In chronic renal insufficiency resulting from destruction of the vast majority of nephrons, the surviving nephrons adapt their functions to the conditions of vigorous haemodynamic and osmolar overloads. They acquire an appropriate behaviour to preserve the principal renal functions and to achieve the balance of inner space. In the long period of time, similarly as in healthy people. Glomerulotubular balance as well as tubuloglomerular balance distinguish the remaining nephron function, while autoregulation of perfusion pressure along the glomerulus rapidly vanishes. All three regulation mechanisms are characteristic of the nephron function under physiologic conditions. Intense work of the remaining nephrons in chronic renal failure is under the high level controls of the group of hormones, among them are rennin-angiotensin system, arginine-vasopressin and atrial natriuretic peptide playing very important and particular roles. Comparison of different published studies emerge the idea that chronically increased arginine-vasopressin levels in chronic renal failure could block the autoregulation of blood flow and hydraulic pressure in glomeruli, which together with other mediator actions give high and fluctuating tense within remaining glomeruli, during every single cardiac cycle. It is probably the main event in the further course of kidney disease progression resulting in definite damage of the overloaded nephrons. Angiotensin II is one of reliably recognised mediators of unfavourable outcome in the process of nephron adaptation in chronic renal failure. Knowing the pathophysiologic processes in the remaining functionally adapted nephrons in chronic renal insufficiency determines a more adequate therapeutic approach in these patients.