Mike Masse, a lawyer and amateur musician, used YouTube to raise money for his son who has brain cancer. Link. Again an example of user generated content and going directly to people without a mass media intermediate.

Mike never divulged how successful the campaign was but he did give an update where he essentially said we have received enough money:

NEJM and the problem with the HGH article from 1990 and since having been shown to be invalid. But quacks continue to link to it. How to deal to deal with this?

Editorial

How Reddit got a transplant patient his medication in the middle of the blizzard of 2013. Some Coverage in the local media.

From the Boston Magazine article:

Afterward, she wrote in to say she'd made the delivery, then signed off for the night. “I had stuff to do, and I didn't log back in until 2 or 3 o'clock the next day. [The post] already had over a thousand [upvotes]. When I'd gone to bed it had like 20. People really liked the story and they were appreciative.”

Since then, the post has received another thousand or so upvotes. Redditors have been looking to give Holdorf her karmic due, and she's been offered dinner or drinks by various users in Belgium, San Diego, Texas, Atlantic City, Jakarta, Singapore, and Atlanta, should she ever visit their regions. She tells us she also received messages from other transplant patients, doctors, and just plain admirers, of which there are no shortage. One commenter noted, “You potentially saved a life and got the gift of beer. Life can be beautiful sometimes.”

​

Malcolm Gladwell on the loose ties of social media. New Yorker 2012

The kind of activism associated with social media isn’t like this at all. The platforms of social media are built around weak ties. Twitter is a way of following (or being followed by) people you may never have met. Facebook is a tool for efficiently managing your acquaintances, for keeping up with the people you would not otherwise be able to stay in touch with. That’s why you can have a thousand “friends” on Facebook, as you never could in real life.

This is in many ways a wonderful thing. There is strength in weak ties, as the sociologist Mark Granovetter has observed. Our acquaintances—not our friends—are our greatest source of new ideas and information. The Internet lets us exploit the power of these kinds of distant connections with marvellous efficiency. It’s terrific at the diffusion of innovation, interdisciplinary collaboration, seamlessly matching up buyers and sellers, and the logistical functions of the dating world. But weak ties seldom lead to high-risk activism.

In a new book called “The Dragonfly Effect: Quick, Effective, and Powerful Ways to Use Social Media to Drive Social Change,” the business consultant Andy Smith and the Stanford Business School professor Jennifer Aaker tell the story of Sameer Bhatia, a young Silicon Valley entrepreneur who came down with acute myelogenous leukemia. It’s a perfect illustration of social media’s strengths. Bhatia needed a bone-marrow transplant, but he could not find a match among his relatives and friends. The odds were best with a donor of his ethnicity, and there were few South Asians in the national bone-marrow database. So Bhatia’s business partner sent out an e-mail explaining Bhatia’s plight to more than four hundred of their acquaintances, who forwarded the e-mail to their personal contacts; Facebook pages and YouTube videos were devoted to the Help Sameer campaign. Eventually, nearly twenty-five thousand new people were registered in the bone-marrow database, and Bhatia found a match.

But how did the campaign get so many people to sign up? By not asking too much of them. That’s the only way you can get someone you don’t really know to do something on your behalf. You can get thousands of people to sign up for a donor registry, because doing so is pretty easy. You have to send in a cheek swab and—in the highly unlikely event that your bone marrow is a good match for someone in need—spend a few hours at the hospital. Donating bone marrow isn’t a trivial matter. But it doesn’t involve financial or personal risk; it doesn’t mean spending a summer being chased by armed men in pickup trucks. It doesn’t require that you confront socially entrenched norms and practices. In fact, it’s the kind of commitment that will bring only social acknowledgment and praise.

