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Cheesecake files: A stadium full John Pickering Aug 06

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As we’ve been enjoying the World Cup and the Commonwealth Games my latest cheesecake appeared in print online. The topic once more is Kidney Attack biomarkers – those pesky little proteins in the urine that appear when your kidney is injured.  This time I have been getting stuck into some math (sorry) to try and understand what it is that affects when these biomarkers appear in the urine after injury.  I call this a biomarker time-course.  A “Pee Profile” may be a better term but it would never get past the editor.  What I care about is whether the type of biomarker and/or extent of injury, affects the pee profiles.

There are three basic types of biomarkers.  First are those that are filtered from the blood by the two million odd filters in the kidney.  Often they are then reabsorbed back into the blood in the little tubules where the pee is produced – that is, they don’t appear in the urine.  Think of it like a stadium with many entrances.  People (biomarkers) come in and sit down (are reabsorbed).  If, though, a section of the stadium has been fenced off because of broken seating from the previous game (the injury), then some of those entering the stadium may end up exiting it again (the pee biomarkers).  The numbers being reabsorbed and exiting will also depend on whether all the entrances are open – if some are closed then this will have a flow on affect on the rate of people leaving the stadium.

The second are preformed biomarkers.  If we change the analogy slightly, imagine these as people already in the stadium (if the analogy was accurate they would have been born there!).  If some terrible injury happens (like the 4th, 5th, 6th and 7th goals of a now famous football match) some of those people would get up and exit quickly.  The overall rate of exit would reflect on the extent of the injury.

The third, are induced biomarkers.  These are ones that don’t already exist, but are produced in response to an “injury.”  Instead of being biomarkers, let us think of the spectators as produces of these biomarkers and let noise be the biomarker.  There is some background noise of course, but when an “injury” (goal, gold medal performance etc) occurs there is a sudden increase in noise which slowly dies down.  Depending on the team and the number of supporters this will be softer or loader and will carry on for shorter or longer periods (Goooooooooooaaaaaaaaaaaa……lllllllllllll).

The upshot of it all were many coloured graphs and a step towards understanding how we may better make use of the various types of novel biomarkers of kidney injury that have been recently discovered.

PlosOneFigs

_____________

Pickering, J. W., & Endre, Z. H. (2014). Acute kidney injury urinary biomarker time-courses. PloS One. doi:10.1371/journal.pone.0101288

 

 

Tagged: Acute Kidney Injury, Biomarkers, Kidney, Kidney Attack, Urine

Cheesecake files: A stadium full John Pickering Aug 06

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As we’ve been enjoying the World Cup and the Commonwealth Games my latest cheesecake appeared in print online. The topic once more is Kidney Attack biomarkers – those pesky little proteins in the urine that appear when your kidney is injured.  This time I have been getting stuck into some math (sorry) to try and understand what it is that affects when these biomarkers appear in the urine after injury.  I call this a biomarker time-course.  A “Pee Profile” may be a better term but it would never get past the editor.  What I care about is whether the type of biomarker and/or extent of injury, affects the pee profiles.

There are three basic types of biomarkers.  First are those that are filtered from the blood by the two million odd filters in the kidney.  Often they are then reabsorbed back into the blood in the little tubules where the pee is produced – that is, they don’t appear in the urine.  Think of it like a stadium with many entrances.  People (biomarkers) come in and sit down (are reabsorbed).  If, though, a section of the stadium has been fenced off because of broken seating from the previous game (the injury), then some of those entering the stadium may end up exiting it again (the pee biomarkers).  The numbers being reabsorbed and exiting will also depend on whether all the entrances are open – if some are closed then this will have a flow on affect on the rate of people leaving the stadium.

The second are preformed biomarkers.  If we change the analogy slightly, imagine these as people already in the stadium (if the analogy was accurate they would have been born there!).  If some terrible injury happens (like the 4th, 5th, 6th and 7th goals of a now famous football match) some of those people would get up and exit quickly.  The overall rate of exit would reflect on the extent of the injury.

