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Review

Live kidney transplant from an unrelated donor

A kidney donor describes and reflects on her experience, from her partner’s diagnosis with kidney failure, through assessment to transplantation and recovery

In this article…

  • Signs and symptoms of renal failure
  • Assessments for both donor and recipient
  • Process and follow-up care for transplant patients
  • Impact of live donation

 

Author

Sharon Smith is principal lecturer; Vimala Sinniah is senior lecturer; both in pre-qualifying nursing at Buckinghamshire New University.

 

Abstract

Smith S, Sinniah V (2013) Live kidney transplant from an unrelated donor. Nursing Times; 109: 27, 12-15.

This article provides an insight into the experience of live donation from the donor and recipient perspectives from diagnosis until 18 months after transplantation. The lead author details the diagnosis of end-stage renal failure in her partner and their decision for her to donate a kidney.

  • This article has been double-blind peer reviewed
  • Figures and tables can be seen in the attached print-friendly PDF file of the complete article in the ‘Files’ section of this page

 

5 key points

  1. Live donation addresses the problem that there are too few kidneys available for deceased donors
  2. Without a kidney transplant people with end-stage renal failure need haemodialysis
  3. Research suggests that survival rates of transplanted kidneys is greater than those of cadaveric organs
  4. Polycystic kidney disease can profoundly enlarge the kidneys, replacing much of the normal structure and reducing kidney function
  5. Around half of patients with the most common type of PKD will progress to end-stage renal failure

 

Howard is 58 years old and, in common with many men, is keen to have as little as possible to do with healthcare providers. In April 2011, I had become concerned about a small wound on his nose caused by ill-fitting glasses; the wound did not appear to be healing as expected and I persuaded him to visit our GP. During this visit the GP measured his blood pressure, which was 161/96 and, in accordance with National Institute for Health and Clinical Excellence (2011) guidelines for stage 1 hypertension, blood tests were requested (Table 1).

The blood results strongly indicated that Howard was suffering from renal insufficiency. He was immediately admitted to hospital, initially for the treatment of his hyperkalaemia (raised serum potassium levels in the blood) and for further investigation to establish the reason for his abnormal blood results.

Reducing the potassium level was a primary concern at this time, as untreated hyperkalaemia can lead to cardiac arrhythmias and arrest (Hudak et al, 1998). This was treated with salbutamol via a nebuliser, which was supplemented with intravenous infusion of glucose and insulin. The insulin promotes movement of potassium from the extracellular space back into the cells (Gross and Pistrosch, 2004). Salbutamol may not lower potassium in all patients, and some studies show that up to 40% of those who have a degree of kidney failure requiring renal replacement therapy (those who are dialysis dependent) are resistant to salbutamol (Gross and Pistrosch, 2004). Although Howard’s full blood picture indicated that he was likely to require dialysis, this treatment succeeded in reducing his blood serum potassium level from 6.2mmol/L to 4.9mmol/L (Table 1). He started on a low potassium diet in the first few days following diagnosis.

The kidneys filter waste and excess fluid from the blood, which are excreted as urine, thereby regulating the levels of potassium, urea and creatinine.

An ultrasound scan showed bilateral polycystic kidney disease (PKD), which is a genetic disorder causing the growth of numerous cysts in the kidneys (Jacob, 2012). These cysts fill with fluid and can profoundly enlarge the kidneys and replace much of the normal structure, resulting in reduced kidney function and leading to renal failure.

Howard was diagnosed with end-stage renal failure (ESRF) secondary to PKD. Without a transplant, he would need three five-hour haemodialysis sessions a week.

Signs and symptoms

Patients with ESRF often experience uraemia. Typically, these patients will have raised blood urea and creatinine (Huether and McCance, 2004), both of which were elevated in Howard’s case.

Uraemia is an increase in blood urea nitrogen, which delays wound healing by preventing the granulation of new tissue (Kindlen, 2003). This may explain why the wound on Howard’s nose had failed to heal, the only outward sign that he was seriously ill.

Huether and McCance (2004) suggest that patients with ESRF normally have problems with fatigue, anorexia, nausea and vomiting. Howard did not complain of any of these symptoms. However, in retrospect his appetite was perhaps reduced and I had been aware of a malodour, which I later recognised as uraemia.

Howard was discharged from hospital once his blood chemistry was within a safe range.

Treatment

Approximately 50% of patients with the most common type of PKD will progress to end-stage renal failure (ESRF) (Table 2). At the point of diagnosis, Howard was found to already be in ESRF (also termed chronic kidney disease stage 5). Patients experiencing renal failure as a result of PKD may require dialysis or transplantation.

The optimum treatment for PKD is a pre-emptive transplant before dialysis is required (Papalois et al, 2000). However, according to Kalble et al (2010), there is little significant difference to the long-term outcome when the patient has been on dialysis for less than six months.

Our first meeting with the renal specialist was 48 hours after Howard had been discharged and it was at this meeting that the decision was made to start dialysis. Dialysis is required when the estimated glomerular filtration rate (eGFR) is below 10 (NICE, 2008) and Howard’s had deteriorated below this level at diagnosis (Table 1).

The implications of the pre-transplant assessment for both Howard and I were discussed. We were fortunate to be able to attend one of the regular patient seminars delivered by the renal transplant coordinator and the transplant team within a few days. This seminar reaffirmed that a live transplant would provide the optimum outcome for Howard in terms of quality of life.

