Regeneration and proteinuria, when albumin makes the difference

Abstract

In chronic kidney disease (CKD) the risk of organ failure is correlated with the severity of proteinuria, which, in its turns, depends on the number of lost podocytes and on the consequent glomerular fibrosis. Nevertheless, several experimental and clinical evidences suggest the possibility of remission of kidney diseases, and in some cases even of regression of the damage, at least if the histology of the organ is not totally compromised. Particularly, these results can be achieved by employing antiproteinuric pharmacological modulators. New experimental evidences suggest why blocking the leakage of proteins in urine is able to allow the remission of CKD. In a recent paper, Peired et al documented for the first time how albuminuria can halt the regenerative process via the sequestration of retinoic acid (RA) by albumin itself. RA is, in fact, a well-know differentiative agent for stem cells’ and progenitor cells’ populations located in various organs. The consequent urinary loss of RA bound to albumin prevents the activation of renal progenitors resident along the Bowman’s capsule, blocking in its first phases the regenerative response, and thus allowing the progression of the CKD.