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Nephrol Dial Transplant (2003) 18: 237-240
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Complement inhibition in renal diseases

Jameel M. Inal1,, Manuel Pascual2, Philippe Lesavre3 and Jürg-A. Schifferli2,3

1 University Hospital Basel, Department of Research, Basel, Switzerland, 2 Massachusetts General Hospital and Harvard Medical School, Transplantation Unit, Boston, MA, USA and 3 INSERM U507, Hôpital Necker, Service de Néphrologie, Paris, France

Keywords: complement; glomerulonephritis; ischaemia/reperfusion injury

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

Introduction

The activation of complement and its deleterious consequences have been observed in many renal diseases. Complement contributes to injury in several forms of glomerulonephritis (GN), in acute and chronic humoral rejection after renal transplantation, and at the time of ischaemia/reperfusion injury. It is also thought to accelerate the progression of chronic renal damage. Most of the evidence for the role of complement in enhancing injury comes from experimental data obtained in murine models, in which the addition of complement inhibitors blocks or reduces damage. The first evidence that excessive complement activation can be reversed in humans has been recently reported by Remuzzi et al. [1]. These authors reported a combined liver and kidney transplantation in a young child with haemolytic uraemic syndrome (HUS) and a mutation of factor H by which they were able to restore the defective factor H activity with no recurrence of the disease. . . . [Full Text of this Article]

Complement

Complement regulators

Complement in glomerulonephritis

Ischaemia/reperfusion injury

Antibody- and complement-mediated rejection after renal transplantation (humoral rejection)

Progression of renal damage

Complement inhibition


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