This increased levels of ApoA-I in urine were attributed to the inclusion of patients with proximal tubulopathies (4.8%), renal dysplasia/CAKUT (8%), glomerulonephritis (8%), and patients in relapse of minimal change disease (MCD) (4.8%) and FSGS (1.3%). Here, APOA1 is linked to focal segmental glomerulosclerosis.