To gain access for dialysis, Howard had a dialysis catheter inserted in early June. The haemodialysis catheter has two lumens, which are inserted into the venous system and positioned with the tips in the right atrium and the superior vena cava, facilitating connection to the dialysis machine. The catheter was used instead of forming a fistula because Howard needed to start haemodialysis three times a week as soon as possible. His haemoglobin continued to fall while on dialysis and did not start to return to a normal level until after the transplant (Table 1).

Before any assessment was made, we were told there was a better than 50% chance that I would be able to donate a kidney to Howard. Kalble et al (2010) have suggested the survival rates of grafts (kidneys) from living donors are higher than those of cadaveric grafts. We were also aware that, if I was able to donate a kidney, the transplant could take place significantly sooner than if we had to wait for a cadaveric transplant.

Assessment

The overall aims of the pre-transplant assessment protocol within guidelines for live kidney transplantation are to ensure both donor and recipient are fit for transplant and that the potential for graft survival is good (British Transplant Association and Renal Association, 2011). In addition, pre-assessment has to establish that the donor will continue to have satisfactory kidney function after donation (Table 3).

The first area of investigation looked at our potential tissue compatibility, which involved blood tests to look at blood groups and antibody levels. These tests confirmed our compatibility; however, some non-compatibility issues can be overcome by medical intervention before transplant. Where the donor and recipient have different blood groups - for example one has group A and the other group B - plasma exchange can be used to remove conflicting antibodies. These are known as ABO-incompatible kidney transplants. If the level of antibody incompatibility cannot be overcome, willing donors can have the option of being entered into a scheme where they donate a kidney to a compatible stranger so that their loved one can receive a kidney from a stranger.

I underwent MRI and ultrasound scans to look at the anatomy of my kidneys, as this varies from one person to another. The donor’s left kidney is the preferred one to use, because the left renal vein is usually longer than the right one, and is therefore easier to join to the recipient’s vein.

Nuclear medicine tests were required to look at the glomerular filtration rate (GFR) of each of my kidneys as my left one was significantly larger than the right. This test demonstrated that my overall kidney function was split 50/50 between each kidney, despite the difference in size. Had there been a 60/40 differential (or more) the transplant would not have taken place as the kidney with the lesser function would not have been enough to sustain satisfactory renal function in either Howard or myself. I also underwent tests to establish my fitness for anaesthetic.

To ascertain Howard’s fitness for transplant, he underwent routine cardiac and respiratory investigations, and a brain scan to rule out cerebral haemorrhage, which is one of the complications of PKD (Jacob, 2012). As he has a close family history of bowel cancer, he also underwent a colonoscopy. It was important to establish if Howard had any pre-existing cancer as the drugs he would need to take for the rest of his life could exacerbate this condition. Immunosuppressive drugs, such as tacrolimus, are given to suppress lymphocyte production.

Once all these tests had established Howard’s fitness for transplant and my appropriateness as a donor, together with my fitness for surgery, non-medical assessment was required. This involved us being interviewed together by an independent assessor, who then saw me on my own to verify that I was not being coerced to donate my kidney. This is in accordance with UK Human Tissue Authority regulations (HTA, 2013).

I had made up my mind that I wanted to be a donor before I understood all the physical implications of having this surgery. The risks were explained to me and I understood that my renal function would not be compromised by having one kidney, although I might experience some fatigue initially while the lone kidney adapted. I very much wanted to be able to give Howard a kidney and trusted the renal team to not put me at any undue risk.

During the build-up to the transplant, my anxiety was far more focused on hoping we would be able to have the surgery than on its implications.

Live kidney transplantation

The investigations caused a high degree of anxiety for us both, but we finally made it to the operating theatre on 15 September 2011. Fig 1 shows the position of a transplanted kidney. It is normal to not remove the diseased kidneys unless they grow excessively large (Jacob, 2012).

After surgery, we both spent two days in the renal high dependency unit. My renal function was closely monitored until it reached satisfactory levels of a GFR over 70ml/min and creatinine below 120µmol/L.

We were discharged home after two weeks when Howard’s creatinine was below 200µmol/L, his wound appeared to be healing and the pharmacist was satisfied that he understood his drug regimen.

Following discharge, Howard continued to be closely monitored by the renal outpatients department. In the first couple of weeks after discharge, this meant visits three times a week, then twice weekly and gradually reducing to once every six weeks. On each visit, his creatinine level was tested, as a significant rise could indicate signs of rejection (Thomas, 2008). If picked up early, this can be rectified by adjusting the dose of anti-rejection drugs.

Howard also had a biopsy of the transplanted kidney at three months and again one year after the transplant. This is because this tissue can show signs of early rejection before creatinine levels change (Thomas, 2008).

I returned to work after a three-month recovery period. Since the transplant, Howard has experienced only one occasion when a raised creatinine level caused him to be readmitted to hospital for 24 hours. This was just after he had been discharged home and the warm weather had caused him to become dehydrated. He has had to learn to increase his fluid level carefully whenever the ambient temperature increases.

The renal team is satisfied that Howard fully understands the importance of correct fluid intake and of adhering to his drug regimen, which means we can now travel abroad. 

Life for both of us has been good since the transplant, culminating in us getting married in August 2012. The transplant journey was challenging but the positive outcome made it worthwhile for us both. We hope our experience will encourage others to grasp the opportunity of live organ donation to enhance the quality of live for those with ESRF.

 

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