Podocytopathies

Abstract

Podocytopathies include a wide spectrum of primary or secondary glomerular diseases that are the consequence of the podocyte injuries. The damage of podocytes can occur due to congenital or acquired disorders of podocyte transcriptional regulators, altered components of the slit diaphragm complex, abnormal assembly, or function of the actin-based cytoskeleton, dysfunction of membranes or cytoplasmic proteins, and mitochondrial injury. Podocytes reactions to injurious stimulus include FP effacement, apoptosis, and loss of podocyte, developmental arrest associated by mild proliferative activity, and dedifferentiation with moderated proliferation. Based on histopathological findings, podocytopathy may be diagnosed such as minimal change nephropathy; focal segmental glomerulosclerosis, diffuse mesangial sclerosis, or collapsing glomerulopathy while in relation to their etiology can be categorized as idiopathic, genetic, and reactive. Podocytopathies may be diagnosed due to podocyte morphological changes, immunohistochemistry, circulating and urine biomarkers, and genetic analysis. The primary clinical focus in prevention should be to reduce the factors that can damage the podocytes and cause hyperperfusion/hypertrophy of the glomerulus. Nowadays, control of systemic and intra glomerular hypertension by pharmacological blockade of angiotensin II is a central in the prevention strategy, while regeneration of podocytes by stem cells is therapeutic strategy of the future.