Proteinuria as a mediator of tubulointerstitial injury

Mauro Abbate, Giuseppe Remuzzi

Research output: Contribution to journalArticlepeer-review

Abstract

Proteinuria is one of the most potent risk factors for renal disease progression in patients with glomerular diseases. Studies in disease models have helped to delineate mechanisms leading to renal structural damage due to persistent dysfunction of the glomerular barrier to proteins, even when the primary immune or non-immune insult to the kidney has ceased. The main focus of this review is the role of the tubular epithelial cell in the induction of interstitial inflammatory and fibrogenic reactions to ultrafiltered proteins. Antiproteinuric drugs (angiotensin-converting enzyme inhibitors, ACEi) while preserving the integrity of the glomerular permselective barrier limit both proteinuria and protein-dependent processes which contribute to tubulointerstitial injury, and in so doing ACEi halt the progression of proteinuric nephropathies toward terminal renal failure.

Original languageEnglish
Pages (from-to)37-46
Number of pages10
JournalKidney and Blood Pressure Research
Volume22
Issue number1-2
DOIs
Publication statusPublished - 1999

Keywords

  • Angiotensin
  • Autoimmunity
  • Chemokines
  • Lymphocyte
  • MHC class II
  • Monocyte
  • Proteinuria

ASJC Scopus subject areas

  • Physiology
  • Nephrology
  • Cardiology and Cardiovascular Medicine

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