Glomerular ultrafiltration and apical tubular action of IGF-I, TGF-beta, and HGF in nephrotic syndrome.
In nephrotic glomerulopathies, there is ultrafiltration of high molecular weight forms of insulin-like growth factor-I (IGF-I), hepatocyte growth factor (HGF), and transforming growth factor-beta (TGF-beta), which are bioactive in tubular fluid and act through apical tubular receptors. Experimental evidence indicates that ultrafiltered IGF-I, HGF, and TGF-beta may contribute to increased tubular phosphate and sodium absorption, synthesis of extracellular matrix proteins, and secretion of chemokines such as monocyte chemoattractant protein-1 (MCP-1). Through these mechanisms, glomerular proteinuria may contribute to tubulointerstitial pathobiology in nephrotic syndrome.
Wang
S N
SN
Division of Nephrology and Hypertension, Harbor-UCLA Medical Center and UCLA, Torrance, California 90509, USA.
Lapage
J
J
Hirschberg
R
R
D000818:Animals; D017228:Hepatocyte Growth Factor / Q000378:metabolism*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000378:metabolism / Q000503:physiopathology*; D007684:Kidney Tubules / Q000378:metabolism*; D009404:Nephrotic Syndrome / Q000378:metabolism / Q000503:physiopathology*; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D014462:Ultrafiltration
D016212:Transforming Growth Factor beta; D017228:Hepatocyte Growth Factor; D007334:Insulin-Like Growth Factor I