Tag Archives: death

Send them home

New Zealand is the home of Home Haemodialysis and Christchurch the hub. Sending people home to dialyse is not only more convenient for them and more cost effective, but also has been shown to reduce mortality.  However, is this reduction in mortality sustained across changes in dialysis medicine over time?  This is an important question as Home Haemodialysis is now being considered seriously in many jurisdictions across the world.  The question was recently addressed by Dr Mark Marshall and colleagues across New Zealand and Australia in an article which appeared online ahead of print a couple of weeks back in the American Journal of Kidney Disease (see here, sadly behind a paywall).

What they did

Step 1 was to extract data from 1998 to 2012 from the Australia New Zealand Dialysis & Transplant Registry which prospectively collects information for all long term renal replacement therapy patients. This is a very important registry and the study highlights the importance of keeping data in this way.

Step 2 Placed patients into one of three time periods according to when they started their dialysis: 1998-2002, 2003-2007, 2008-2012.

Step 3: Identified the exposure of the patients to one of: Facility lead haemodialysis (facility HD), Home haemodialysis (home HD), or Peritoneal dialysis (PD).

Step 4: Compared rates of death for patients starting in each time period for each of the dialysis modalities after accounting for age, sex, ethnicity, primary kidney disease, and glomerular filtration rate at the start of therapy (ie how well the kidney was functioning).

What they found (with my commentary)

there is demonstrable survival benefit associated with recent era irrespective of the landmark initiation time.

Indeed, it was a 25% lower (adjusted) mortality for those starting dialysis in  2008-2012 compared to the 1998-2002.

Well done kidney docs – they are getting better and keeping people alive.

There is significant effect modification by modality [type of dialysis] (P <0.001), and separate models were developed in each subgroup: there is a 23% corresponding reduction for those on facility HD therapy, a 29% reduction for those on PD therapy, and a 46% reduction for those on home HD therapy

In other words, all things being equal, survival was improved more on home haemodialysis than either of the other types.

Hazard ratios for death according to era and mode of dialysis.  Lower numbers are better!  From: Marshall, M. R., Polkinghorne, K. R., Kerr, P. G., Agar, J. W. M., Hawley, C. M., & McDonald, S. P. (2015). Temporal Changes in Mortality Risk by Dialysis Modality in the Australian and New Zealand Dialysis Population. American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. doi:10.1053/j.ajkd.2015.03.014

Hazard ratios for death according to era and mode of dialysis. Lower numbers are better! From: Marshall, M. R., Polkinghorne, K. R., Kerr, P. G., Agar, J. W. M., Hawley, C. M., & McDonald, S. P. (2015). Temporal Changes in Mortality Risk by Dialysis Modality in the Australian and New Zealand Dialysis Population. American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. doi:10.1053/j.ajkd.2015.03.014

I note patients were only around 60 years old on average when they first initiated dialysis, yet 37% died before the end of the study period or could receive a transplant.  Folks – do your damnedest to avoid kidney disease – starting with avoiding diabetes.

Conclusions

  1. Survival has increased during the past 15 years
  2. Survival of peritoneal dialysis patients has increased more than facility haemodialysis patients
  3. The relative survival of home haemodialysis patients has improved the most

Has home haemodialysis caused people to survive longer?  This study can’t say, because it is an association study not one set out to demonstrate causation. However, it is evidence that supports the continued use and possibly even expansion of home dialysis in New Zealand and Australia.

For further reading, refer to the paper itself:

Marshall, M. R., Polkinghorne, K. R., Kerr, P. G., Agar, J. W. M., Hawley, C. M., & McDonald, S. P. (2015). Temporal Changes in Mortality Risk by Dialysis Modality in the Australian and New Zealand Dialysis Population. American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. doi:10.1053/j.ajkd.2015.03.014

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.

91467137

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/

References

  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.

 

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

1300

Today’s number brought to you by Funeral Directors of New Zealand.

 

1300

 

Kidney Attack (aka Acute Kidney Injury) is responsible for at least 1300 deaths a year in New Zealand.  It used to be said that people died with Acute Kidney Injury rather than of Acute Kidney Injury.  The paradigm has shifted in the last few years.  Now it is recognised that an acute attack on the kidneys is a killer all by itself.  Of course, the attack is still most often precipitated by another event – heart attack, serious infection, cardiac surgery etc etc etc.

How did I come up with 1300?

A comprehensive study of nearly 20,000 hospital admissions showed that there was a 4.1 times increase in risk of death in hospital for those with Kidney Attack compared to those without.  The Ministry of Health in New Zealand do not report hospital mortality data, but a very helpful MOH information analyst, Chris Lewis (thanks Chris), dug out some numbers for me.  There were 7582 patients out of 548,965 discharges from public hospitals in 2011/12 who were “Discharged Dead”, Died in the emergency department, or Discharged for organ donation.  This does not necessarily capture all deaths (eg Private Hospitals are not included).  However, it gives me enough to go on using the proportion who died overall, the increased odds of death with Kidney Attack (4.1), the estimated number of Kidney Attack patients (30,000), and a little bit of math. The result is at least 1300 Kidney Attack deaths.