Tag Archives: Acute Renal Failure

Hot oil baths and other things to do on World Kidney Day 2015

“In ancient times the Persian philosopher Avicenna [Ibn Sina] noted that urine may be retained in crisis of fever (s393) and prescribed hot oil baths (s413)(1). Unfortunately, apart from the supportive therapy of dialysis, there has been little progress since in the treatment of acute kidney injury (AKI).”(2)

Given that getting AKI at least doubles your chance of dying in hospital “no progress” is a major health issue.

Today is World Kidney Day and I get to post quite possibly the first blog post in the world on this day. I believe Avicenna would be thrilled with the attention paid to the organ which delivers urine. He may not be so thrilled that hot oil baths have been abandoned. Of course there is the obvious safety issues of scalding and drowning. Also, as Herod the Great found out, syncope (sudden loss of consciousness) is also a possible side effect (probably just because the heat constricted his blood flow [vasoconstriction] causing too little oxygen to reach his brain [cerebral anoxaemia].(3) Nevertheless, I think Avicenna is the type of person who would have welcomed a randomised controlled trial of hot oil baths verse today’s standard treatment.


The statue of Avicenna (Ibd Sina) to be found in Hamaden, Iran. http://www.panoramio.com/photo/91467137

If you don’t fancy a hot oil bath this World Kidney Day, then there are other things to do to minimise the possibility of Acute Kidney Injury. Have you got high blood pressure, diabetes or Chronic Kidney Disease? Be warned, ~10% of the adult population have Chronic Kidney Disease, many of whom are not aware, and many more are at risk of developing it. All add to your risk of multiple illnesses any one of which can trigger acute kidney injury. If you happen to have a heart attack or sepsis (very serious infection) you are more likely to get AKI and more likely to die because of these underlying conditions.

So, on the assumption that readers of this blog are smarter than the average bear, I shall give you some sound advice – for the sake of yourselves and your family LOOK AFTER YOURSELF (yes, I’m shouting and therefore sinning against the internet protocol police – but this is important). Cut the sugar intake, quit smoking, take a walk around the block. It ain’t rocket science (one of the simpler sciences that involves cylinders with fins and lots of explosives) – it’s easier than that.

Former World Kidney Day posts

2014 A day to celebrate https://100dialysis.wordpress.com/2014/03/13/a-day-to-celebrate/

2013 Happy WKD https://100dialysis.wordpress.com/2013/03/14/happy-wkd/

2012 I am a pee scientist https://100dialysis.wordpress.com/2012/03/07/i-am-a-pee-scientist/


  1. Avicenna: The Canon of Medicine [Internet]. 2nd ed. New Yourk: AMS Press; 1973. Available from: http://archive.org/stream/AvicennasCanonOfMedicine/9670940-Canon-of-Medicine_djvu.txt
  2. Pickering JW, Endre ZH: The definition and detection of acute kidney injury. Journal of Renal Injury Prevention 2014; 3:19–23 http://www.journalrip.com/Archive/3/1
  3. Retief FP, Cilliers JFG: Illnesses of Herod the Great. S Afr Med J 2003; 93:300–303

Cheesecake files: Just how deadly is it?

Everyone said it did, but how did they know and by how much?  Statements like

“The development of AKI [Acute Kidney Injury] after CPB [Cardiopulmonary Bypass Surgery] is associated with a significant increase in infectious complications, an increase in length of hospital stay, and greater mortality.” (Kumar & Suneja, Anaesthesiology 2011 14(4):964)

are common place in the acute kidney injury literature.  When I started to look at the references for such statements I realised that they were all to individual, normally single centre, studies and that the estimates of the increased risk associated with AKI after CPB varied considerably.  Furthermore, the way AKI is defined in these studies is quite varied. This lead to two questions?

  1. Just how deadly is getting AKI after CPB?
  2. Does it matter how we define AKI in this case?

These questions are important as the answer to them helps a surgeon and patient to better assess the risk associated with choosing to have cardiopulmonary bypass surgery and what the importance is in monitoring kidney function after such a surgery.  To answer these questions required a meta-analysis the results of which I have just published (a.k.a earned a cheesecake).  A meta-analysis involves systematically searching through the literature, a sentence which takes seconds to write but months to serve, for all articles reporting an association between AKI and mortality after CPB.  Then there is learning how to put all the, sometimes disparate, data together (I had to learn a lot of R for this one) and to report on it.  As this was my first meta-analysis, I was fortunate to have the assistance of two highly competent scientists & nephrologists with meta-analysis experience, namely Dr’s Matt James of Calgary, and Suetonia Palmer of my own department in the University of Otago Christchurch.

