N-acetylcysteine ameliorates acute kidney injury but not glomerular hemorrhage in an animal model of warfarin-related nephropathy

摘要

The most conspicuous feature of WRN is the presence of numerous renal tubules obstructed by RBC casts. On this basis, it has been assumed that the tubular obstruction was the principle mechanism of the AKI in WRN. It was recognized, however, that in both patients and animals with WRN and severe reductions in glomerular nitration rate (GFR), only a small percentage of the tubular cross sections in any given slide showed complete obstruction by RBC casts (7, 31). To explain the discrepancy between the degree of tubular obstruction and the degree of GFR decrease, it was assumed that the degree of tubular obstruction shown in any given slide represented only the "tip of the iceberg" of obstructed tubules. On the other hand, the discrepancy between the degree of tubular obstruction and the degree of GFR decrease also raised the possibility that mechanisms, in addition to tubular obstruction, could be involved in the AKI of WRN. For example, warfarin coagu-lopathy could influence glomerular hemodynamics or the hydraulic conductivity of glomerular nitration barrier (7). Alternatively, the AKI or WRN could be the result of a problem more widespread than complete tubular obstruction by RBC. For example, the AKI could be the result of oxidant damage to tubules by RBC, even though the RBC do not obstruct the tubule.