The barrier function of glomerular capillaries in vivo, which prevents the leakage of plasma proteins and cellular elements, depends not only on the basic morphological and physico-chemical fine structure of the glomerular capillary wall, but also on a functional barrier maintained by components obtained from blood. Together, both restrict the leakage of plasma proteins and cells in vivo. Two types of morphological defects are claimed to represent the normal condition: a larger type of leak, which enables the passage of red cells through the glomerular capillary wall one after the other without interruption by a plasma pulse and which must be present more frequently in thin basement membrane disease. This type of leak is sealed by penetrating cells and uncovered for protein filtration in the isolated (cell-free) perfused rat kidney. A smaller type of leak cannot be sealed by red cells, but also contributes to the enhanced protein permeability in perfusion with a monocomponent albumin solution. This type of leak is uncovered in vivo by angiotensin or catecholamines and is the basic route responsible for the unselective "functional proteinuria" of different types. Mechanisms which induce lesions under pathological conditions may also be active under everyday conditions, although to a smaller extent.