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Tytuł oryginału: Thrombotic microangiopathy in renal transplantation.
Autorzy: Chiurchiu Carlos, Ruggenenti Piero, Remuzzi Giuseppe
Źródło: Ann. Transplant. 2002: 7 (1) s.28-33, tab., bibliogr. 76 poz.
Sygnatura GBL: 313,259

Hasła klasyfikacyjne GBL:
  • transplantologia
  • hematologia
  • nefrologia
  • neurologia

    Typ dokumentu:
  • tytuł obcojęzyczny

    Streszczenie angielskie: The term thrombotic microangiopathy (TMA) encompasses syndromes of thrombocytopenia, microangiopathic haemolytic anaemia, neurologic deficits, renal dysfunction and variable signs of organ impairment. Childhood cases of TMA with predominant renal failure are usually referred as Haemolytic Uremic Syndrome (HUS), and adult cases with major neurological involvement as Thrombotic Thrombocytophenic Purpura (TTP). Exotoxins, produced in most cases by E. Coli O157:H7, have been related to diarrhea associated HUS(D+HUS). Anticancer (mitomycin), immunosuppressive drugs (cyclosporin, tacrolimus and OKT3) and as well as some antiplatelet agents (ticlopidine, clopidrogel) have been associated with both HUS and TTP. Defective factor H or vWF protese activity have been found familiar and recurrent forms. Endothelial damage and dysfunction is most likely the initial event of the pathogenic process that eventually leads to plateled aggregation, microvascular thrombosis and tissue ischemia. TMA may occur de novo in the native kidneys of patients who received a non-kidney transplant or in the transplanted kidney patients who progressed to ESRD because of a disease other than HUS. Calcineurin inhibitors and vascular rejection are most often involved in these cases. The disease may also recur on the transplanted kidney in patients who progressed to ESRD because of HUS/TTP. The risk of postransplant recurrence is negligible for D + HUS but is close to 100 p.c. in familial/recurrent forms associated with low C3 and decreased factor H bioavailability or activity...

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