So – what did we find?

  1. If you get AKI after CPB you about 4 time more likely to die compared to if you do not get AKI after CPB even after accounting for things like age, diabetes, and other risk factors.
  2. Somewhere between 37 and 118 lives per 10,000 CPB operations could be saved if we could find a way to eliminate AKI.
  3. How AKI was measured did not make any difference to the results.
  4. AKI after CPB was also associated with increased risk of stroke.
Figure 1 from Pickering et al, AJKD 2014

A teaser of a figure from Pickering et al, AJKD 2014

Pickering, J. W., James, M. T., & Palmer, S. C. (2014). Acute Kidney Injury and Prognosis after Cardiopulmonary Bypass: A Meta-analysis of Cohort Studies. American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. doi:10.1053/j.ajkd.2014.09.008

ps. Sorry about the paywall folks, but as I’ve said before, if we want to put this data in front of the people it is most relevant to we haven’t the budget to always make them Open Access.


Can Doctors and Nurses help Dialysis patients recover?

In the case of dialysis dependent acute kidney injury patients this is a question which Dr Dinna Cruz  and colleagues (University of California San Diego) are asking and seeking opinions from both nephrologists and non-nephrologist doctors and nurses involved in care of dialysis patients.  It was a question which arose out of discussions at this year’s Continuous Renal Replacement Therapies conference (CRRT 2014). Personally, I think it is a brilliant starting point for research to go out and seek the opinion of those “at the coal face” actually treating patients. If that includes you, please take a moment to complete the survey. If it includes someone you know, please pass this request to participate on.  Here is Dr Cruz’s request:

Currently there is much interest regarding the recovery aspect of AKI. A specific area of interest is how to enhance recovery in patients who remain dialysis-dependent at the time of discharge. It is hypothesized that patients with potential for renal recovery may require a different care plan than the “usual” ESRD patient.

Therefore we are asking your opinion regarding the post-discharge care of such patients, using this short survey. It will take only a few minutes of your time, and represents a starting point for developing potential strategies for these patients. We think it is very important to have the input of specialists from different healthcare settings and countries to give a more balanced view.

Kindly complete the survey appropriate for your specialty, then please share both these links with other colleagues so we get more responses from around the world

For nephrologists:


For non-nephrologists, including acute and chronic dialysis nurses:


Thank you very much for your help!

Source: Anna Frodesiak-Wikimedia Commons

Source: Anna Frodesiak-Wikimedia Commons

Cheesecake files: Too little pee

This week’s post is really about the coloured stuff & why too little of it is dangerous.  Note, I say coloured stuff because it aint just yellow – check out this herald article if you don’t believe me (or just admire this beautiful photo).

 A rainbow of urine from a hospital lab. Credit:  laboratory scientist Heather West.

A rainbow of urine from a hospital lab.
Credit: laboratory scientist Heather West.

Story time

A long time ago, when Greeks wore togas, and not because they couldn’t afford shirts, a chap named Galen* noted that if you didn’t pee you’re in big trouble.  It took 1800 more years before the nephrologists and critical care physicians got together to try and decide just how much pee was too little.  This was at some exotic location in 2003 where these medics sat around for a few days talking and drinking (I’m guessing at the latter, but I have good reason to believe…) until they came up with the first consensus definition for Kidney Attack (then called Acute Renal Failure, now called Acute Kidney Injury)1.  It was a brilliant start and has revolutionised our understanding of just how prevalent Kidney Attack is.  It was, though, a consensus rather than strictly evidence based (that is not to say people didn’t have some evidence for their opinions, but the evidence was not based on systematic scientific discovery).  Since then various research has built up the evidence for or against the definitions they came up with (including some of mine which pointed out a mathematical error2 and the failings of a recommendation of what to do when you don’t have information about the patient before they enter hospital3).  One way they came up with to define Kidney Attack was to define it as too little pee.  Too little pee was defined as a urine flow rate of less than half a millilitre per kiliogram of body weight per hour over six hours (< 0.5ml/kg/h over 6h).  Our groups latest contribution to the literature shows that this is too liberal a definition.

