BKV AFTER TRANSPLANT.
Posted: Tue Sep 29, 2015 11:30 am
BKV After Transplant.
So there you are, so excited about your new kidney, (in my case 5 months after transplant) the thought of no dialysis and hoping to get a semblance of normal life back when BANG, your bloods start going haywire. Creatine starts rising, white blood cells start dropping and it is clear something is wrong.
In my case by chance a registrar (junior Doctor) noticed that my white blood cell count was very low and as a precaution asked for a series of different blood results. At the same time, although typically the Creatine level worsens gradually, mine jumped from 140/150 to 250 between two 3 week tests.
That was just 10 days ago and I remember sitting there opposite the kidney specialist while he picked up the phone to call the specialist transplant ward upstairs to see if there was a spare bed to admit me. Man my life fell apart in those few seconds. Over and above that I had become a bit lax on the water front, only drinking about 2 L a day. Big shock and wake up call.
Anyway a bit on the epidemiology of the virus.
Humans are the natural host for BKV, JVC and SV40 and it is thought up to 80% of the population carry it in it’s dormant state. The way we get it is varied and may be faecal-oral, food prepared by someone who has not washed their hands for example, respiratory, transplacental, or from donor tissue.
BK virus infection is considered to be contagious between people. Generally the infectious agent may be transmitted by saliva, air, cough, faecal-oral route, surfaces, blood, needles, blood transfusions, sexual contact, mother to foetus, etc.
Begs the question which I will ask at my next clinic visit, why is more separation not given for patients visiting the clinic with this virus? It just so happens that a lady I know who has also just had the virus, sits next to me and chats every time we go to clinic, did catch it from her?
BKV is the consequence of modern potent immunosuppression aimed at reducing acute rejection and improving allograft survival which suppresses the immune system so well that dormant and or caught viruses can take hold.
BKV infections lead to kidney allograft dysfunction or loss.
Decreased immunosuppression is the principle treatment but predisposes to acute and chronic rejection. The only way to treat BKV is to reduce the immunosuppression allowing the immune system to fight the virus but as we are aware this also predisposes a transplant patient to rejection. It becomes a tightrope situation, too little suppression = rejection, too much = BKV killing your kidney.
There are no antiviral drugs that can help.
Just by way of incidence, the emergence of polyomavirus nephropathy (BKV) has coincided with the use of new potent immunosuppressive medications. It is usually associated with BKV, affects up to 8% of recipients, and frequently results in allograft loss or permanent dysfunction. However as already mentioned dormant BKV in one study was found in 80-88% of pre-transplant patients.
A bit about the treatment of BKV virus.
The principal treatment for BKV nephropathy is reduction in immunosuppression.
Various strategies include reduction or discontinuation of any calcineurin inhibitor and/or adjuvant agent, changing from MMF to steroids and in really bad cases from tacrolimus (Prograf) to cyclosporine or commonly known as Gengraf or Sandimmune or Neoral.
The net result of this should be an improvement in your creatine levels, then stabilisation and an increase in your white blood cell count.
When BKV nephropathy (worsening performance of kidney measured by creatine level) is diagnosed early within the first 6 mo after transplantation and the creatinine is stable, survival is improved compared with when the diagnosis is made later and the creatinine is elevated.
In my case the noticed my white blood cell count was very low, after investigation realised my creatine had worsened badly, did more tests and found the BKV traces. Immediately stopped the MMF (cellcept) and started me on a steroid, which by the way is also a form of immune suppression but less aggressive with a side effect of encouraging white blood cell growth necessary to fight the virus.
I will keep adding as and when new developments happen.
So there you are, so excited about your new kidney, (in my case 5 months after transplant) the thought of no dialysis and hoping to get a semblance of normal life back when BANG, your bloods start going haywire. Creatine starts rising, white blood cells start dropping and it is clear something is wrong.
In my case by chance a registrar (junior Doctor) noticed that my white blood cell count was very low and as a precaution asked for a series of different blood results. At the same time, although typically the Creatine level worsens gradually, mine jumped from 140/150 to 250 between two 3 week tests.
That was just 10 days ago and I remember sitting there opposite the kidney specialist while he picked up the phone to call the specialist transplant ward upstairs to see if there was a spare bed to admit me. Man my life fell apart in those few seconds. Over and above that I had become a bit lax on the water front, only drinking about 2 L a day. Big shock and wake up call.
Anyway a bit on the epidemiology of the virus.
Humans are the natural host for BKV, JVC and SV40 and it is thought up to 80% of the population carry it in it’s dormant state. The way we get it is varied and may be faecal-oral, food prepared by someone who has not washed their hands for example, respiratory, transplacental, or from donor tissue.
BK virus infection is considered to be contagious between people. Generally the infectious agent may be transmitted by saliva, air, cough, faecal-oral route, surfaces, blood, needles, blood transfusions, sexual contact, mother to foetus, etc.
Begs the question which I will ask at my next clinic visit, why is more separation not given for patients visiting the clinic with this virus? It just so happens that a lady I know who has also just had the virus, sits next to me and chats every time we go to clinic, did catch it from her?
BKV is the consequence of modern potent immunosuppression aimed at reducing acute rejection and improving allograft survival which suppresses the immune system so well that dormant and or caught viruses can take hold.
BKV infections lead to kidney allograft dysfunction or loss.
Decreased immunosuppression is the principle treatment but predisposes to acute and chronic rejection. The only way to treat BKV is to reduce the immunosuppression allowing the immune system to fight the virus but as we are aware this also predisposes a transplant patient to rejection. It becomes a tightrope situation, too little suppression = rejection, too much = BKV killing your kidney.
There are no antiviral drugs that can help.
Just by way of incidence, the emergence of polyomavirus nephropathy (BKV) has coincided with the use of new potent immunosuppressive medications. It is usually associated with BKV, affects up to 8% of recipients, and frequently results in allograft loss or permanent dysfunction. However as already mentioned dormant BKV in one study was found in 80-88% of pre-transplant patients.
A bit about the treatment of BKV virus.
The principal treatment for BKV nephropathy is reduction in immunosuppression.
Various strategies include reduction or discontinuation of any calcineurin inhibitor and/or adjuvant agent, changing from MMF to steroids and in really bad cases from tacrolimus (Prograf) to cyclosporine or commonly known as Gengraf or Sandimmune or Neoral.
The net result of this should be an improvement in your creatine levels, then stabilisation and an increase in your white blood cell count.
When BKV nephropathy (worsening performance of kidney measured by creatine level) is diagnosed early within the first 6 mo after transplantation and the creatinine is stable, survival is improved compared with when the diagnosis is made later and the creatinine is elevated.
In my case the noticed my white blood cell count was very low, after investigation realised my creatine had worsened badly, did more tests and found the BKV traces. Immediately stopped the MMF (cellcept) and started me on a steroid, which by the way is also a form of immune suppression but less aggressive with a side effect of encouraging white blood cell growth necessary to fight the virus.
I will keep adding as and when new developments happen.
Prograf