Virtually all renal diseases progress to terminal renal failure relatively independently of the initial disease. Arresting the rate of the deterioration of kidney failure has a great impact on reducing the number of patients reaching the stage of expensive renal replacement therapy. Understanding the mechanisms of the progression of kidney disease has greatly been improved during recent years. The nature of the progressive renal damage with various etiologies includes various well-known factors where hemodynamics, renin-angiotensin system (RAS) and progressive proteinuria play the central roles. Proteinuria has to be shown as an independent risk factor for renal disease progression. Also, disturbances in lipid metabolism as well as the later structural lesions contribute to the progression. Various modalities have been used for the prevention of progressive renal disease, e.g. low-protein diet, antihypertensive therapy, antifibrotic therapy. Many recent experimental and clinical studies have shown that besides the systemic blood pressure lowering effect, RAS blocking agents provide renal protective effects via direct, hemodynamic, and indirect, non-hemodynamic, pathways: (1) lowering intraglomerular capillary hydraulic pressure, and increasing the glomerular ultrafiltration coefficient; (2) lowering proteinuria; (3) lowering hyperlipidemia; (4) diminishing kidney growth; (5) diminishing infiltration of macrophages; (6) downregulation of proinflammatory cytokines. Therefore, RAS blocking agents are widely prescribed not only for antihypertensive but also for renoprotective purposes in diabetic and non-diabetic nephropathies.