The evangelists of social media don’t understand this distinction; they seem to believe that a Facebook friend is the same as a real friend and that signing up for a donor registry in Silicon Valley today is activism in the same sense as sitting at a segregated lunch counter in Greensboro in 1960. “Social networks are particularly effective at increasing motivation,” Aaker and Smith write. But that’s not true. Social networks are effective at increasing participation—by lessening the level of motivation that participation requires. The Facebook page of the Save Darfur Coalition has 1,282,339 members, who have donated an average of nine cents apiece. The next biggest Darfur charity on Facebook has 22,073 members, who have donated an average of thirty-five cents. Help Save Darfur has 2,797 members, who have given, on average, fifteen cents. A spokesperson for the Save Darfur Coalition told Newsweek, “We wouldn’t necessarily gauge someone’s value to the advocacy movement based on what they’ve given. This is a powerful mechanism to engage this critical population. They inform their community, attend events, volunteer. It’s not something you can measure by looking at a ledger.” In other words, Facebook activism succeeds not by motivating people to make a real sacrifice but by motivating them to do the things that people do when they are not motivated enough to make a real sacrifice. We are a long way from the lunch counters of Greensboro.

Read more: http://www.newyorker.com/reporting/2010/10/04/101004fa_fact_gladwell#ixzz2O3VYbjw3

Facebook does organ donation cards. The Hastings Center does a post mortem​.

Unfortunately the effect was short lived and in a month or two we were at baseline.​

Patients like us

Today I received a tweet from @MedCalc. I have a bit of an appCrush on MedCalc. I Began using it on the Palm and continued with the Treo and iPhone.

This is a question I use in my IV fluid lecture. The lesson goes like this:

It starts by me asking the students what's the highest glucose they have ever seen. I go around the room and find the highest. Sometimes they'll have a cool story of a DKA or HONK. Then I tell them that they haven't seen anything until they've had an ESRD patient in DKA. Since dialysis can't make urine they escape the osmotic diuresis. The blood sugar doesn't have an escape route so the plasma levels sky rocket. Additionally the lack of profound volume loss allows these patients to delay treatment by avoiding the life threatening shock that typically hospitalizes the patient with DKA. I have seen blood sugars of 2,700 mg/dL.

After that lead in, I ask the students to guess what the concentration of glucose in D5W. Someone will say 50 mg/dL, but quickluy they will arrive at a consensus of 500 mg/dL. If someone says 5,000 it is quickly forgotten as unreasonable.

Then I pick on one student and walk through the trivial conversion of g/dL to mg/dL. I like to get a Canadian or foreigner since they are metric natives.

Once the students get that the concentration of glucose in D5W is 5,000 mg/dL the questions turns to why.

Why would anyone want a routine, off the shelf fluid, to have a such wildly non-physiologic glucose concentration?

At least one student  knows the answer or I coach a dim group to the answer without much difficulty. The glucose is needed to make D5W iso-osmotic. If we Infused sterile water we would trigger  hemolysis.

The last step in the lesson is showing the students that they already know how to calculate the osmolality of D5W

In the previous acid-base lesson the students learn to calculate an osmolar gap. In America one needs to convert the BUN and glucose from mg/dL to mOsm/L. This means dividing by the molecular weight and multiplying by 10. The equation looks like this:

So all we need to do to figure out the osmolality of the glucose is divide by 180 and multiply by 10. I have someone take 5000 and divide by 18 = 278 mOsm/Kg water, isosmotic to plasma. Its a great 5 minute diversion that teaches the students something important. It shows that these rules all fit together. I try to impress on them that fluids and electrolytes are internally consistent like math.

So it was rather embarassing to find out I have been wrong. The actual osmolality of D5W is 252 not 278. Here was my erroneous reply to @medCalc

The author, Michelle Lin chimed in with her reference. Nice work

The first thought was that the discrepancy was due to osmolarity versus osmolality.

Science teacher extradonair Gary Abud weighed in:

Brian Lee was the first to nail it. We are not using dextrose, but dextrose monohydrate. (You remember, Molecule of the month in March of 2008)

Michelle Lin then came up with the correct molecular weight. It's just glucose at 180 plus a water at 18 = 198

Then Bryan Hayes a pharmacist gives his stamp of approval.

