Polarity signaling through the aPKC-Par polarity complex is essential for the development and maintenance of the podocyte architecture and the function of the glomerular filtration barrier of the kidney. To study the contribution of Par3A in this complex we generated a novel Pard3 podocyte-specific knockout mouse model by targeting exon six of the Pard3 gene. Genetic deletion of Par3A did not impair renal function neither at birth nor later in life. Even challenging the animals did not result in glomerular disease. Despite its well-established role in aPKC-mediated signaling Par3A appears to be dispensable for the function of the glomerular filtration barrier. Moreover, its homolog Par3B and not Par3A, is the dominant Par3 gene expressed in podocytes and found at the basis of the slit diaphragm where it partially colocalizes with podocin. In conclusion, Par3A function is either dispensable for slit diaphragm integrity or compensatory mechanisms and a high redundancy of the different polarity proteins including Par3B, Lgl or PALS1 maintain the function of the glomerular filtration barrier even in the absence of Par3A.