CD44 expression in IgA nephropathy

Sandrine Florquin, Raffaele Nunziata, Nike Claessen, Frank M. Van den Berg, Steven T. Pals, Jan J. Weening

Research output: Contribution to journalArticle

Abstract

Immunoglobulin A (IgA) nephropathy is a frequent, chronic renal disease characterized by a broad spectrum of clinical presentations and pathologic findings. CD44, a family of type I transmembrane glycoproteins involved in cell-cell and cell-matrix interactions, may orchestrate partially the cascade of inflammation, accumulation of myofibroblasts, and fibrosis leading to end-stage renal disease. To clarify the possible role of CD44 in the progression of IgA nephropathy, the expression of CD44 in glomeruli and the tubulointerstitial compartment was analyzed in 25 renal biopsy specimens of patients with IgA nephropathy and was correlated to histopathologic, serologic, and urinary parameters. The expression of CD44 correlated significantly with the degree of glomerular and interstitial damage, even better than the accumulation of α-smooth muscle actin-positive myofibroblasts, which is recognized as a reliable marker for the progression of IgA nephropathy. A positive correlation also was found between proteinuria and the expression of CD44 in the tubulointerstitial compartment. The glomerular and tubulointerstitial expression of CD44 correlated with the degree of renal damage in IgA nephropathy and could be a reliable marker of the progression of IgA nephropathy. CD44 may have a pivotal role in the cascade of renal inflammation and fibrosis.

Original languageEnglish
Pages (from-to)407-414
Number of pages8
JournalAmerican Journal of Kidney Diseases
Volume39
Issue number2
Publication statusPublished - 2002

Keywords

  • CD44
  • Classification
  • Fibrosis
  • Immunoglobulin A (IgA) nephropathy
  • Myofibroblasts
  • Prognosis

ASJC Scopus subject areas

  • Nephrology

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    Florquin, S., Nunziata, R., Claessen, N., Van den Berg, F. M., Pals, S. T., & Weening, J. J. (2002). CD44 expression in IgA nephropathy. American Journal of Kidney Diseases, 39(2), 407-414.