During human kidney development, the cells of the proximal part of the nephron gradually differentiate into podocytes and parietal epithelial cells (PECs). Podocytes are terminally differentiated cells that play a key role in normal kidney function, and are damaged in glomerulopathies. The possibility of their regeneration or replacement with a cell population like PECs would be crucial in the treatment of glomerular diseases, especially podocytopathies such as focal segmental glomerulosclerosis (FSGS). In this paper, we investigated the development of podocytes and PECs in the fetal kidney, postnatally in the healthy kidney and in patients with congenital nephrotic syndrome of the Finnish type (CNF) and idiopathic FSGS by analyzing markers of cell proliferation and epithelial-mesenchymal transition (EMT) and markers typical for immature and mature podocytes. Our sample contains tissue from 20 developing human kidneys, postnatal kidneys and kidneys from patients with CNF and FSGS. Immunofluorescence staining for the proliferation marker (Ki-67) and EMT markers (WNT4, NOTCH2, JAGGED1, and SNAIL) and podocyte markers (nestin, synaptopodin, nephrin) was performed to prove the composition of the cytoplasmic extensions bridging the urinary space. The ultrastructure of bridging cytoplasmic appendages was analyzed on samples prepared for electron microscopy. In the developing kidney, PECs have a higher proliferation rate than podocytes. Nestin is expressed only in podocytes. In the early fetal period, all markers of EMT are expressed. In the later fetal period, the expression of WNT4, NOTCH2 and JAGGED1 was moderately increased in podocytes, and significantly increased in PECs, and the expression of SNAIL was also increased in PECs. This expression is no longer found in the postnatal kidney. The expression of WNT4 was decreased in podocytes and PECs in patients with CNF and patients with FSGS, the expression of NOTCH2 was decreased in patients with FSGS and the expression of JAGGED1 in patients with CNF. The expression of SNAIL was increased in podocytes and PECs in both groups of patients, the expression of NOTCH2 was increased in patients with CNF, and the expression of JAGGED1 in patients with FSGS. Immunofluorescence and electron microscopy showed cellular processes bridging the urinary space between podocytes and PECs in fetal and postnatal kidneys. These cellular bridges express podocyte markers. Patients with CNF and patients with FSGS have numerous bridging cellular processes and all analyzed proteins are expressed in them. Mechanisms of gene expression control during nephrogenesis are reactivated in pathological conditions, so their further investigation could point to the mechanism of podocyte regeneration induction from PECs.