Novel approaches to treatment of glomerulonephritis.
Our improved understanding of the mechanisms of glomerular injury has allowed the design of novel therapeutic strategies to treat glomerulonephritis. While elimination of the etiologic factors continues to be a difficult task, modulation of the inflammatory response seems more promising at present. Several proinflammatory mediators have been identified as therapeutic targets and their inhibition has ameliorated glomerular injury in experimental animals. The role of anti-inflammatory molecules and the phenomenon of immunotolerance have gained particular attention and may prove to be useful therapeutically. Mediators of tissue repair have been found to contribute to glomerular destruction, and their inhibition was protective in a variety of experiments. In this review we discuss some of these novel approaches which may be targeted against human glomerulonephritis in the near future.
Dept. of Internal Medicine, Baylor College of Medicine and Houston Veterans Affairs Medical Center, Texas, USA.
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Nassar
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Badr
D000818:Animals; D001093:Arachidonate 15-Lipoxygenase; D001094:Arachidonate 5-Lipoxygenase; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology / Q000628:therapy*; D006801:Humans; D006893:Hydroxyeicosatetraenoic Acids; D018836:Inflammation Mediators; D007375:Interleukin-1; D015289:Leukotrienes; D044045:Lipoxins; D008222:Lymphokines; D010982:Platelet-Derived Growth Factor; D013237:Stereoisomerism; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha
D006893:Hydroxyeicosatetraenoic Acids; D018836:Inflammation Mediators; D007375:Interleukin-1; D015289:Leukotrienes; D044045:Lipoxins; D008222:Lymphokines; D010982:Platelet-Derived Growth Factor; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; C040527:lipoxin A4; D001093:Arachidonate 15-Lipoxygenase; D001094:Arachidonate 5-Lipoxygenase