The morphological consequences of acute or chronic renal ischemia may consist of an anemic kidney infarction, bilateral cortical necrosis, acute tubular lesions in circulatory renal failure, so-called subinfarction, as well as arteriosclerotic endstage kidney. In renal biopsies obtained from patients with acute renal failure, renal dysfunction can be morphologically explained by acute intra- and extracapillary necrotizing glomerulonephritis in 50% of cases, and by solely acute tubular lesions in 30% of cases. It is suggested that the development of acute tubular lesions during circulatory insufficiency might be favoured by an angiotensin II-dependent vas efferens constriction, leading to a reduction of peritubular blood flow in the presence of preserved glomerular filtration. The balance between demand and supply of oxygen within the tubular epithelial cells might thereby be critically disturbed.