Lupus: a special report
Published on 01 July 2011
Two years ago former Times gardening correspondent George Plumptre donated a kidney to his brother Francis, when lupus caused his kidneys to fail. Now chief executive of the National Gardens Scheme, which made Arthritis Research UK its guest charity in 2010–11, he tells how his donation transformed his brother’s life.
George’s living legacy
On 20 March 2009 I underwent an operation to give a kidney to my younger brother, Francis. Aged 53, over a period of months I was introduced to the remarkable world of transplant surgery and living donorship which is, in these days of so much criticism of and despair about our health service, a beacon of positiveness and quality.
But before describing the transplant experience some background about Francis’s health is necessary. Francis, who is 46, had had a long history of kidney failure. A serious accident involving major head injuries when he was 13 resulted in many years of ill health, and he contracted lupus in 1987. Lupus is an autoimmune disease and analysis at the time and afterwards confirmed that the onset of lupus resulted from Francis having previously contracted Henoch-Schönlein purpura, a type of vasculitis.
Total renal failure
The lupus took hold rapidly and a few months later he suffered total renal failure. Emergency treatment saved his life and led to a programme of dialysis to keep him alive. Despite the short-term devastating effect of the lupus, over a period of years it was controlled by careful medication until the threat receded for good.
Dialysis was a wonderful invention and offers life to people who, a generation ago, would have died. But it is a mechanical alternative to a complex bodily function and can never provide the same service. In 1993 the long-awaited breakthrough was offered when he had his first transplant, with a cadaver kidney as was the norm at that time. But the transplant failed, Francis rejected the kidney and after a period of life-threatening illness he had no option but to return to the bleak routine of dialysis three times a week.
Just before Christmas 1997 he was told by the renal unit at Guy’s, where he had been a dialysis patient for some years, that they could give him a new transplant with another cadaver kidney. This was a success and he returned home to embark on a more normal life than had been possible for a decade. But cadaver kidneys have a limited life of often little more than 10 years. In late 2007 Guy’s confirmed that his kidney was deteriorating and that he had a maximum of two years before it ceased functioning.
Having had two transplants and with his long history of ill-health and associated medication, Francis was an unusual patient. Most significantly, he had built up powerful antibodies in his blood so a new kidney had to be very well matched. And that is where I came in. We are a family of five brothers, Francis the youngest, me the third. Largely for reasons of practicality (such as one brother living in Australia) I was the one who took the decision to be tested as a potential donor first.
I had the crucial blood test at Guy’s on 24 September 2008, the results of which would show whether I was a compatible blood group and, crucially, whether I was a good tissue match. Tissue matching is measured from 1/6 to 6/6 and we knew that anything below 5/6 would cause complications because of Francis’s antibodies.
I was a perfect tissue match
When my result came through it confirmed I was a perfect 6/6 tissue match.
Making the decision to proceed was easy, I knew I could offer Francis the best possible chance of improved health and long life and I was conscious of the privations he had suffered since his youth. Nonetheless, as a donor you are voluntarily putting yourself on the line and introducing great turmoil into your life.
During the period of four months that I underwent different tests my main worry was that some problem would prevent me from being a donor. The operation was originally scheduled for late January but queries thrown up by my tests caused a delay until 20 March. During the delay Francis’s kidney function deteriorated unexpectedly fast and he had been forced to start dialysis.
On the operation day I was told by my surgeon that they had found I had a hernia, which he would deal with at the same time as removing my kidney, the whole operation to be performed laparoscopically (key-hole surgery). Perhaps because of the impact of the hernia as well, when I first came round from the anaesthetic I was in considerable pain and it was a real shock. But after six days I was discharged from hospital to recuperate at home and was amazed at the noticeable rate of my recovery during the weeks that followed.
For Francis, the fact that the kidney started working straight away had the immediate effect of making him feel better, even while he was recovering from the operation. It was amazing to watch and I do not think any of us had been prepared for the transformation of his daily quality of life which it brought about and which continues today, more than two years later.
