Tuesday, June 30, 2009
When you see community acquired pneumonia and the ICU intern mentions that there was a lot of blood during the intubation your mind needs to starting thinking about pulmonary-renal syndromes. Ask the family about a history of sinusitis, pay extra-attention to the red cells on the U/A, fire off that ANCA and anti-GBM ab. It is the job of the nephrologist to consider this diagnosis, if you don',t no one will and a week later when the ICU and ID teams begin scratching their collective heads on why this patient is not behaving like a typical pneumonia you will have the reason and prevent a low yield and dangerous bronchoscopy because you will have the serologic evidence you need to get the renal biopsy for the win.
The cryptic case of acute kidney injury starts off just like the banal case of acute renal failure, a rise in creatinine. If you open your eyes to the faint threads that don't quite fit the standard narrative you will be more receptive to seeing the clues you need to make that rare diagnosis.
Monday, June 29, 2009
Sugar is a carbohydrate, one of three macronutrients in our diet (carbohydrate, protein and fat).
Table sugar or sucrose is disaccharide made of the joining of glucose with fructose. Lactose another disaccharide is made from the joining of glucose with galactose.
Fructose is he sweetest monocachide, about twice as sweet as glucose. Most high fructose corn syrup is about 50-60% fructose about he same amount of fructose as found in table sugar. Honey is 70% fructose. Almost all of the fructose we get in our diet comes from sweeteners added to foods.
The drive to eat sweet foods is inherent in our humanness. We don't need to be taught that fruit tastes better than vegetables. Johnson lays out a teleological argument that follows:
- sweet foods offer a survival benefit by promoting weight gain due to their caloric density.
- weight gain is enhanced by the fact that they don't promote satiety, so you can over eat, an advantage when food is in short supply and spoilage prevents storing leftovers
- the tendency of fructose to raise blood pressure may have offered a survival advantage to ancestors living on salt poor diets who suffered from chronic hypotension
India was the first country to boil the juice from the New Guinea sugar cane to produce crystalized sugar.
Persian invaders brought home sugar and then the Arab invaders of the 7th century spread sugar from Persia to the rest of the Middle East.
The crusades brought sugar back to England in 1099.
Sugar was thought to have medicinal values and sold at pharmaceutical like prices. In 1319, sugar cost the equivalent of $50 per pound.
Sugar was one of the crops which supported the slave trade between Africa, North America and Europe.
England became a dominant producer of sugar and by 1700, the English were ingesting 4 lbs of sugar a year.
The democratization of sucrose accelerated following the discovery of the by which sugar could be extracted from beets.
In 1866 scientists in Buffalo invented a way to convert corn starch into sweet tasting corn syrup. Corn syrup is made of glucose chains of varying lengths. There is no fructose in corn syrup, so it is not as sweet as sucrose.
In the 1960s, glucose isomerase was discovered. THIS enzyme could convert some of the glucose in corn syrup to fructose ushering in high fructose corn syrup (HFCS).
HFCS is cheaper than sugar mainly because of the phenomenal overproduction of corn in this country. See the Omnivore's Dilemma. By the end of the 70's Americans were eating 10 pounds of HFCS every year.
In 1982 the US Government began to limit the amount of sugar which could be imported every year and by 1984 both Coke and Pepsi converted from sucrose to HFCS as the primary sweetener in their respective colas. The sweetwener in most colas is HFCS-55 which has 55% fructose only slightly more than sucrose, 50%.
Johnson states that another common variety of HFCS found in non-carbonated fruit juices is HFCS-42 (42% fructose).
He then claims that much of the harm from HFCS is not because it is anymore toxic than equal amounts of sucrose but rather that, its low-cost has resulted in more consumption.
This explains the expansion in the sizes an portions over the last 20 years. He points out the change in the size of a single serving of Coke. In the fifties it was 6.5 oz and now I am seeing 1 liter bottles (33 ozs) for sale.
The conclusion of the chapter has this wonderful sentence:
More to the point, the composition of basic nutrients that most people eat today is vastly different from what early humans consumed, or even what the typical American ate a century ago.
Friday, June 26, 2009
Thursday, June 25, 2009
Wednesday, June 24, 2009
Friday, June 19, 2009
No one outside of AT&T and Apple know for sure the duration of AT&T's exclusivity. In August of last year USAToday said the contract lasts until 2010 .
My thought is that if the exclusive contract ran out at the end of 2009 or by June of 2010 then AT&T would be behaving differently right now. Instead of telling people whoose contracts expire in a year to get lost for a year they would be rolling out the red carpet to extend their contract for another 2 or 3 years.
Eventually the exclusive deal will end and an early sign of that day will be AT&T offering current customers a deal to extend their contract. AT&T's current behavior signals that the exclusivity is here for at least a couple more years.
Thursday, June 18, 2009
Just a quick review of FGF-23 so I'm not an idiot when this rock star nephrologist starts talking. (FYI don't let the clean cut pic above fool you, he came to the lecture in full rock-star fashion with the long hair, groupies (supplied by Genzyme) and everything)
FGF-23 is produced by osteocytes.
Klotho seems to be a required co-factor for FGF-23, such that mice that are Klotho deficient mimic the phenotype of FGF-23 deficiency.
FGF-23 increases renal phosphorous clearance by blocking Na-Phos reabsorbtion in the proximal tubule. FGF-23 also inhibits 1-alpha-hydroxylase, decreasing 1,25 OH-vitamin D.
Some of the biology is still a mystery. The highest density of fgf-23/klotho receptors are located in the distal tubule but the biologic effects stem from the proximal tubule.
FGF-receptor and Klotho are also found in the parathyroid gland but the exact role it plays is unclear. Some data points to direct stimulation of PTH and both molecules tend to rise together but this may be due to FGF-23 surpressing 1,25 OH D and secondary increases in PTH.
Increased phosphate and 1,25 vitamin D both stimulate the production of FGF-23. [Note Wolf provided data that phosphate levels do not increases FGF-23. He proposed that it is phosphate balance that is important, his supporting data included lupron treated patients bump their phosphorous by half a point but FGF-23 doesn't budge, I couldn't find this article on Google]. The Phex endopeptidase cleaves and inactivates FGF-23 so that is another control factor. [Wolf also discussed iron infusions causing phosphorous wasting due to excess FGF-23 ref pubmed related search]
Wednesday, June 17, 2009
Sunday, June 14, 2009
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.
Monday, June 8, 2009
Thursday, June 4, 2009
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.
Wednesday, June 3, 2009
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:
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.
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.
Tuesday, June 2, 2009
Incredibly the BCA has won the first legal round.
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.
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.
Monday, June 1, 2009
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:
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.