Great article in the New Yorker summarizing books on obesity


See XXXL

Elizabeth Kolbert reviews the current crop of what she calls obesity books

Though weight-loss books will doubtless always be more popular, what might be called weight-gain books, which attempt to account for our corpulence, are an expanding genre.

It is very good. Nothing on uric acid or fructose or an infectious etiology but a lot of interesting thoughts on our expanding wastlines.

My first two lectures to the IM Intern Class of 2012

On July first I gave a lecture on IV fluids, total body water and hyponatremia. This handout is similar to the lecture I give to the medical students titled sodium and water. It adds a half baked section on potassium but this handout really needs to have th sodium section tightened up and shortened, the potassium section finished and short sections on the treatment of phos, magnesium and calcium disorders.

  • Here is the PDF
  • Here is the native Pages documentin case you use Pages and are interested in finishing this work in progress.

On July 9th I gave a lecture on acute renal failure. The handout is 28 5.5 x 8.5 pages. The book is designed as a workshop with questions and points for discussion throughout.

  • Here is the PDF of the 28 page handout. It is very readable and one of the best handouts I have put together.
  • Here is the native Pages document in case you use Pages and are interested in editing my masterpiece.

Happy July 1st, and don’t worry about the July phenomenon. All myth.

According to this article in Newsweek from last July:

the July medical-training period is associated with between 1,500 and 2,750 accelerated deaths every year. In a study of the July phenomenon from which initial findings were released in 2005 by the National Bureau of Economic Research, Harvard Business School health-care economists Robert Huckman and Jason Barro compared mortality rates in teaching and non-teaching hospitals around the country. They found that there are 4 percent more incidences of accelerated death in average-sized teaching hospitals in July and August.

They also found length of stay increased 2%. It is not clear from the above paragraph but the 1,500 to 2,750 deaths is also part of the same study by Huckman and Barro. A good review of the paper is found on this blog, A New Start. Here is a link to the abstract, full article costs $5.

A study done on hospitals in Ohio found no increase in mortality in ICU patients admitted in July through September. It looks like a massive study with rigorous methodology and it is more recent by nearly a decade.

In analyses of over 48,000 patients admitted to ICUs in 5 major teaching hospitals, using a validated method of adjusting for admission severity of illness, several important findings emerge. First, in-hospital mortality and LOS were similar in patients admitted to intensive care units from July through September and during later months of the academic year. Moreover, results were consistent when July, August, and September were analyzed separately, and there was no discernible pattern of variation when examining outcomes for individual months over the entire year. Furthermore, we were unable to detect differences when individual academic years, surgical and nonsurgical patients, and individual hospitals and ICUs were examined separately. These results were all similar in analyses of roughly 108,000 patients admitted to minor teaching and nonteaching hospitals.

With its unremarkable findings and disruption of the common wisdom is it any wonder that it is given short shift in the Newsweek article.

Cool article on Hippocratics Aphorisms

The authors describe aphorisms as:

…terse and trenchant, facilitating maximum comprehension in minimum expression. The Hippocratic aphorisms are just that: concise, often pithy, and memorable statements of literal truths and frequently obvious wisdoms.

Sounds like Hippocrates would have had a ton of followers on Twitter.


This aphorism is probably the first description of casts associated with ATN.

Here is the article

My philosophy of consult nephrology

If, on every consult for acute kidney injury, you limited your differential to pre-renal azotemia, obstruction and run-of-the-mill ischemic ATN you would be capable of reaching the right diagnosis 95% of the time. Common causes of renal failure are common. All the time we spend learning and teaching about glomerulonephritis, interstitial nephritis, vasculitis and the other zebras of acute renal failure is usually time wasted. However, your job as a consult nephrologist is to hunt down and flush these zebras. I strive to try and fit every clinical scenario into one of these alternative rare diagnosis. Because if you are not actively hunting a zebra, you will never find one.

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.

Stay vigilant and stay hungry

The Sugar Fix: Chaper Two: Raising Cane

The Sugar Fix: Chapter 2: The birth of dietary sugar comes about 10,000 years ago in New Guinea. Johnson states that this moment is one that alters history as few other discoveries have.

Source Sugar Fix and USDA Economic research service

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.

Sucrose. Note: glucose is on the left and fructose on the right

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

He suspects that ancient humans ate only 15-20 grams of fructose a day (equivalent to two pieces of fruit) this compares to contemporary humans eating 70-80 g a day.

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.

Patient missed a whole mess of dialysis in June

One of my dialysis patients suffers from chronic cryptogenic diarrhea. Because of the diarrhea she does not get volume overloaded or hypertensive. This week I received a call from the dialysis unit telling me she has missed 5 treatments in the first 3 weeks of the month. Sure enough the next day she ends up in the hospital, suffering the effects of chronic uremia. She had a bicarbonate of 4, a BUN of 120, and Cr of 16. Potassium was fine at 3.9 but the phos was 16.8 mg/dL. I don’t think I have seen one that high, outside of rhabdo.