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Nephrol Dial Transplant (2000) 15: 173-183
© 2000 European Renal Association-European Dialysis and Transplant Association

Inflammatory mediators in human renal dysplasia

Catherine M. Cale1, Nigel J. Klein2, Paul J. D. Winyard1 and Adrian S. Woolf1

1 Nephrourology Unit and 2 Immunobiology Unit, Institute of Child Health, UCLMS, London, UK

Correspondence and offprint requests to: Dr Catherine Cale, Department of Clinical Immunology, Great Ormond Street Hospital for Children NHS Trust, Great Ormond Street, London WC1N 3JH, UK.

Background. Cytokines regulate many processes in the immune system and have recently been implicated in normal organogenesis. We previously demonstrated that the archetypal inflammatory cytokine tumour necrosis factor-{alpha} (TNF-{alpha}) is expressed in the murine metanephros, and exogenous TNF-{alpha} inhibits nephrogenesis and increases macrophage numbers in vitro (Cale et al., Int J Dev Biol 1998; 42: 663–674). The phenotype seen, with an arrest of ureteric bud branching and failure of mesenchymal to epithelial conversion, is similar to human renal dysplasia.

Methods and results. In normal human fetal kidneys we demonstrated the presence of macrophages and T cells and also documented TNF receptor expression on ureteric bud derivatives. In contrast to normal tissues, TNF-{alpha} protein was detected in dysplastic kidneys. This factor was also detected in the urine of fetuses with obstructive uropathy and TNF receptors were expressed in dysplastic tubules. Furthermore, we noted a fetal distribution of macrophages and T cells in dysplastic tissues and persistent expression of the adhesion molecules neural cell adhesion molecule and intercellular adhesion molecule.

Conclusions. We suggest that abnormal expression of cytokines early in renal development dysregulates normal patterns of adhesion molecule expression and inflammatory cells, and may contribute to the pathogenesis of renal dysplasia.

Keywords: ICAM-1; macrophage; NCAM; renal dysplasia; TNF-{alpha}


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