The pathophysiology of the hemolytic uremic syndrome

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43 Citations (Scopus)

Abstract

The hemolytic uremic syndrome is an important cause of acute renal failure and leads to substantial morbidity and mortality. In pediatric patients, the hemolytic uremic syndrome usually follows hemorrhagic colitis caused by verocytotoxin-producing Escherichia coli. Several well-publicized outbreaks of hemorrhagic colitis and hemolytic uremic syndrome have highlighted the morbidity and mortality of infection with verocytotoxin- producing Escherichia coli. Recent studies have further demonstrated the role of verocytotoxins in mediating renal cell injury and the mechanisms of verocytotoxin cell injury. Although the endothelial cell appears to be the major target of verocytotoxin-mediated cell injury, studies have also shown that mesangial cells, renal tubular epithelial cells, monocytes and cells derived from the monocytic cell line are also targets of verocytotoxin- mediated biological effects. It has also been shown that inflammatory cytokines are likely to play an important role in hemolytic uremic syndrome. Serum levels of IL-8 and TNF-α are elevated in hemolytic uremic syndrome and verocytotoxins promote the generation of inflammatory cytokines from monocytes and monocyte-derived cell lines. These new findings have important implications for current therapy and potential future therapy of hemolytic uremic syndrome.

Original languageEnglish
Pages (from-to)459-464
Number of pages6
JournalCurrent Opinion in Nephrology and Hypertension
Volume8
Issue number4
DOIs
StatePublished - 1999

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Hemolytic-Uremic Syndrome
Monocytes
Colitis
Wounds and Injuries
Cytokines
Escherichia coli
Morbidity
Cell Line
Mesangial Cells
Mortality
Interleukin-8
Acute Kidney Injury
Disease Outbreaks
Endothelial Cells
Epithelial Cells
Pediatrics
Kidney
Therapeutics
Infection
Serum

ASJC Scopus subject areas

  • Nephrology
  • Internal Medicine

Cite this

The pathophysiology of the hemolytic uremic syndrome. / Andreoli, Sharon.

In: Current Opinion in Nephrology and Hypertension, Vol. 8, No. 4, 1999, p. 459-464.

Research output: Contribution to journalArticle

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