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De Novo and recurrent thrombotic microangiopathy (TMA) after renal transplantation: current concepts in management

Urology & Nephrology Open Access Journal
Fedaei Abbas,1,2 Sara Fedaei Abbas3

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Thrombotic   microangiopathy   (TMA)   is   a   well-recognized   complication   of   kidney   transplantation that leads frequently to allograft failure. This serious outcome depends greatly on the underlying etiology as well as the timing of therapeutic interventions. TMA syndromes may occur with no previous history of TMA, i.e., de novo TMA, mostly due to medications or infection, or more frequently recurs after kidney transplantation i.e., recurrent TMA in patients with ESRF due to the atypical hemolytic uremic syndrome (aHUS). On the other hand, patients with shiga-toxin induced HUS (classic HUS), particularly in childhood has a favorable prognosis. One of the fundamental tools of management of this disease is the genetic screening for abnormal mutations, determination of which will recognize the tools of therapy and consequently outcome of the disease to a large extent. While patients with CFH  and  CFI  mutations  have  a  worse  prognosis,  other  patients  with  MCP  mutations-for  example- have a more favorable prognosis. Accordingly, plan of therapy can be thoroughly drawn with a better chance of cure. Unfortunately, the successful use of the biological agent “eculizumab”, an anti-C5 agent, in some of these syndromes is largely impeded by its high cost linked to its use as a life-long therapy. However, a new therapeutic option has been recently admitted ameliorating this drawback and improve the cost-effectiveness balance.


thrombotic microangiopathy- de novo tma - recurrent tma - renal allograft