An equally important component of disease progression and lack of response to steroid therapy is tubulointerstitial fibrosis and tubular damage in FSGS, which are reflected by an increase in the level in the urine of lumican and cystatin C. These processes are also evidenced by an increase in vitamin D-binding protein and retinol-binding protein 4 in the urine of FSGS patients with impaired renal function [18,19,20,21,37]. Here, RBP4 is linked to focal segmental glomerulosclerosis.