Progression versus regression of chronic kidney disease.

Chronic kidney disease (CKD) is a major cause of morbidity and mortality worldwide, and is characterized by relentless progressive scarring of renal parenchyma that ultimately results in end-stage renal disease with the need for dialysis or transplantation. Scarring is, however, not an inherently irreversible process, as it may be modulated in, for example, skin, heart and large arteries. However, the kidney has unique challenges in remodelling of glomerulosclerosis, in that nephron development ends in late gestation, and generation of new glomeruli is not possible after term birth. The apparent inexorable progression characteristic of CKD is postulated to start with disease-specific initial scarring that then activates compensatory but ultimately maladaptive changes in the remaining nephrons. These compensatory changes include haemodynamic alterations and altered growth responses that promote further scarring and fuel this vicious circle [1]. It is of interest that this sclerotic process is not static, in that even glomeruli with advanced sclerosis have ongoing cell turnover. Thus, there is a potential for modulation of these processes.