The immuno-inflammatory process related to the deposition of immune complexes in the glomeruli with damage of podocytes (podocytopathy) is considered to be the main cause of proteinuria in patients with chronic glomerulonephritis. Proteinuria can also result from the accumulation of VEGF and hyposialylized ANGPTL4 in the podocytes. The tacrolimus in non-immunosupressive doses affects VEGF while N-acetyl-D-mannosamine (ManNAc) increases sialylization ANGPTL4. Both substances reduce proteinuria in the experiments and in patients. Klotho, antagonist glucocorticoid receptors mifepreston and inhibitors of monocyte chemoattractant protein-1 (MCP-1) also provide anti-proteinuric effect. This article reviews the mechanisms of action of these antiproteinuric factors.
Chronic glomerulonephritis, podocytopathy, proteinuria, angiopoietins.