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

Eur Cytokine Netw. 2012 Mar 1;23(1):12-4. doi: 10.1684/ecn.2012.0300.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Antibodies / adverse effects
  • Creatinine / blood
  • Creatinine / urine
  • Glomerular Basement Membrane / immunology
  • Glomerulonephritis / chemically induced
  • Glomerulonephritis / immunology*
  • Glomerulonephritis / metabolism
  • Kidney / pathology*
  • Lipopolysaccharides / immunology*
  • Lipopolysaccharides / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Proteinuria / urine*
  • Rabbits
  • Recombinant Proteins
  • Time Factors
  • Tumor Necrosis Factor-alpha / immunology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antibodies
  • Lipopolysaccharides
  • Recombinant Proteins
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Creatinine