[Physiopathology of acute renal insufficiency]

Various physiopathological mechanisms are involved in acute renal failure (ARF). Renal cortical ischemia is frequent but is not a constant finding. The fall in glomerular filtration rate is related to the decrease in glomerular capillary pressure, the increase in tubular pressure, and/or the decrease in ultrafiltration coefficient. Emphasis is placed on the role of tubular obstruction (in some toxic and in postischemic ARF), and of imbalance between pre- and postglomerular vascular resistance (as in captopril or enalapril-induced ARF in patients with artery stenosis of a solitary kidney). Recently attention has been focused on cellular events in ARF. In aminoglycoside-induced ARF, phospholipids accumulate in tubular cell lysosomes. In post-ischemic ARF, cell depletion in adenine nucleotides (ATP, ADP) and increase in Ca++ play a role. Administration of calcium antagonists improves experimental post-ischemic ARF. In conclusion, there is no single physiopathological mechanism of ARF. It should be borne in mind that the mechanisms triggering ARF may be different from those perpetuating it, and may necessitate different preventive and therapeutic measures.