Circulating levels of ICAM-1, VCAM-1, and MCP-1 are increased in haemodialysis patients: association with inflammation, dyslipidaemia, and vascular events.

Background: Increased levels of circulating adhesion molecules and chemokines have been reported in haemodialysis (HD) patients but the influence of the HD membranes on their secretion, as well as their pathophysiological implications, remains largely unknown.

Methods: Circulating levels of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1) were measured by immunosorbent assay (ELISA) in 81 HD patients (45 male, mean age 57+/-13 years) and 35 normal subjects. All patients had been stabilized on renal replacement therapy for >3 months and were free of active infection.

Acute nephrotoxic serum nephritis in complement knockout mice: relative roles of the classical and alternate pathways in neutrophil recruitment and proteinuria.

Background: The importance of complement in the pathophysiology of renal disease is still being appreciated. To further address the role of this mediator system, we evaluated the influence of absolute deficiency of C3 and C4 on acute nephrotoxic serum nephritis (NSN).

Methods: Selective 'knockout' of C3 and C4 was routinely confirmed in null mice by ELISA.

Circulating vascular cell adhesion molecule-1 in pre-eclampsia, gestational hypertension, and normal pregnancy: evidence of selective dysregulation of vascular cell adhesion molecule-1 homeostasis in pre-eclampsia.

Objective: Our purpose was to investigate circulating levels of vascular cell adhesion molecule-1 in the peripheral and uteroplacental circulations during normotensive and hypertensive pregnancies.

Study Design: This prospective observational study involved 2 patient groups. Group 1 consisted of 22 women with pre-eclampsia and 30 normotensive women followed up longitudinally through pregnancy and post partum.

Cytokines, growth factors, and other inflammatory mediators in glomerulonephritis.

Over the past decade, research has been centered on the identification of factors that mediate glomerular immune injury and the assessment of their roles in this disease process. The spectrum of mediators identified to date encompasses a diverse array of bioactive molecules such as phospholipids, including cytokines and growth factors, and lipid-derived mediators such as eicosanoids. Given the extensive number of potentially important mediators in glomerulonephritis (GN), I focus only on some of them, for which strong in vitro and in vivo data suggest a major role in the pathogenesis of immune-mediated renal injury.