The whole thing tumbled out from question to blog post in about 6 hours.

The biggest problem is my cool story problem and interactive lesson is off by about 10%.

Ahh the weight of a water molecule

Protein in the urine is one of the most common signs of kidney disease. One of the earliest tests a kidney specalist does is measure how much protein is in the urine. What is remarkable is how increasing degrees of proteinuria correlate with poor outcomes. proteinuria can vary from a few milligrams to thousands of times that. As the proteinuria increases there are a few milestones:

• 30 mg per day is lower limit for a condition called microalbuminuria. More albumin in the urine than 30 mg per day is a risk factor for future full blown diabetic nephropathy
• 300 mg of protein is the threshold for proteinuria. Below this the patient has microalbuminuria. Above this it is proteinuria. This is the threshold for finding protein on a traditional dipstick urinalysis.
• 3,500 mg is the threshold for nephrotic syndrome. At this point the proteinuria is so heavy that it will cause illness merely from the loss of protein. The most prominant symptom is edema. Typical signs include hypercholesterolemia, low albumin and a tendency to clot.

These three thresholds, each roughly separated by an order of magnitude represent the major milestones in renal disease. This post is going to focus around the highest range. Low levels of proteinuria are due to non-specific renal damage. Inciting events include inflammation, fever, hypertension and diabetes. As the proteinuria grows toward 3 grams the list of diseases begins to change to a collection of conditions, often primary renal diseases that include membranous nephropathy, diffuse proliferative GN, focal segmental nephropathy, multiple myeloma and others. Though many of these conditions can be suggested by blood tests, definitive diagnosis and effective therapy depends on a kidney biopsy.

Unexplained nephrotic range proteinuria (around 3g/day) is an indication for a kidney biopsy and mild proteinuria of about 300 mg is not an indication for a biopsy. The space in between is a bit nebulous. I will almost always biopsy at 2 grams a day. I, in the past, have biopsied a few patients with proteinuria around 1 gram. But in the few cases that I did biopsy I didn't find anything that changed my treatment. I satisfied some personal curiosity but wasn't able to offer the patient anything but certainty about the reason for their proteinuria. Because of this I no longer recommend these patient go for a kidney biopsy that, though generally safe has some real potential consequences.

Because of this I know have collected a cohort of patients that all match the following general characteristics:

• Stable proteinuria from 800-1,700 milligrams a day
• Stable and renal function
• Negative serologic work-up. This means they do not have evidence of lupus, viral infection, vasculitis, inflammatory damage to the kidney after extensive blood tests.
• Agreed to be a bit in the dark about the cause of their kidney disease

I then use ACEi or ARBs often with spironolactone to try to lower the proteinuria as much as possible. I am usually at peace with not knowing what is going on but occasionally I worry that I'm not doing the best I can for these patients. A couple of weeks ago I tweeted this after seeing one of these patients:

I got an an avalanche of response:

Essentially everyone agreed with me with two nuggets of information that were novel to me. The first was the possibility of orthostatic proteinuria. This is a benign diagnosis that is usually made in children. These patients have proteinuria while up and about during the day but no proteinuria at night.

The other possibility is IgA nephropathy as mentioned by Jason Prosek. I had toyed with this diagnosis and really is the reason I am not totally at peace with my decision not to biopsy. It wasn't the diagnosis that was new it was the information that the KDIGO guidelines recommend a trial of steroids if ACE inhibition , low sodium diet and blood pressure control does not reduce the proteinuria below 1 gram.

A couple of notes: as soon as Dr. Prosek mentioned the KDIGO guidelines, the thread went silent. Literally that was the last tweet on this subject. It was as if he had thrown the KDIGO trump card down and no one wanted to go on record as being unfamiliar with the guideline or as practicing outside of the guideline. This is a shame because the evidence for this guideline is not A level. It should generate discussion.