubble-mania to me. What do you think?



Via Brian Hall's Smart Phone Wars

Write your own text book, save money

I bet this becomes a real trend as school districts become short for cash.

Anoka-Hennepin teachers write their own online textbook, save district $175,000

Instead of mass-produced textbooks, the more than 3,100 sophomores in the state's largest district are learning from an online curriculum developed by their teachers over the summer with free software distributed over the web.

 For the extravagant tuition charged at medical schools it seems they should throw in the course materials for free. No?

Dynamed versus uptodate

I received the following announcement from our hospital librarian

We are conducting a trial of the online clinical resource Dynamed for the month of November.  We wanted to get some feedback on this product as an alternative to UpToDate, or possibly as an addition to our electronic resources before we negotiate with UpToDate.

So to check it out I did a quick tour of UpToDate and then the same tour on DynaMed. I recently diagnosed a patient with Goodpastures so I looked that up in both databases.

UpToDate

UpToDate has a great autocomplete system for search terms. Not sure if Goodpasture is one or two words? Don't worry, typing "Good" is good enough.

The number of topics on Goodpastures is remarkable.

I love how the topic outline slides opens on the right when you hover over a topic. When I selected Treatment of anti-GBM antibody (Goodpasture's) disease I was treated to 3500 words (excluding references, of which there were 32) written by an editor team that puts their name to the review. In this case the authors are all tops in glomerulonephritis:

The article is long, detailed and tells the reader exactly how to treat the patient. What drugs, alternative treatments, how to pheresis including replacement fluid, schedule, dose and duration. It is beautiful in its completeness.

DynaMed

I typed in Good, no autocomplete at all. I searched Good and good pastures is not on the first page of search results. 

I searched Goodp and got nothing.

Searched Goodpastures and...jackpot! They even have the roll-over see the outline trick from UpToDate. Nice

The actual article though, is terrible compared to UpToDate. They have a single entry on Goodpastures which is barebones outline of the condition.

The treatment section contains 159 words, and really gives you no idea how to treat this condition. In fact, about a third of the treatment section is dedicated to combination ACEi and ARB therapy, a window dressing issue in the treatment of this rapidly progressive and potentially fatal disease. I would give this reference a failing grade. You read all 159 words and have no idea what to do. You need to go to a second source.

Their is no author associated with the outline of Goodpastures. Dynamed's editorial team does not list any nephrologists. The editorial board does have a single nephrologist, which is exactly how many podiatrists they have on the board.

As my colleague, Dr Steigerwalt, said, it should be spelled DinoMed as in Dinosaur.

AJKD launches a blog

Say hello to eAJKD. Kenar Jhaveri of Nephron Power is the editor and he has enlisted much of the nephrology blogosphere, including your humble author to assist him on this endeavor.

Recently some of the all guard of media have started compelling blogs (see the New York Times' page of blogs for an example). Medical publishing seems to have lagged in this phenomenon.

All of the interesting medical bloggers are independent agents, though The Lancet, JAMA and NEJM have all launched blog initiatives.

I hope that eAJKD aspires to be something special, I'll do my best to assist it.

It should be a fun adventure.

Crazy numbers: the lowest hemoglobin I have ever seen

When I was a resident I saw a really low hemoglobin. I don't remember what the number was but I remember the circumstances. I was working the ER at Riley Children's hospital and EMS pulled up with a infant who was short of breath. The family had been feeding him cows milk instead of formula and as a result he had severe iron deficiency anemia. Great case and after a few transfusions and some parental education, everyone lived happily ever after.

Last week I saw another lowest hemoglobin. Since I wasn't blogging when I was a resident I don't know if this hemoglobin is lower than that poor kid but here it is:

Hemoglobin of 3.6 g/dL. The hematocrit is still a double digit number, but still that's a really low hemoglobin.

This is a dialysis patient who started having some vomiting that looked a little "dark" but didn't really bother him. A day or so later he developed some dark colored diarrhea. Still didn't bother him. Then he found himself short of breath, like he missed a treatment and got volume overloaded. This kept getting worse so he finally decided to get in his car and drive to the ER. The admitting hemoglobin was 3.7 followed by a repeat by I'm sure a disbelieving ER doc.


Diagnosis duodenal ulcer and after a half dozen transfusions and a prescription for BID omeprazole he was discharged home to lived happily ever after.

Articles that changed the way I practice: ACCOMPLISH

I was searching PBFluids and could not find any posts about ACCOMPLISH which surprised me. I then went to the Renal Fellow Network and found a similar lack of commentary. Dito for Nephron Power, and Nephrology on Demand. Even The Kidney Doctor with 100+ posts (and in the process putting the rest of the nephrology blogosphere to shame) in the last 2 months comes up empty handed.

Now some of this may be due to faulty blog search and some of this may be due to the fact that the study is approaching 3 years of age, but regardless ACCOMPLISH is important enough that it should get higher profile coverage.

