From the transplant clinic to the dialysis unit (and back again?)


On the monthly ward round of your satellite dialysis unit you come across a new patient: a man in his mid-50s, originally from Cyprus, who has recently been discharged from the renal ward and transferred to your unit in the last week.

From his discharge paper work and chatting to the patient you learn the following:

Having being labelled as having ‘small kidneys’ this gentleman spent 3 years on haemodalysis before receiving a deceased donor transplant 6 years ago. This transplant was complicated by 2 early episodes of rejection and his creatinine never got much below 180umol/l.

Concordance with clinic appointments and medicines was always deemed an issue by the medical team and 9 months ago the patient ceased to attend appointments.
It transpires that this was because a doctor in the transplant clinic had suggested that the current graft would reach the end of its useful life soon and, as a result, the patient had returned to Cyprus to try and find family members who could be potential live donors.

On return to the UK, he was admitted via A&E short of breath, oedematous and of a weight approx 13kg in excess of that recorded at his last clinic visit. Serum creatinine on admission was approx 600umol/l.  He was aggressively medically diuresed and re-established on dialysis given his fluid overload and symptomatic uraemia. A transplant biopsy was performed which showed widespread fibrosis and some nodular hyalinosis within arterial walls.

During his absence from the UK the patient had continued to see a renal doctor in Cyprus and remained on his Tacrolimus and MMF immunosuppression.  He has a few letters from this Cypriot doctor which document ‘therapeutic’ FK levels throughout this time.  They also refer to him having had a number of UTIs, none of which warranted hospital admission.  The treatment of these infections is listed but there are no visible positive microbiology results.

In the unit today, he is well and denies any concurrent medical problems. In particular he never experiences exertional chest pain and can climb several flights of stairs.

He is still slightly oedematous with a pre-dialysis BP of 180/90. Given his recent move to your satellite unit there is no useful information about inter-dialytic weight gains and he tells you he is still passing ‘about 1 litre’ of urine/day.

His current medicines are: Tacrolimus 2mg BD, MMF 500mg BD, Frusemide 250mg OD, Irbesartan 150mg BD, Atorvastatin 40mg OD, one Calcichew with meals and the unit’s favourite epo.

Since returning to the UK the patient has resurrected his painting and decorating business, which he claims was always the cause of his poor concordance and he tells you he has a potential live donor travelling to the UK in the next few weeks.

1 – What issues need addressing prior to listing this gentleman for transplantation?
2 – What would you do with his existing immunosuppressive regime?
   – Would this strategy be influenced if he were to be listed for live donor transplantation in the near future?
3 – Would you continue his high dose loop diuretic? Why?

2 thoughts on “From the transplant clinic to the dialysis unit (and back again?)”

  1. Some initial thoughts:

    1) Practically speaking it sounds as if adherence is going to represent the greatest barrier to retransplantation and input from a liason psychologist to explore and address this will be invaluable.

    It would be nice to invest more thought in the aetiology of the first allograft’s failure given its relatively premature demise. Was there evidence of chronic antibody mediated damage in the recent biopsy (eg PTC multilamination, or C4d positivity), to substantiate poor compliance? Was there any evidence of recurrent disease? The latter is particularly pertinent in a man of Cypriot origin with an uncertain primary disease, given the recent description of CFHR5 nephropathy in this population, a highly penetrant autosomal dominant disease leading to C3 glomerulopathy and progressive renal impairment, with documented potential to recur in the allograft. This would, of course, also have implications for selection of a suitable donor. How substantive were the urinary tract infections and does his bladder need further assessment?

    2) Regarding immunosuppression after return to dialysis, local practice at my centre has been to rapidly withdraw CNI but maintain a low dose of MMF (+/- steroid) in order to encourage persistent residual graft function with attendant benefits in volume management. I recognize that this conflicts with the popular view that risk of infection outweighs such benefits in this setting. A ‘ready to go’ live donor might sway you more towards keeping some IS onboard (probably the tac) to prevent troublesome symptomatic rejection in the lead-up to transplantation.

    3) I’d definitely continue the high dose loop diuretic while he has significant residual graft function. Although there is no prospective RCT data to support this, there is circumstantial evidence that associates diuretic use with improved survival in HD patients (DOPPS data) and conceptually it makes sense to maximize diuresis, minimize UF requirements and reduce IDWGs, especially as the risk of harm (eg ototoxicity) seems to be low with oral therapy.

  2. Interesting fact about CFHR5 nephropathy – apparantly the most recent data, obtained by screening every accessible Cypriot haemodialysis patient, suggests that the minimum prevalence of the allele among Greek Cypriots is 1:8500 – about 2.5x more common than Huntington’s disease, and only 8x less common than ADPKD – and the likelehood (given that the early stages manifest only as microscopic haematuria) is that this is a very conservative estimate.

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