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Podocyturia: Potential applications and current limitations
1Nephrology Service, Hospital Británico de Buenos Aires, Buenos Aires 1280AEB, Argentina. cenefrologia@hbritanico.com.ar.
Insights
Podocyte loss causes chronic kidney disease progression and proteinuria. Identifying urinary podocytes (podocyturia) may enable earlier diagnosis and tailored therapies for kidney diseases.
Area of Science:
- Nephrology
- Pathology
- Cell Biology
Background:
- Chronic kidney disease (CKD) affects millions globally, increasing cardiovascular risks.
- Diabetes, hypertension, and glomerulopathies are primary CKD causes.
- Proteinuria and glomerulosclerosis are key indicators of kidney disease progression.
Purpose of the Study:
- To elucidate the central role of podocytes in CKD pathogenesis.
- To investigate the relationship between podocyte loss, proteinuria, and glomerulosclerosis.
- To explore the potential of urinary podocyte detection (podocyturia) for early CKD diagnosis and management.
Main Methods:
- Review of existing literature on podocyte biology and CKD.
- Analysis of the link between podocyte function, proteinuria, and glomerular histology.
- Discussion of podocyturia as a potential biomarker for glomerulopathies.
Main Results:
- Podocyte damage and loss are directly linked to proteinuria and glomerulosclerosis.
- Podocyte shortage is the primary driver of irreversible kidney damage.
- Podocyturia precedes proteinuria, indicating it as an earlier marker of kidney injury.
Conclusions:
- Podocyte integrity is crucial for maintaining glomerular filtration barrier function.
- Tissular podocyte deficiency is the cause of proteinuria and CKD progression.
- Urinary podocyte detection offers a promising avenue for early assessment and targeted treatment of glomerular diseases.
Abstract:
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.
