Open Access

ARTICLE

Inflammation augments the development of experimental glomerulonephritis by accelerating proteinuria and enhancing mortality

Eva Pfeifer, Johannes Polz, Daniela N. Männel, Sven Mostböck

Department of Immunology, University of Regensburg, D-93042 Regensburg, Germany

* Corresponding Author: DN Männel,

European Cytokine Network 2012, 23(1), 12-14. https://doi.org/10.1684/ecn.2012.0300

Accepted 06 February 2012;

Abstract

Proteinuria represents a parameter for a damaged filtration capacity of the kidney. We investigated how inflammation influences the development of experimental, immune complex-mediated glomerulonephritis by monitoring proteinuria.Mice pre-treated with LPS or TNF, one day before induction of glomerulonephritis, excreted high levels of protein in the urine immediately after the induction of glomerulonephritis, in contrast to non-treated mice where proteinuria increased steadily after day 3. Protein levels in the urine of pre-treated mice remained elevated over the 15-day observation time. The severity of proteinuria at later times correlated with the degree of tissue pathology and mortality in individual mice. Pre-treatment with inflammatory agents accelerated the development of proteinuria and induced more severe kidney damage.

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