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Getting another abstract (or two) ready for Renal Week 2009

We are racing the deadline for our ASN abstract. We have a great data set on geriatric patients in a structured CKD clinic. We need to define stable renal function. Our first try used the CKD stages. Our cohort is restricted to CKD 3b and 4. So stable was any patient who began and ended the study in the same CKD stage. This has been done in the literature, so there is some precedence but it doesn’t feel right to me.

Think about two participants in our study, both GFRs fall by 3 cc/min over three years, just about what the Baltimore Longitudinal Study on aging predicts. Patient A started with an eGFR of 31 mL and Patient B started with an eGFR of 33. These patients have the same clinical course and outcome but Patient A goes from 31 to 28 mL/min and hence from CKD Stage 3 to 4 while Patient B goes from an eGFR of 33 to 33 so his stage does not change.

I need a definition of stable renal function. You can help by filling this 5 question anonymous survey. We are looking

How would you define stable renal function:

Candidate A: Change in GFR less than 2 cc/min/yr (essentially 3x the average rate determined by the Baltimore Longitudinal Study on Aging).

Candidate B: Change of GFR of less than 20% from baseline to the end of the study

Candidate C: Change of less than 10 mL/min from the baseline visit

Note: baseline visit is the 1st contact with us with a GFR<45 mL/min(CKD stage 3b), we removed any patient who does not have a second eGFR < 45 at least 3 months before the initial measurement.

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Online endocrine textbook

This looks pretty cool.

Here is the link to the section on kidney stones written by Murray Favus. On my brief overview it looks good.

Being in the textbook business in the era of free online textbooks, UpToDate and wiki’s has got to be a world of hurt.

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Renal stents for preservation of renal function with atherosclerotic renal artery stenosis

The annals has an article this week on renal stents and again they fail.

Stent Placement in Patients With Atherosclerotic Renal Artery Stenosis and Impaired Renal Function

They randomized 140 patients with GFR <>50% stenosis (CT angio, MRA or digital subtraction angiography) with in 1 cm of the origin of the renal artery. They also excluded patients with uncontrolled blood pressure (>140/90) this was done because if patients randomized to medical management developed uncontrollable blood pressure they could cross over and receive a stent.

The end point was a persistant 20% reduction of GFR by Cockcroft-Gault for more than a month.

Results: No significant difference between the two treatment strategies.

The Kaplan-Meier curves confirm this. The top graph is the primary outcome and the bottom graph is primary outcome plus death:
Renal angioplasty resulted a variety of complications:

Two patients in the stent group died of procedure-related causes within 30 days after stent placement. In 1 of the patients, embolization of a perforated renal artery was required; the patient subsequently developed pulmonary edema and needed mechanical ventilation, and died of a massive ischemic stroke 3 days later. The second patient had perforation of a renal artery branch; the artery was embolized, but despite re-intervention, the patient went into hypovolemic shock and experienced the acute respiratory distress syndrome, and died of multiorgan failure after 1 week.

The most common complications after stent placement were minor and mainly consisted of hematoma at the puncture site (11 patients [17%]). In 1 of these patients, secondary infection in the groin required surgical reconstruction. The patient thereafter developed end-stage renal failure, pulmonary edema, and heart failure and died 6 months after the procedure. In 2 other patients, stent placement was complicated by false aneurysm of the femoral artery. Injury to the kidney or renal artery occurred in 5 patients; however, this was never associated with loss of renal function and additional intervention was never required.

One patient in the stent group who had repeated angiography required permanent dialysis after cholesterol embolism.

So another negative trial of renal artery revascularization. We are still waiting for the publication of ASTRAL, a much larger and more definitive trial. CORAL is another trial which is ongoing and will shed further light on this subject.

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Will the UK courts squash scientific discourse?

This article about Simon Singh‘s battle with the British Chiropractic Association is frightening.

The consequences of letting the libel law loose on scientific debate are horrendous. Science proceeds by peer review. A researcher’s colleagues must submit his or her ideas to scrutiny without fear of the consequences. If they think they could lose their homes and savings in the libel courts, however, they will back off.

For alternative therapists are not the only ones answering their critics with lawyers. NMT, an American health giant, is suing a British doctor for questioning one of its treatments.

Incredibly the BCA has won the first legal round.

The BCA sued for libel. And on May 7th Sir David Eady, a high-court judge, ruled, in a preliminary hearing, that the “natural and ordinary meaning” of the phrase (the relevant legal test) was that the BCA was being consciously dishonest and knowingly promoting quack treatments.

The key to the court case is a claim that chiropractic treatments for problems outside of backpain are bogus that Singh made in Trick or Treatment: The Undeniable Facts about Alternative Medicine, a book he coauthored on alternative medicine.

Advancing medicine and science is impossible if writers have to self-censor themselves when discussing scientific claims.

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Nike+ iPod imprecision

I have been running off-and-on for the last 3 years (mostly off) and running regularly for the past 15 months. I love how lightweight it is the antithesis of biking or backcountry hiking with their emphasis on gear. Running is nearly completely free of equipment and gear. All I do is strap on my shoes, plug in the headphones and go. The exception to this is my Nike+ iPod pedometer. This is a cool gadget that consists of a sensor which goes in your shoe and a receiver which plugs into the 30-pin connector on the bottom of the iPod Nano. If you use an iPod Touch you don’t even need the receiver.

