Monthly Archives: March 2012

Getting the users perspective

I can’t possibly expect to be able to comment on what it is like to be on dialysis – I’ve only observed the process.  To try and understand more I have begun to search out some blogs by those on dialysis.  Here are two:

The Facts on The big D. is a blog post by Ellie.  Ellie is a young woman (the same age as my wife) in New York in need of a transplant.  Ellie comes across as a straight shooter.  She’ll tell us when it stinks and she’ll count her blessing aloud.  Sitting in a dialysis centre is the last place she wants to be. Thanks for the honesty Ellie.

D(ialysis) Day   Joe has just begun dialysis for the third time in his life.  This is his first blog post from the chair. He first began dialysis at 15, underwent a transplant from his mother which lasted a couple of years, went back on dialysis for 4 years, underwent a second transplant which lasted 10 years and has now returned to dialysis.  What strikes me is just how long Joe needed to wait for that second transplant.  The same is here in New Zealand.  Folks, it is really very very important that you tell your family if you are prepared to donate your organs – Do not rely on there being something on your driver’s license, this has no legal effect and is often ignored by grieving relatives.  Have that conversation – today.

New visions:

No one will need to wait more than 6 months for a transplant

$100 dialysis will be portable so most will not need to spend 5 hours, 3 days a week, sitting around with tubes in them.

By the way, both these people have End Stage Renal Disease following Chronic Kidney Disease (CKD). Joe’s form of CKD appears to be from a heredity disease.  Ellie does not say.  Neither are overweight or appear to have anything other than a normal life.  CKD affects about 13% of the population (many do not know).  Do not be complacent. If in doubt, get your kidney’s checked.

Hold that Rice, it may be dangerous or perhaps not…

“White rice could cause diabetes”   The Independent UK

“White rice link seen with type II diabetes”  Yahoo News

“White rice raises T2 diabetes risk”  The Telegraph

Those were the headlines of the last few days.  Of the three posted, one is really wrong, one is sort of OK, one is almost OK and all are meaningless.  The headlines come out of a “meta-analysis” of population studies of risks associated with diabetes.  Meta-analysis are important because they consider the quality of studies and combine their results which, if done well, reduces the chance of giving erroneous results.  In this case there were only four studies included in the meta-analysis.  The paper was published in the British Medical Journal and is available here if anyone wants to read it.

So – the real question, is “can we keep eating rice?”  The overwhelming answer is “yes we can!”

To answer why, you may need to learn something about (in a whisper) statistics.  If you are new to reading medical journals then one of the terms you will run across and need to understand is “Relative Risk.”  What the number means is the increase in risk (chance of having the disease) of one group compared to another.  A Relative Risk of 1.5, then, means that one group is 1.5 times as likely to get the disease as another.  Right away, you can see that it is easy to get a high relative risk by comparing groups with very low absolute risk to those with high absolute risk.  Eg, for Type 2 diabetes if we compared healthy normal weight individuals with obese individuals then the relative risk would be high for the obese individuals.  In this meta-analysis they compared the group with the lowest consumption of rice with those with the highest consumption of rice.  Before I give the numbers, remember that most people do not have either the lowest or the highest consumption, but somewhere in between.  Anyway, for Western populations the relative risk was 1.12 and for Asian populations it was 1.55.  This looks like those Westerners eating heaps of rice are about 12% more likely to get Type 2 diabetes than those eating the least.  However, the devil is in the details…

Stats lesson number 2.  The 1.12 is presented with some numbers after it in brackets: 1.12 (0.94 to 1.33).  These numbers are crucial.  They are even more important than the 1.12 itself!  They are what is called a confidence interval. In this case a 95% confidence interval.  They are an indication of just how good the estimate of 1.12 really is.  In this case, not very good.  The authors are saying that they are 95% confident that the true relative risk (i.e. the number we would get if we included everyone in the world in the study) is somewhere between 0.94 and 1.33.  Because this number straddles 1 there is a good chance (maybe ~25%) that the real relative risk is actually less than 1, in other words that eating the least amount of rice has a greater risk than eating the most!  In the Asian population the relative risk was 1.55 (1.20 to 2.01) which suggests that it is unlikely that the real relative risk is less than 1.20.

OK then, let us for a minute assume that if we measured everyone in the world and found a true relative risk of 1.2 for those eating the most rice compared with those in the group eating the least.  What does that mean to you and me.  Probably nothing, because what is important is Absolute risk.  As far as Type II diabetes goes the equation is simple – if you are obese then you are at high absolute risk of Type II diabetes.  Eating rice is going to make next to no difference.  If you eat heaps of rice it is probably  because you eat heaps of food.  Cut back on the rice, but for goodness sake do not replace it with pasta or spuds or anything else for that matter.  If you eat well and exercise a bit and happen to prefer rice to spuds….then there is no big deal…bon appetite.

I am a pee scientist

I’m often asked “What do you do?”   In order to avoid those glazed over looks, and in honor of World Kidney Day, I present to you Dr John’s five minute intro to his study of Acute Kidney Injury (AKI).

What is Acute Kidney Injury and why does it matter?

AKI is the very rapid loss of kidney function.   As the kidney is a big filter designed to clean your blood this means you won’t be able to get rid of the nasties and that ain’t good news (see this previous post for some of the other great things kidneys do).

AKI is not about getting punched in the kidneys.  Lots of things can cause the kidney to fail.  If the blood ceases to run to the kidneys for a short time (e.g. during a heart attack) then no oxygen gets delivered to them.  All cells need oxygen, so lack of it means curtains for some cells.  Other causes are when parts of the kidney get poisoned.  Given that the kidney concentrates the nasties in the blood, it is the first place to get hit by poisons.

About one third of people entering the intensive care have or get AKI.  That’s heaps annually (heaps is a technical term used by scientist to mean “more than we can get funding to count”).  If you have AKI you are more likely to die, need dialysis, get Chronic Kidney Disease and you will spend more time in hospital.  So, it’s kinda important (bean counters – note: it costs billions annually).  These things are all summarised in my latest minfographic below.

Acute Kidney Injury

What do I study?

Most of my work is about how to figure out people have AKI.  The problem is that for the last 70 years or so AKI has been able to be detected only a day or three after it has occurred!  This is too late to do much about it (dialysis only supports the kidney, not cures).  Think about this analogy (remember the kidney is a big filter):  Imagine you a running water in the sink. It goes down the plughole OK.  You are defrosting some meat (the old fashioned way), so you wander away and leave the water running.  Unknown to you, there is some hair stuck down the drain (yuk), which gets shifted around a bit until it largely blocks the drain.  The inevitable happens and the drain and then sink fill up and, of course, overflow.  What my colleagues and I do is to look at the other end of the drain for any tell-tale signs that there is something amiss (yep, we look in the urine.  I guess that makes us pee scientists).   That something amiss is a very small molecule which only the clever scientists in the labs can extract from the urine and quantify.  For the past decade or so there have been many such small molecules discovered (new techniques and technology have helped) which are potential early indicators of AKI.  We call these “biomarkers.”  My job is to analyze the numbers the lab people give me.  I try and see if and when particular biomarkers are in greater concentrations in the urine and try and match this to the clinical outcomes of patients.  The hope is that we will learn enough about these biomarkers to know when and how to use them in clinical practice.  If we can detect AKI when it first occurs, then we should be able to develop new treatments and finally be able to do something about the death rates and other poor outcomes.