Diseases are frequently caused by disorders of basic cell biological mechanisms that govern the functions of individual tissues and organs [1]. Detailed knowledge of the molecular pathogenesis is a prerequisite for the design of specific therapies, and recent progress in this field was encouraging. Examples are malfunctions caused by genetic defects, such as in storage diseases in which the lysosomal segment of the endocytic pathways lacks the correct digestive enzymes [2]. Another cause is the corruption of specific cellular mechanisms by parasites, such as viruses which use niches in housekeeping mechanisms to enter the host cells, to multiply, and to leave the infected cells again [3]. Yet another possibility is the blockade of basic cellular mechanisms by autoantibodies and subsequent functional and physical damage of the target system, such as antibodies to the acetylcholine receptor in myasthenia gravis [4], or to the myelin basic protein in allergic encephalitis and multiple sclerosis [5].

It recently has become evident that the glomerular cells, including the podocytes, also contribute to the initiation and propagation of glomerular damage. Although most of the pathological conditions of podocytes are mere phenomenology because the underlying cell biological mechanisms are not or only rudimentarily known at present, I will attempt to outline a few examples of how some basic cell biological functions of podocytes can turn into focal points of glomerular diseases. The examples chosen are: (i) the glycocalyx, with particular reference to the correct synthesis of negatively charged anionic molecules; (ii) the cell adhesion to the glomerular basement membrane; (iii) the cellular organelles and compartments which mediate endocytosis; and (iv) the de novo synthesis of proteins and other compounds under stress situations.