The story of our research is that as part of a PhD program Dr Azrina Md Ralib (an anaesthesist from Malaysia) conduct an audit of pee of all patients entering Christchurch’s ICU for a year.  She did an absolutely fantastic job because this meant collecting information on how much every patient peed for every hour during the first 48 hours as well as lots of demographic data etc etc etc. Probably 60-80,000 data points in all!  She then began to analyse the data.  We decided to compare the urine output data against  meaningful clinical outcomes – namely death or need for emergency dialysis.  We discovered that if patients had a flow rate of between 0.3 to 0.5 ml/kg/h for six hours it made no difference to the rates of death or dialysis compared to those with a flow rate greater than 0.5.  Less than 0.3, though, was associated with greater mortality (see figure).  For the clinician this means they can relax a little if the urine output is at 0.4 ml/kg/h.  Importantly, they may not give as much fluid to patients. Given that in recent times a phenomenon called “fluid overload” has been associated with poor outcomes, this is good news.

The full paper can be read for free here.

Proportion of mortality or dialysis in each group. Error bars represent 95% confidence intervals.From Ralib et al Crit Care 2012.

Proportion of mortality or dialysis in each group. Error bars represent 95% confidence intervals.From Ralib et al Crit Care 2013.


*Galen 131-201 CE.  He came up with one of the best quotes ever: “All who drink of this remedy recover in a short time, except those whom it does not help, who all die.”

1.     Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky PM, Acute Dialysis Quality Initiative workgroup. Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004;8(4):R204–12.

2.     Pickering JW, Endre ZH. GFR shot by RIFLE: errors in staging acute kidney injury. Lancet 2009;373(9672):1318–9.

3.     Pickering JW, Endre ZH. Back-calculating baseline creatinine with MDRD misclassifies acute kidney injury in the intensive care unit. Clin J Am Soc Nephro 2010;5(7):1165–73.

Cheesecake files: Injury, function, and death

When they say your tests are positive for a disease just what do they mean?  If it is a simple blood or urine test often they mean that the concentration measured is outside (above or below) some  reference range.  In my field of Kidney Attack (a.k.a. acute kidney injury: AKI) two tests of the same substance (plasma/serum creatinine) are needed a day or two apart . The difference in the concentrations is what is important.  If the creatinine concentration has increased by >0.3 mg/dl within 48 hours or by more than 50% within a week then the diagnosis of AKI is made.  What happens, though, when someone comes along with a new test?  How do we know it is any better (or worse) than the original test? In my view what is required is that both the old and the new tests should be compared to a third, clinically relevant, variable.  For example, a new prostate cancer test may be compared to the present (poor) PSA test  by referencing both to the more definitive biopsy results.

In AKI the reason the creatinine threshold of 0.3 mg/dl was included as diagnostic was because research(1) had shown this level of increase to be associated with a four fold increase in the likelihood of premature death. If you’ve seen any of my previous posts on my research you will know that I am interested in new biomarkers (plasma and urine proteins mainly) that could be used to diagnose AKI earlier than creatinine.  While creatinine is a marker of changes in kidney filtration function, most of these new biomarkers reflect structural injury itself.  An analogy is that movement of a finger hurt in a rugby tackle tells us if the finger is functioning, whereas an x-ray is needed to tell us if it is broken or not.

Sam Whitelock damaged his finger during a game.  It had enough function to let him continue to play.  X-rays later showed it was broken. Picture: TV3

Sam Whitelock damaged his finger during a game. It had enough function to let him continue to play. X-rays later showed it was broken.
Picture: TV3


My latest publication(2) describes a method to determine appropriate biomarker thresholds.  It is quite simple.  First, I determine the sensitivity of the creatinine threshold to predict a meaningful clinical outcome – the need for dialysis or death within 30 days. The sensitivity is simply the proportion of all those who end up having the outcome who had a measure above the threshold.  I then take that sensitivity and work out what the biomarker threshold needs to be in order to yield that same sensitivity.

An early sketch of mine as I worked out how to determine structural biomarker thresholds

An early sketch of mine as I worked out how to determine structural biomarker thresholds

(1) Chertow, G. M., Burdick, E., Honour, M., Bonventre, J. V., & Bates, D. (2005). Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. Journal of the American Society of Nephrology : JASN, 16, 3365–3370. doi:10.1681/ASN.2004090740

(2) Pickering, J. W., & Endre, Z. H. (2013). Linking Injury to Outcome in Acute Kidney Injury: A Matter of Sensitivity. PloS one, 8(4), e62691. doi:10.1371/journal.pone.0062691.t001

The Face of Kidney Attack Part II

This guy crawls through bat dung for fun.  He also runs incredibly long distances and then cycles or kayaks more.  If you’ve not guessed already, our Face of Kidney Attack is multisport and adventure racer Sir Steve Gurney (He’s not really “Sir” but anyone who does what he does deserves some sort of honorific and all other honorifics he’s been called are not printable).

