No abstract

Background:In the critically ill, ischemia secondary to decreased renal blood flow (RBF) is believed to be central to the pathogenesis of acute renal failure (ARF); however, the scientific basis for this conclusion has not been systematically evaluated. Methods: Systematic interrogation of the Pubmed database, and screening bibliographies of retrieved reports, for studies of human ARF where RBF was measured. Results: Thirty-two articles published between 1944 and 2008 describing RBF in 373 patients with ARF were identified. Overall, mean RBF during ARF was 387 ml/min. It was 329 ml/min when estimated by clearance-based techniques (15 studies) and 471 ml/min when measured with nonclearance-based techniques (17 studies). Only 46 patients had measurements in the intensive care unit where mean RBF was 306 ml/min. Normal RBF was reported in 14 publications, mean 1,192 ml/min. Conclusions: Limited information is available on RBF during ARF in the critically ill. Measurements in contemporary patients are required to further our understanding of this condition.

In hyperdynamic sepsis, intrarenal infusion of a highly selective inducible nitric oxide synthase inhibitor did not reduce the elevated renal blood flow or improve renal function. In contrast, renal blood flow was reduced by infusion of a nonselective NOS inhibitor or a high dose of a partially selective inducible nitric oxide synthase inhibitor. The renal vasodilatation in septic acute kidney injury may be due to nitric oxide derived from the endothelial and neural isoforms of nitric oxide synthase, but their blockade did not restore renal function.