The third, are induced biomarkers.  These are ones that don’t already exist, but are produced in response to an “injury.”  Instead of being biomarkers, let us think of the spectators as produces of these biomarkers and let noise be the biomarker.  There is some background noise of course, but when an “injury” (goal, gold medal performance etc) occurs there is a sudden increase in noise which slowly dies down.  Depending on the team and the number of supporters this will be softer or loader and will carry on for shorter or longer periods (Goooooooooooaaaaaaaaaaaa……lllllllllllll).

The upshot of it all were many coloured graphs and a step towards understanding how we may better make use of the various types of novel biomarkers of kidney injury that have been recently discovered.

PlosOneFigs

_____________

Pickering, J. W., & Endre, Z. H. (2014). Acute kidney injury urinary biomarker time-courses. PloS One. doi:10.1371/journal.pone.0101288

 

 

Tagged: Acute Kidney Injury, Biomarkers, Kidney, Kidney Attack, Urine

Cheesecake files: Of bathtubs and kidneys John Pickering Jun 11

Sitting in the bathtub you notice that there is a slow leak around the plug.  You adjust the taps to maintain a flow of water that exactly counteracts the loss due to the leak; the water level stays constant.  This is called a steady state and the same thing happens with out kidneys and the molecule used to assess their function.  Our bodies generate creatinine at a constant rate which finds its way into the blood.  Under normal circumstances our kidneys excrete that creatinine into the urine at the same constant

rate.  The creatinine concentration in the blood, therefore, stays constant.  When our kidneys get injured (as they very often do in hospitalised patients) this is like plugging the leak.  Just as the water level in the bathtub would rise slowly – undetectable at first – so too does the creatinine concentration rise slowly.  It normally takes a couple of days to be noticed.  Most of my work has been about trying to detect this injury to the kidney early.  However, if the kidneys start to recover then excess creatinine is only slowly cleared from the blood by the kidney – a process that similarly can take a day or two before it is detected.  Just as not knowing if the kidneys have been harmed makes treatment and drug dosing difficult for the nephrologists and intensivists, so too is not knowing if they have recovered.  My latest publication (aka a cheesecake file) that has appeared in press presents a simple tool for the physicians to try and determine if kidney function has recovered after having been compromised.

This particular piece of work began when a St Louis Nephrologists (a kidney doc), Dr John Mellas, contacted me to say that although a manuscript of his had been rejected by reviewers, he thought there was merit and could I help him (he found me through a search of the literature).  I confessed to being one of the reviewers who had rejected the manuscript!  Fortunately, John was forgiving.  His problem was that he was called in to the intensive care unit to look at a patient with high blood creatinine concentration.  Should he put the patient on dialysis or should he wait?  If he knew if the kidney was already recovering, then he would be less likely to put on dialysis. We talked about the issue for a while and eventually settled on a possible tool which we could test by looking at the behaviour of creatinine over time in abut 500 patients in the ICU.  The tool is quite simple.  It is the ratio of the creatinine that is excreted to the creatinine that is generated.  If more creatinine is being generated than excreted then probably the kidney function is still below normal, however, if more is excreted than generated then probably the kidney is recovering.  The difficulty is that there is no way to measure in an individual what the creatinine generation is.  We ended up using equations based on age, sex, and weight to estimate creatinine generation.  This is a bit like using an equation which takes into account pipe diameter, mains water pressure, and how many turns of the screw the tap has had to determine the rate of water flow.  Creatinine excretion, though, can be easily measured by recording total urine production over several hours (we suggest 4h) and multiplying this by the concentration of creatinine in the urine.

We discovered that by using the ratio between estimated creatinine generation and creatinine excretion we were able to tell in most patients if the kidney was recovering or not.  My hope is that physicians will test this out for themselves.  The good thing is that it requires only minimal additional measurements (and costs) beyond what are already made in ICUs, yet may save many from expensive and invasive dialysis.