For those of you who are not New Zealanders or who were asleep the last couple of decades, Steve made his name in the incredible Coast-to-Coast race which involves cycling, kayaking and mountain running from the West to East coast of the South Island of New Zealand through the Southern Alps.  Arduous does not begin to describe this race – that Steve does it in under 12 hours and has won the race 9 times are mere numbers which can not possibly describe the punishment he put his body through and the mental toughness he developed.  However, in 1990 a Kidney Attack almost halted the adventure and very nearly killed Steve.

In the 90s Raid Gauloises were the toughest races of them all. Now known as Adventure races they involve hiking, mountain biking, canoeing, and scrabbling across the toughest terrain for days on end.  The first race in 1989 had been the NZ Grand Traverse. The lure of such a race in Borneo with Christchurch adventure race guru John Howard was too much for Steve in 1994 – a prize of $55,000 was a pretty good incentive as well.  John and Steve arrived in Borneo where John had arranged for three Malaysian athletes to join them (all adventure race novices).  The race was expected to take 10 days.  The race was famous for four things, first John organised the team to take minimal equipment and supplies – previously heavily laden backpacks had been the order of the days, second John and Steve became the first athletes to win two such races, third they did the race in 5 days not the expected 10, and fourth, is what happened to Steve.

Early in the race Steve suffered heat stroke having mountain biked up a steep hill (just to show he could, the others walked their bikes!).  He vomited and was quite sick.  Water was in short supply (remember they took minimum supplies) and it was very humid “jungle” weather.   This was the first “hit” his kidneys took – dehydration is not good.  One of the primary roles of the kidney is to regulate body water so as to keep the right balance between water and salts.  This process was obviously under stress as Steve lost water through vomiting and sweat and may not have replaced enough.

Later in the race the racers had to crawl through the Mulu caves.  This was an 8 hour trek that involved getting down on hands and knees and squeezing through gaps in the rock.  The caves were home to bats and the floor was covered in bat dung.  By the time they finished the trek Steve, wearing shorts at the time, was covered in scratches.  It is likely that here he picked up the bacteria  that causes leptospirosis from the bat dung. “Hit” number two. This is an infectious bacterial disease which grows great in neutral or acidic pH as found in renal tissue.  The body’s response is inflammation, hypotension (low blood pressure), decrease blood flow to the kidneys (low oxygen to the tissue, therefore death to cells), and decrease in renal filtration.  There can also be direct invasion of renal cells causing necrosis. The severity of disease determines severity of the kidney attack.

Hospital2 Hospital3While the Kidney Attack began during the race, it was not until a few days later Steve got real sick.  As the team waited for the other teams to finish, he began to feel unwell – fever and headaches.  He was determined to enjoy the post race party on Saturday 29th October, so took a couple of aspirin (!).  He made it to the party, but only just. By Sunday afternoon his friends were in emergency mode organising for him to get on a flight to reach the nearest hospital in Kuching.  Steve quite literally crawled off the plane and waited for an ambulance to take him to hospital.  It was a small hospital and after 5 days, most of it sedated, without improvement, Steve was evacuated to Mt Sinai Hospital in Singapore.  There leptospirosis was diagnosed (it’s difficult to diagnose because of similarity of symptoms with other diseases of the tropics like typhus, dengue fever, Hanta virus infection).  Steve spent 10 days in ICU undergoing regular dialysis to support his kidneys and nearly all the time under sedation.  He was very lucky to survive.  His story of leaving Singapore, a $91,000 medical bill*, and continued hospitalisation in Christchurch with further dialysis is a harrowing one and can be found in his autobiography, “Lucky Legs.”

In the next instalment of the Face of Kidney Attack I will look at life after Kidney Attack.


*Steve had insurance provided by the race organisers, but it was woefully inadequate.  Only with the support of friends, family, and a public appeal did he avoid loosing his house.  I’ve considerable experience in assessing medical and travel insurances (long story why).  Never travel without at least $500,000 medical cover and preferably unlimited!  I choose myself to use Uni-Care outbound (http://www.uni-care.org)

The Face of Kidney Attack

The Face of Acute Kidney Injury.  (Published with permission).

The Face of Acute Kidney Injury. (Published with permission).

It ain’t pretty, it’s Acute Kidney Injury.  This case was probably brought on by leptospirosis.  This is the face of a well known New Zealander.  Do you recognise him?  He’s kindly lent his name to my research on AKI.  I will reveal that name in future posts as I tell his remarkable story.