Podocytopathies, Minimal Change Disease (MCD) and Focal Segmental Glomerulosclerosis (FSGS), represent the main causes of nephrotic syndrome worldwide [1]. However, its causes are still not well defined.

The immune system appears to play a significant role in the pathogenesis of these diseases, and specifically, the activation of the complement system has been recognized as a cause of injury [2] and also as a poor prognostic factor in FSGS [3]. Thus, reports demonstrate that complement system activation fragments are higher in the plasma and urine of patients with FSGS compared to controls, and this plasma increase is correlated with the severity of the disease [4].

Moreover, several glomerulopathies such as FSGS, MCD and diabetic nephropathy show an increase in IgM in renal biopsy. Therefore, it is believed that glomerular IgM and complement system activation may represent a common final pathway of glomerular injury, leading to disease exacerbation [5]. It was demonstrated in an experimental study with a FSGS model that IgM contributes to the disease's progression, binding to the damaged glomerulus, activating the complement system, and intensifying glomerular injury [6].

However, there are still few studies addressing the complement system in podocytopathies, especially in MCD. Therefore, the present study aims to better elucidate the mechanisms of injury in these diseases by investigating the deposition of immunoglobulins and complement system particles in renal biopsies of patients with podocytopathies, relating them to the laboratory data of these patients.