Glomerular ultrafiltration and apical tubular action of IGF-I, TGF-beta, and HGF in nepbrotic syndrome

In nephrotic glomerulopathies, there is ultrafiltration of high molecular w eight forms of insulin-like growth factor-I (IGF-I), hepatocyte growth fact or (HGF), and transforming growth factor-beta (TGF-beta), which are bioacti ve in tubular fluid and act through apical tubular receptors. Experimental evidence indicates that ultrafiltered IGF-I, HGF, and TGF-beta may contribu te to increased tubular phosphate and sodium absorption, synthesis of extra cellular matrix proteins, and secretion of chemokines such as monocyte chem oattractant protein-1 (MCP-1). Through these mechanisms, glomerular protein uria may contribute to tubulointerstitial pathobiology in nephrotic syndrom e.