[Pathophysiology of renal ischemia].
Renal ischaemia results, early in its course, in cell swelling of those tubule segments which are specifically susceptible to damage. These segments are the straight proximal tubules in the outer stripe of the outer medulla and the medullary thick ascending limb of the loop of Henlé in the outer and inner stripe of the outer medulla. One causal predisposing factor for both nephron segments is the sharp decline in the partial pressure of oxygen in the outer medulla. Another important cause for the vulnerability of the thick ascending limb is its strict dependence on a continuous supply of metabolic substrates. The cell swelling caused by ischaemia can be explained, for all nephron segments, as an unchanged uptake of Na+ across the luminal membrane in the face of a reduced pump rate of the basolateral (Na+ + K+)-ATPase. The swelling can be prevented if, for example, in the thick ascending limb the Na+ uptake is inhibited by furosemide. In addition to cell damage by cell swelling, other pathomechanisms are operative in ischaemia. One such mechanism is the damage caused by oxygen radicals. The concentration of these radicals is increased during ischaemia, especially during the initiation of reperfusion. Additionally, the concentration of radical scavengers such as glutathion, is reduced during ischaemia. Future work is needed to define more closely the damage produced by oxygen radicals in terms of lipid peroxidation, ATP and enzyme degradation.
Greger
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Lehrstuhl II Physiologie, Albert-Ludwigs-Universität, Freiburg.
D000818:Animals; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply*; D007684:Kidney Tubules / Q000098:blood supply; D010101:Oxygen Consumption; D014882:Water-Electrolyte Balance
Pathophysiologie der renalen Ischämie.