The study was published in the NEJM in 2008

The acronym is an obviously:

• Avoiding 
• Cardiovascular events through 
• COmbination therapy in 
• Patient 
• LIving with 
• Systolic 
• Hypertension

From the title, if not the acronym, the point of the study should be clear: The study pits benazepril and amlodipine (Lotrel) against benazepril and hydrochlorothiazide (Lotensin).

The politics of this fight are interesting as this study tries to right one of the possible mis-steps in the wake of ALLHAT. ACCOMPLISH used the thiazide diuretic that is actually most often used in the U.S. and the only thiazide that is used in combination pills, hydrochlorothiazide (yes I know I'm ignoring Tenoretic, atenolol and chlorthalidone, but every other combination pill uses hydrochlorothiazide). ALLHAT used chlorthalidone as its diuretic and when this largest-ever hypertension study concluded that there was no difference among chlorthalidone, amlodipine and lisinopril on fatal coronary heart disease and non-fatal heart attacks, thiazides became institutionalized as the primary agent to treat hypertension.

Figure depicting the primary outcome from ALLHAT

The money shot from JNC7 (pdf) institutionalizing thiazide-type diuretics

The problem stems from the fact that hydrochlorothiazide and chlorthalidone are unique molecules with significant biologic and pharmacokinetic differences.

This year Dorsch et al re-analyzed data from the MRFIT trial. This was a long-term primary prevention trial from the 70's that changed protocols mid-stream and converted patients from HCTZ to chlorthalidone. This allowed Dorsch's team to look for differential effects of the two diuretics. They found a 21% reduction in cardiovascular events with chlorthalidone:

If you are interested in the reasons behind the differences read John Flack's editorial associated with Dorsch's analysis and look at a 2004 review by Carter et al.

So ACCOMPLISH set out to show that the ACEi CCB combination is superior to the ACEi HCT combination. They randomized 11,506 patients to one of these two arms. The dosing titration seems fair:

1. 20 benazepril and either 5 of amlodipine or 12.5 of dydrochlorothiazide
2. if BP is not < 140/90 (130/80 in CKD and DM) increase to 40 mg of benazepril
3. if BP is not < 140/90 (130/80 in CKD and DM)  increase to 10 of amlodipine or 25 of hydrochlorothiazide
4. if BP is not < 140/90 (130/80 in CKD and DM)  add additional agents as needed

The cohort was rather sick with previously diagnosed hypertension and an additional history of at least one of the following:

• Coronary events
• Impaired renal function
• Peripheral artery disease
• LVH
• Diabetes.

The end point was time to first cardiovascular event, or death from cardiovascular disease.

The study was well run but the blood pressures were not perfectly equal between groups with a small but statistically signifigant difference in the blood pressures between the two groups:

• 131.6/73.3 in the Benazepril-Amlodipine group
• 132.5/74.4 in the Benazepril-Hydrochlorothiazide group
• A difference of 0.9/1.1 in favor of the Benazepril-Amlodipine group

The study was terminated early because the data and safety monitoring committee observed a difference between the two groups that exceeded the pre-specified stopping rule. They found a 20% risk reduction in only 30 months. This represented an absolute risk reduction of 2.2% which translates into a Number Needed to Treat of only 45.

Entering EBM free zone:

To my eyes, ACCOMPLISH better represents the patients I see than ALLHAT. All of the patients that come to my CKD clinic have high blood pressure and almost all also have the additional co-morbidities needed for enrollment. After fully digesting ACCOMPLISH I have made two changes in my practice pattern:

1. I am starting patients with ACEi + CCB or ARB + CCB. I have been impressed by the effectiveness of Lotrel and Exforge as single pill solutions to a lot of hypertension.
2. I avoiding hydrochlorothiazide where ever possible. This usually requires re-jiggering a number of medications but a common switch will be to move patients from a list that looks like this:
1. Lisinopril HCT
2. Amlodipine

          To a list that looks like this:

1. ACEi CCB combination pill
2. Chlorthalidone

This results in significant improvement in blood pressure control.
I have to thank ACCOMPLISH to opening my eyes to this change.

Nephrology blog-together at Kidney Week

Next week is ASN's Kidney Week in Philadelphia. Some of the kidney bloggers are going to be getting together to clink glasses and talk blogging, kidneys, MedEd and whatever else spills from our lips. We are meeting at McGillin's Olde Ale House.

When you get there look for the nerdy guys who look like they spend too much time staring at an screen.


Friday, November 11th at 8 pm
McGillin’s Olde Ale House
1310 Drury Street
Philadelphia, PA 19107
215/735-5562
www.mcgillins.com

Hope to see some of you there, and remember when you are tweeting about Kidney Week use the hashtag #kidneywk11

No! No! No! Never! Give a dialysis patient a Fleets Enema!

