Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
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Nephrol. Dial. Transplant. · Jan 2001
Comment Letter Case ReportsTranexamic-acid-induced acute renal cortical necrosis in a patient with haemophilia A.
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Nephrol. Dial. Transplant. · Jan 2001
ReviewContinuous renal replacement therapy in critically ill patients.
Acute renal failure is an evolving syndrome in which new pathogenetic mechanisms have recently been elucidated. The evolution of the field of haemodialysis has led to a parallel development in the therapeutic approach to patients suffering from this syndrome. In particular, acute renal failure is more frequently seen as part of a more complex syndrome, defined as multiple organ failure. ⋯ Classic indications, but also alternative non-renal indications, have been proposed for these techniques. The most advanced indication is the multiple organ dysfunction occurring in septic patients. The possible removal of proinflammatory mediators may permit a blockade of the systemic inflammation, a modulation of the altered immune response in these patients, and it may lead to a partial or total restoration of the lost homeostasis.
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Nephrol. Dial. Transplant. · Jan 2001
ReviewEffects of nitric oxide synthase blockers on renal function.
Three isoforms of nitric oxide synthase (NOS) [neuronal NOS (bNOS), inducible NOS (iNOS) and endothelial NOS (eNOS)] are expressed in the kidney. The use of pharmacological inhibitors of these enzymes has been a major experimental tool to determine the role of nitric oxide (NO) in renal physiology and pathophysiology. Studies performed in both human and experimental animals demonstrate that NOS blockade increases renal vascular resistances and decreases the glomerular ultrafiltration coefficient. ⋯ Renal iNOS activity is significantly increased in various pathophysiological conditions including autoimmune tubulointerstitial nephritis and sepsis. Interestingly, recent evidence suggests that high NO levels secondary to increased iNOS activity may inhibit eNOS activity and through this mechanism lead to renal vasoconstriction and reductions in glomerular filtration rate. The use of NOS blockers has generated a great deal of information on the role of NO in the control of renal function and has also allowed us to begin to understand the high level of complexity of this system.