Pickering, J. W., & Mellas, J. (2014). A Simple Method to Detect Recovery of Glomerular Filtration Rate following Acute Kidney Injury. BioMed Research International, 2014. doi:10.1155/2014/542069

 

Tagged: Acute Kidney Injury, AKI, cheesecake, Creatinine, Dialysis, Intensive Care Unit, Kidney, kidney function, Nephrology

A day to celebrate John Pickering Mar 13

If it weren’t for your kidneys where would you be?

You’d be in the hospital or infirmary,

If you didn’t have two functioning kidneys.

(with apologies to John Clarke aka Fred Dagg)

Happy World Kidney Day everyone.

This blog started off life as $100 Dialysis because I believe that if we can make a computer for $100 then surely we can do the same for dialysis!  Dialysis is a life saver, yet its cost kills as so many can not afford the treatment.

There’s some good news in the dialysis world.

Schematics of the zeolite nanonfibres and how they may look in practice

Schematics of the zeolite nanonfibres and how they may look in practice

Just last week the MANA – International Centre for Materials NanoArchitectionics announced  they have developed a method to remove waste from the blood using an easy-to-produce nanofibre mesh.  Importantly, they claim it is cheap to produce.  Details were published in Biomaterials Science (free access).  Despite the photograph, there have been no human studies yet, but I expect that won’t be too long in the future.

Dr Victor Gura and the Wearable Artificial Kidney (WAK)

Dr Victor Gura and the Wearable Artificial Kidney (WAK)

In the meantime, the FDA gave approval last month for human trials of a wearable dialysis device produced by Blood Purification Technologies Inc (the WAK).

New Zealand, and Dunedin and Christchurch in particular, lead the way in Home Dialysis.  One Dunedin tradesman has even taken Home Dialysis a step further and turned it into portable dialysis by dialysing in his work van during his lunch hour. Of course, those needing a holiday may go on the road in specially equipped camper vans (http://www.kidneys.co.nz/Kidney-Disease/Holiday-Dialysis/).

Cause for celebration in the New Zealand kidney community was the gong (Office of the New Zealand Order of Merit) given to Adrian Buttimore who for 40 years managed Christchurch’s dialysis service.

These are just a few pieces of good news as doctors and scientists work around the world to improve the lives of dialysis patients.

_________________

Hot off the Press… I couldn’t resist adding this…. Pee, the answer to the world’s energy problems. http://www.bbc.com/future/story/20140312-is-pee-power-really-possible

 

Tagged: Dialysis, Home dialysis, Kidney, Nephrology, pee, Urine, Wearable Artificial Kidney, World Kidney Day

Too little pee John Pickering Jun 26

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.

Tagged: Acute Kidney Injury, Acute Renal Failure, AKI, Fluids, Intensive Care, Kidney, Kidney Attack, Urine

Two new Health Research Council grants worth crowing about John Pickering May 07

This week’s announcement by the HRC of Feasibility Study and Emerging Researcher grants have many great projects.  Two in particular are worth crowing about (because they have some relationship to kidneys and they involve two excellent people).  I have put summaries in their own words below, but first my comments.

Dr Palmer (Department of Medicine, University of Otago Christchurch), who has appeared on this blog site before, conducts what in the trade are called “meta-analyses” and “systematic reviews.”  Simply put, these are methods to extract the best possible evidence from all the studies that have been done for the effectiveness of a treatment.  Just as one person may toss a coin 4 times in a row and get 4 heads, so too can any one trial give a mistaken impression that a treatment is efficacious (or not) when it really isn’t (or is).  By pooling together many treatments Suetonia provides the very best quality evidence available.  Given that Chronic Kidney Disease affects a large and growing proportion of us, knowing which treatments have the best outcomes is of national significance, not merely to our health but also to the national budget.  A particular problem is that after a trial it can be many many years until meaningful health outcomes are know (e.g. if the treatment delays dialysis need or reduces mortality).  Suetonia’s study will assess the effectiveness of surrogate endpoints for clinical trials.  Surrogate endpoints, such as plasma creatinine which I’ve discussed many time in this blog, are physiologically related to the functioning of an organ or to a disease state as well as statistically associated with future hard outcomes.  However, their use in trials is limited by how well they are associated and how they are used.  I look forward to finding out what Suetonia discovers.