What is wrong with this picture?

Sevelamer and Fleet Enema. They go together like a honey baked ham and Chanukah. Fleets enemas have an obscene amount of phosphorous and sevelamer (Renvela) is a phosphorous binder. They should never co-mingle on the same MAR. So while some may see a couple of benign medications, I see a Chanukah ham.

A  Fleets enema, or any typical sodium phosphorous enema, is roughly 4 onces or 120 ml. The active ingredient is sodium phosphorous, to the tune of 26g of sodium phosphate per dose, some articles quote a phosphorous concentration of 13,000 mg/dL. Remember, a normal diet has about 1 gram of phosphate and only 700 mg of that is actually is absorbed; so we are talking about a potentially massive overdose.

I love that someone scanned the entire packaging

No patient with kidney disease or on dialysis should get this drug without talking to their doctor. Its written right on the damn package.

I guess, if you are in the hospital and the doctor orders it, that is essentially the same thing as asking your doctor. Too bad that over and over again doctors express their ignorance about dangerous this seemingly innocuous medication can be by ordering it in patients with kidney disease.

A rogues gallery of bad outcomes from the lowly Fleets Enema

The sodium phosphorous enema can be lethal to a patient with kidney failure.

Here is a case report regarding a patient who developed hypocalcemic tetany and coma following a single enema

My favorite quote in the case report is the hyperphosphatemia review of systems:

...the family denied that other drugs or unusual food such as star fruit was given by them- selves.

They gave the patient a couple of amps of calcium gluconate and then dialyzed him on hospital day 6, 7 and 8.

The situation is even more harrowing if you give the enema orally. This results in massive sodium and phosphorous absorption. In this case report the team gave it to the patient...twice:

They ran in to trouble while treating a toxic theophylline level. They gave activated charcoal to bind the theophylline. Subsequently, the patient developed an illeus and was given 120 mL of a sodium-phosphorous enema down the NG tube. The next day he received 4 liters of polyethylene glycol via the NG and finally another 120 ml sodium phosphorous enema enterally.

Then he arrested.

They resuscitated him. Here are his post-code labs:

• Na 177
• K 2.8
• CO2 18
• Cr 3.4
• phosphate 59.6
• calcium 5.2
• Ca x Phos product: TFTC*
• pH 7.12/37/40

* Too frightening to calculate

After resuscitation the patient was too hemodynamically unstable for dialysis and died during a subsequent arrest.

Look at that phosphorous! A phosphorous over fifty is like a traffic accident, can't tear your eyes away.
Here's a simple rule:

If the medicine is supposed to go in the butt, don't feed it to your patient.

As high as the phosphorous is however, the symptoms are due to the low calcium. The high phosphorous complexes with the calcium driving the ionized calcium down.

Severe hyperphosphatemia and hypocalcemia: a dilemma in patient management

JASN published a tight review in 1996. They discuss an unfortunate case where a gentleman was prescribed two enemas for a flexible sigmoidoscopy prep. The patient however, mistakenly ingested them orally rather than, you know, using them the right way. 191 mmol of sodium and 208 mmol of phosphorous down the hatch. The patient presented to the ER complaining of foot and hand pain along with diarrhea and difficulty swallowing and speaking. Data on presentation:

• QTc 0.6 sec (prolonged)
• ionized calcium 0.34 mmol/L
• total calcium 4.5 mg/dL
• Na 154 mmol/L
• phosphate 44.8 mg/dl
• anion gap 39

The patient was managed with insulin and dextrose, aluminum hydroxide and IV calcium gluconate along with IV fluids. Dialysis was delayed for 4 hours due to difficulty gaining IV access. He was dialyzed against a high (3.5 mg/dl) calcium bath

One of the points I tried to highlight in the graph is the rapid drop in the phosphorous prior to the dialysis. The conservative therapy of IV fluids, insulin, and aluminum hydroxide look highly effective. Also note how effective dialysis is at raising the calcium.

The authors make an excellent point regarding the acidosis. The patient had an initial pH of 7.28 and an anion gap of 39. The anion gap is from the high phosphorous. The authors point out that treating the acidosis with alkali will further drop the ionized calcium and is contraindicated until the calcium is corrected.

The discussion of the paper is delicious and addresses a situation I have found myself debating with fellows. The question is what to do when the phosphorous is really high and the patient has hypocalcemic symptoms. Does the administration of calcium lead to metastatic calcification to the detriment of the patient? The authors feel that calcium should be given to treat the symptoms of hypocalcemia and delay full treatment of hypocalcemia until the phosphorous is restored to normal levels.

In terms of personal experience, the MAR from the top of the post comes from a dialysis patient who did receive a Fleets enema while in the hospital. His phosphorous went from 3.5 to 11.7, overnight. He remained asymptomatic but the whole experience terrified me.

No. No. No Never. Give a fleets enema to a dialysis patient.