The most important component of the filtration apparatus of the renal glomeruli is specialized visceral epithelial cells podocytes. The normal physiological function of podocytes is critically dependent on the proper regulation of the intracellular Ca2+ content; excessive Ca2+ influx in cells can lead to a disorder of cell morphology, podocytopathy, apoptosis and subsequent glomeruli damage. Podocytopathy is one of the primary characteristics of proteinuria and focal segmental glomerulosclerosis. One of the key proteins responsible for Ca2+ influx in podocytes is the TRPC6 channel. Since the first discovery of a mutation in a gene encoding TRPC6, the attention of the scientific community has been focused on studying the role of this ion channel in the onset and development of kidney diseases. Both an increase and a decrease in the functional activity of TRPC6 are associated with the manifestation of severe nephrotic syndromes leading to the end-stage of chronic kidney disease. The review contains materials related to the regulation of TRPC6 activity and the role of this channel in the pathogenesis of glomerular diseases.