Living donation is the key feature to future success
Living donation has revolutionised kidney transplants and any renal surgeon or physician will tell you that it is the key to future success. The first successful living donor transplant was carried out between two identical twins in 1954. But thereafter a lack of effective immuno-suppression drugs (which prevent rejection of the transplanted kidney) meant that the few times the operation was tried again most ended in failure. Not until the introduction in 1983 of the first reliable immuno-suppression drug called cyclosporin were improved rates of success made possible, and since then refinement of these drugs has been the key to successful living donor transplants.
In the space of a few years, medical advance has brought about a multi-faceted revolution: a change in legislation; better conditions and results for transplant recipients; and a cultural change in renal units like the one at Guy’s because the possibility of living donorship is now discussed at an early stage with patients suffering from kidney failure. The select group who opt to become living donors go through self-inflicted pain and upheaval before discovering an intense feeling of altruistic achievement, and an enriching reward that very few people are privileged to experience and which, I am sure, lasts a lifetime.
• Sections of this article originally appeared in the Mail on Sunday in 2009.
• Arthritis Research UK currently spends £6.5 million on research into lupus, including lupus nephritis.
A PDF version of our new information booklet on lupus is available on our website. Alternatively please call 0300 790 0400 or email us at firstname.lastname@example.org for a free paper version.
Looking for the genes that may cause lupus
Arthritis Research UK is currently running the UK’s biggest-ever study to discover the genes that cause lupus. And the scientist behind the study believes it could considerably advance understanding of the disease and could also result in a genetic test predicting who is most likely to develop the condition.
Professor Tim Vyse and his team at King’s College London are taking advantage of the latest advances in gene technology to analyse DNA samples from 5,000 people with lupus from all over the UK, Europe and Canada, in order to identify the full set of genes that predispose them to getting the condition.
They are being funded by a grant of £1.7 million from Arthritis Research UK through the generosity of a private donor.
As well as finding out how many genes contribute to the development of lupus, the team also wants to establish whether genes that cause the condition also influence the severity or type of lupus and whether particular organs of the body such as the heart or kidneys are likely to be involved. In the future a genetic test could become available to help speed up the diagnosis of lupus in patients with suspected auto-immune, inflammatory forms of arthritis.
In the short term the main aim is to discover many more genes that cause the disease. The team will then go on to determine how these genes increase the risk of developing lupus.
Professor Vyse, professor of molecular medicine at King’s College London, said: “There is a significant risk to the development of lupus; for example, the brother or sister of an affected person is over 29 times more likely to develop it than the rest of the population. Our group, among others, has already identified some of the genes implicated.
“However, we have only identified the ‘tip of the lupus genetic iceberg’, as the studies conducted so far have not been large enough. Our study is more than twice as big as all the other studies combined, so we are hoping that we will be able come up with some really useful results in order to identify the ‘how and why’ of lupus.”
The team expects to produce the first set of research papers of early results later this year.
Professor Alan Silman, medical director of Arthritis Research UK, said the charity had high hopes of Professor Vyse’s genetic research: “The drugs for lupus are not as effective as we would like. Discovering how many genes contribute to disease development is crucial so that we can work to produce new therapies.
“Because lupus mimics so many other forms of inflammatory arthritis, there are often long delays in diagnosing the condition, and in the shorter-term tracking down the genes responsible could also help speed up this process.”
What is lupus?
Also known as systemic lupus erythematosus or SLE, lupus is a serious inflammatory disease that affects the skin, joints and internal organs, and in severe cases can be fatal. There is no cure and people with the condition may have to take medication for the rest of their lives. However, current drugs are not particularly effective and many sufferers have a poor quality of life.
For more information on Lupus you can read our new booklet online (PDF version): Lupus
Alternatively please call 0300 790 0400 or email us at email@example.com for a free paper version