NGAL (neutrophil gelatinase-associated lipocalin) has recently generated great interest as an early marker of renal injury. However, like many other endogenous biomarker molecules, it is not produced by just one cell type and different pathologies in different tissues can all provoke responses. Results must be interpreted with due regard to concurrent conditions in the individual patient in order to make optimal use of this sensitive marker.

Investigations on the performance of neutrophil gelatinase-associated lipocalin (NGAL) as an early marker of renal injury have certainly not stood still since my short introductory article in CLI [1]. Papers on NGAL are appearing at a rate of over two a week, and the main emphasis is indeed on its role as a marker of renal injury. However, other aspects of this fascinating molecule have not been ignored. Its pathophysiology and its role as a marker in adenocarcinomas are receiving attention, as are its roles in inflammation, atheroma and thrombi, as well as what may be its main function: a binder and transporter of siderophore iron.