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NDT Advance Access originally published online on June 12, 2009
Nephrology Dialysis Transplantation 2009 24(9):2623-2627; doi:10.1093/ndt/gfp282
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Haemophagocytic syndrome—a life-threatening complication of renal transplantation

Claudio Ponticelli1 and Ornella Della Casa Alberighi2

1 Division of Nephrology, IRCCS Istituto Clinico Humanitas, Rozzano, Milano 2 IRCCS G. Gaslini, Clinical Pharmacology, Genova, Italy

Correspondence and offprint requests to: Claudio Ponticelli; E-mail: claudio.ponticelli@fastwebnet.it

Keywords: haemophagocytic syndrome; macrophage activation; transplant complications

The first 150 words of the full text of this article appear below.



   Introduction
 
Haemophagocytic syndrome (HPS), also referred as macrophage activation syndrome (MAS) or haemophagocytic lymphohistiocytosis, is a clinicopathologic entity caused by systemic proliferation of benign haemophagocytic cells of the monocyte–macrophage–histiocyte lineage. Criteria for diagnosis include fever, hepato-splenomegaly, neurological dysfunction, pancytopaenia, hypertriglyceridaemia, hypofibrinogenaemia, hyperferritinaemia and haemophagocytosis. Five of the following eight diagnostic criteria needed to be met: (1) fever, (2) cytopaenia of two lines, (3) hypertriglyceridaemia and/or hypofibrinogenaemia, (4) hyperferritinaemia (>500 µg/L), (5) haemophagocytosis, (6) elevated soluble interleukin-2 receptor (CD25), (7) decreased natural killer (NK)-cell activity and (8) splenomegaly can also commonly be found in patients with sepsis, systemic inflammatory response syndrome (SIRS), multiorgan dysfunction syndrome (MODS) and MAS [1–3]. A tissue biopsy, but more commonly bone marrow aspiration examination, may reveal haemophagocytosis characterized by proliferation of mature histiocytes actively ingesting other blood cells. However, the typical haemophagocytic features may be absent in 30% of cases. [1–4]. Two forms . . . [Full Text of this Article]

Primary HPS
Reactive HPS
HPS in renal transplant recipients
Diagnosis of posttransplant HPS
Pathogenesis of posttransplant HPS
Prognosis of posttransplant HPS
Treatment of posttransplant HPS


   Conclusions
 

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