Published online Sep 6, 2017. doi: 10.5527/wjn.v6.i5.221
Peer-review started: March 28, 2017
First decision: May 4, 2017
Revised: July 18, 2017
Accepted: July 21, 2017
Article in press: July 23, 2017
Published online: September 6, 2017
Processing time: 159 Days and 22.7 Hours
Chronic kidney disease is a prevalent condition that affects millions of people worldwide and is a major risk factor of cardiovascular morbidity and mortality. The main diseases that lead to chronic kidney disease are frequent entities as diabetes mellitus, hypertension and glomerulopathies. One of the clinical markers of kidney disease progression is proteinuria. Moreover, the histological hallmark of kidney disease is sclerosis, located both in the glomerular and in the interstitial compartments. Glomerulosclerosis underscores an irreversible lesion that is clinically accompanied by proteinuria. In this regard, proteinuria and glomerular sclerosis are linked by the cell that has been conserved phylogenetically not only to prevent the loss of proteins in the urine, but also to maintain the health of the glomerular filtration barrier: The podocyte. It can then be concluded that the link between proteinuria, kidney disease progression and chronic kidney disease is mainly related to the podocyte. What is this situation due to? The podocyte is unable to proliferate under normal conditions, and a complex molecular machinery exists to avoid its detachment and eventual loss. When the loss of podocytes in the urine, or podocyturia, is taking place and its glomerular absolute number decreased, glomerulosclerosis is the predominant histological feature in a kidney biopsy. Therefore, tissular podocyte shortage is the cause of proteinuria and chronic kidney disease. In this regard, podocyturia has been demonstrated to precede proteinuria, showing that the clinical management of proteinuria cannot be considered an early intervention. The identification of urinary podocytes could be an additional tool to be considered by nephrologists to assess the activity of glomerulopathies, for follow-up purposes and also to unravel the pathophysiology of podocyte detachment in order to tailor the therapy of glomerular diseases more appropriately.
Core tip: Podocytes are cells that do not proliferate under normal conditions. Their loss in the urine, a process known as podocyturia, antedates proteinuria. When the number of podocytes per glomerulus is less than 80%, glomerulosclerosis is triggered and if not stopped, it will eventually lead to chronic kidney failure and end-stage kidney disease. A prompt and standardized assessement of podocyturia should lead to better results related to glomerular disease outcomes.