Mrs Rachael Parke (Auckland DHB) is an experienced nurse undertaking a PhD. Ensuring patients have adequate fluids on board is particularly crucial to the kidneys and other organs. Obviously with surgery any blood loss needs to be compensated for. However, there are also physiological changes in where fluid is distributed throughout the body.  Cardiopulmonary bypass, used in cardiac surgery, is a particular risk factor for Acute Kidney Injury. In the past the practice has been to give large amounts of fluid in order to ensure adequate fluid is given.  However, recent research has shown that too much fluid can have a negative impact (increased mortality).  A more restrictive fluid regime may have very meaningful outcomes.  Rachael is investigating, in a randomised controlled trial, if restricting fluid improves outcomes.  The outcome she is most interested in is how long patients stay in the hospital.  This is a very practical outcome for both patient and budget.  I am particularly pleased that this study is nurse-led.  Nurses play an incredibly important role in research as well as patient management.

In their own words:

Dr Suetonia Palmer: Making better clinical decisions to prevent kidney disease

More than ten percent of adults will develop chronic kidney disease. The effectiveness of many treatments used to improve outcomes in kidney disease is tested against surrogate (indirect) markers of health (e.g., cholesterol levels or blood pressure).

Unexpectedly, subsequent systematic analysis has identified little evidence to show that treatment strategies based on these surrogate markers translate to improved health for patients. Serum creatinine and proteinuria levels are commonly-used markers of kidney function to guide treatment.

The research involves using systematic review methods to summarise the quality of evidence for using proteinuria and serum creatinine as markers of treatment effectiveness in clinical trials. It will be determined whether using these markers to guide clinical care improves patient health or, conversely, leads to treatment-related harm or excessive use of ineffective medication.

These summaries will help clinicians and patients make better shared decisions about which therapeutic strategies actually improve clinical outcomes in kidney disease.

Mrs Rachel Parke: Fluid therapy after cardiac surgery – A feasibility study

Following cardiac surgery, patients receive large amounts of fluid in the intensive care unit. This may cause problems with wound healing and delay hospital discharge. A planned randomised controlled trial of a restrictive fluid regime as compared to a more liberal approach utilising advance hemodynamic monitoring, aims to reduce the amount of fluid patients receive and reduce hospital length of stay. This feasibility study aims to determine whether this nurse-led protocol is practicable and feasible and will help answer the research question. This study is simple and inexpensive and if it demonstrates a decreased length of hospital stay then this will represent a significant benefit for both individual patients and the health system.

Tagged: Acute Kidney Injury, auckland dhb, Cardiac Surgery, Cardiopulmonary Bypass, Chronic Kidney Disease, Intensive Care Unit, Kidney, Kidney Attack, metaanalysis, university of otago

The Face of Kidney Attack Part III John Pickering Apr 24

He didn’t die, quite.  But later thought he may well of.  Steve Gurney’s episode of Acute Kidney Injury (see Part II) didn’t finish him after he was discharged from his third hospital (one each in Malaysia, Singapore and New Zealand) – 4 weeks after the event. While media outlets clamoured to hear the story of this amazing athlete’s brush with death, he had a $92,000 medical bill and was so weak he could barely walk.  He couldn’t return to his own home because it was on a hill and he couldn’t make it up the steep track.

Steve did all the right things.  He began exercising by walking to the letterbox and gradually increased it from there.  He lived on fruit, vegetables, nuts, legumes and meat – nothing pre-processed.  While his body began to be restored, it was the mental anguish – so often hidden from others – that really shook him up.  This from his book “Lucky Legs”:

“I’d gone from top dog in my sport to lowly turtle.  My aim to compete as a mountain biker in the Olympics had disappeared down a mud puddle.  I’d lost 15 kilograms, mostly muscle, there was a possibility of permanent kidney damage and my career as a pro athlete was in question.  My fuzzy mind reasoned that the ‘mat of my expertise’ had been jerked from under my feet now that I had been robbed of my fitness, too.  It was like the bottom had fallen out of my world and I was falling, out of control, with nothing to ground me.  ….The depression went on for six months … death seemed like a realistic solution  … But there was a tiny spark that said, ‘Don’t jump. … hang in there … like a long endurance race …”

Steve’s story of recovery is one of endurance and it is one of reaching out for help.  Some of the help Steve got was from practices which scientifically speaking don’t have a leg to stand on, yet the process of reaching out and talking with people concerned and willing to help was, and is to anyone in similar situations, so very important.  Steve didn’t go for homeopathy, but I’ve been told be someone who acknowledges it is a load of nonsense that they think it valuable to have in the community because of the power of the placebo affect.  She may well be right (needs a study).

Steve wins again

Steve wins again

The story continues and is one of anguish and triumph.  The two time winner of the Coast to Coast returned to it three years after his brush with death and won again, and then won another six years in a row.  Steve’s experiences had strengthened him mentally and focussed him on the things that mattered most to him.  As he said, “Contracting leptospirosis … was a good thing.”

There is an ancient Hebrew concept of health called “shalom.”  Often translated simply as “peace” it is actually much broader than that.  Unlike the common idea of health being merely an absence of illness, it encompasses the notion of being in right relationships – spiritually, physically, environmentally, and communally.  Those of us working in medical science do well to be reminded of shalom.

Tagged: Acute Kidney Injury, Coast to Coast, health, Kidney, Kidney Attack, leptospirosis, mental-health, Renal Failure, Steve Gurney

Cooking up a new kidney John Pickering Apr 15

The Boston Kidney Recipe

  1. Take an unwanted kidney.
  2. Disconnect from plumbing.
  3. Wash away cells (use plenty of detergent).
  4. Take resultant scaffold and reseed with a few cells obtained from someone needing the kidney.
  5. Place in bioreactor and “cook” for 3 to 5d (or until done)
  6. Place regenerated kidneys into the transplant recipient and connect to plumbing.
  7. Pee.

In Nature Medicine today Massachusetts General Hospital based researchers have announced the successful removal of an unwanted kidney from one rat, the removal of cells from that kidney, regeneration with stem cells from another rat, transplantation into that animal and the observation of  urine production*.  A  small step for a rat, a giant leap for anyone waiting for a transplant.  Why is this so important?  As the authors’ state:

“A bioengineered kidney derived from patient-derived cells and regenerated ‘on demand’ for transplantation could provide an alternative treatment for patients suffering from renal failure.”

While this study is “proof of context”, it is a beautiful proof and one which should bring hope to millions. There are many more people with End Stage Renal Disease than kidneys available for transplant.  Some donated kidneys currently considered not good for transplant may become viable in the future if the cells are stripped off and the patient’s own stem cells can be used to grow a new kidney over the scaffold of the old one.  By using the patient’s own cells the immune response may be reduced.  This will mean less dependence of immunosuppressant drugs and therefore fewer side effects, including  cancer, and less transplant rejection. This is the vision and one that can not come soon enough.  Have a look at the video and if you want to get into details, check out the paper* .

*Regeneration and experimental orthotopic transplantation of a bioengineered kidney. Jeremy J Song, Jacques P Guyette, Sarah E Gilpin, Gabriel Gonzalez, Joseph P Vacanti & Harald C Ott1. Nature Medicine. Advance Publication Online. http://dx.doi.org/10.1038/nm.3154

Tagged: bioengineering, End Stage Renal Disease, End stage renal failure, Kidney, Renal Failure, Transplant, Urine

The Face of Kidney Attack Part II John Pickering Apr 10

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)

Tagged: Acute Kidney Injury, Acute Renal Failure, Kidney, Kidney Attack, leptospirosis, Mulu Cave, Steve Gurney

A list of effective treatments for a Kidney Attack John Pickering Mar 12

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Tagged: Acute Kidney Injury, Acute Renal Failure, Kidney, Kidney Attack, World Kidney Day

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