I was blown away by the accuracy of the device and have been rediculously satisfied with this $30 gadget. Two events brought home how accurate the pedometer was: I ran a Cinco de Mayo 5k in Brooklyn with my sister a few years ago. The pedometer signaled 5k on the very footfall that crossed the line finishline. It was accurate to the step. Amazing:

I had a similar experience in the Detroit Marathon Relay in 2007. I ran a short segment from Downtown to Belle Isle. As soon as I crossed the timing blocks the iPod signaled I had reached my goal:

Last fall when I did the half marathon the accuracy fell a bit. It recorded 13.6 for a 13.1 mile route but I felt that 5% slosh was okay:

I had the same over estimate occur during the martian Marathon 10k. With the devic recording 6.5 miles for a 6.2 mile run. Again a 5% error:

What inspired this post was the new finding that in 2009 the error has swung in the opposite direction, now the Nike+ is underestimating my distance and speed. I first noted this during an 8.5 mile loop I ran with PBFluids reader and fellow nephrologist Steve Rankin. The Nike+ only recorded 7.98 miles:

Yesterday I did the Dexter-Ann Arbor half marathon and again the Nike+ iPod underestimated the distance and speed:

In the end it was only off by 0.6 miles over 13.1, so 5% but on my next run my Nike+ odometer will cross 1000 miles and its a little less satisfying thinking that I already crossed that milestone at some unrecognized time in the last month or so.

Update: Just discovered that the New York Times recently did a review of the Nike+iPod system.

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The Sugar Fix: Chapter One: The Fructose Factor

Johnson starts The Sugar Fix with the assertion that a century ago heart disease, diabetes and obesity were rare conditions.

In 1890 a survey of 5,000 US citizens revealed that only 3.4% of Americans were obese and they were typically isolated to the upper class. This compares to a contemporary rate of 32%. Two thirds of Americans are either overweight or obese. This includes one third of school children. This obesity rate has doubled since 1976 (CDC Source). The rapid increase in girth cannot be explained by genetics. Johnson feels that the rapid change in the frequency of obesity exonerates genetics as the cause, he states that the human genome has been relatively stable going back a few thousand years.

This leaves an environmental change. He then considers and discards changes in physical activity as the etiology. This is supported by the most recent analysis revealed at the 2009 European Congress on Obesity.

Johnson goes on to implicate fructuse. He states that fructose intake has increased 30% since the 1970’s. Fructose is the main source of sugar in fruit. It is half of the molecule sucrose, table sugar. In 1970 the average American consumed half a pound of High Fructose Corn Syrup. By 2000 that had increased to 42 pounds a year. Though HFCS consumption has risen by two orders of magnitude, fructose exposure has only gone up by 30%. This likely means that HFCS has largely replaced the prior source of fructose in the diet, table sugar. The authors don’t address that inconsistancy in this chapter.

Fructose causes obesity through multiple mechanisms:

  • fructose causes more and faster weight gain than seen with other sugars
  • fructose does not satisfy your appetite resulting in more calorie intake
  • increased fructose dulls the brains responce to the normal satiety signals so that following chronic fructose exposure subjects eat more as they don’t sence “fullness”
  • fructose upregulates enzymes which promote obesity

Johnson believes that other conditions have increased in prevalence in lockstep with the increased exposure to fructose including:

  • hypertension: 73 million Americans
  • diabetes: 20 million Americans (CDC Source)
  • kidney disease: 20 million Americans
  • liver disease: emergence of NASH, now effect 2-5% of Americans (NIDDK Source)
  • metabolic syndrome 55 million Americans

The mechanism linking fructose and these problems comes from multiple metabolic consequences of fructose:

  • fructose is the only sugar which increases the production of uric acid which leads to hypertension
  • fructose increases the production of triglyceridesand lowers HDL
  • fructose causes insulin resistance
  • fructose causes kidney disease

This last section is not supported by any references or data but Johnson promises to reveal the details later in the book.

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Great spoof ad on the impending Palm Pre

The heavy guy in blue is Roger McNamee, co-founder of Elevation Partners, a private equity group with a huge position in Palm. The video is a riff on episode a few months ago where McNamee caused quite a stir by overstoking the hype on the Pre, from Fortune:

In early March, McNamee caused a stir by telling a wire-service reporter that he thought the Pre was so good that customers would give up their iPhones as soon as their AT&T contracts expired. Palm was forced to file a statement with the SEC calling his comments “premature” and “an exaggerated prediction of consumer behavior.”

The slender guy is Jon Rubenstein, one of the creators of the iPod from Apple and the lead designer of the Palm Pre.

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The Sugar Fix: The Introduction

In the introduction of The Sugar Fix, Johnson uses a broad brush to establish the scope and purpose of what he intends to prove in the subsequent 300 pages.

  • He gives a brief anecdote about the increasing prevalence of obesity. His uric acid hypothesis is going to explain this huge health problem.
  • He outlines how he was initially looking for the cause of hypertension when he realized the weight-loss potential of a low fructose diet.
  • He then speeds through a handful of clinical studies, both epidemiologic and interventional, which implicate uric acid as a powerful risk factor for cardiovascular disease, i.e. uric acid as the new cholesterol. He admits that the scientific establishment has not accepted his theory as facts and that uric acid today is where smoking was in the 50s and cholesterol was in the 60s.

He concludes the chapter by disclosing two potential sources of bias. He is the Dr. Cade Professor of Medicine at the University of Florida and that his salary and research is supported by sales of Gatorade by the PepsiCo corporation. This is an interesting disclosure because the cola companies are the principle villains in this morality tale. I wonder if part of the reason for the release of Pepsi Throwback (sucrose rather than high-fructose corn syrup (HFCS) as the principle sweetener) is the pushback against HFCS partially lead by Dr. Johnson.

He also explains that he has applied for multiple patents that could financially benefit him if the relationship of uric acid and cardiovascular disease bears fruit.

(pdf)