Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
-
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.
-
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.
-
Several therapeutic approaches have been tried in patients with membranous nephropathy. Corticosteroids have been largely used, but a meta-analysis of the available controlled trials did not show any benefit of corticosteroids either in favouring remission of the nephrotic syndrome or in preventing renal dysfunction. Controversial results have been obtained with cytotoxic agents. ⋯ A number of non-controlled studies and a randomized trial also showed the efficacy of cyclosporine in reducing proteinuria. In many but not all cases, proteinuria reappeared when cyclosporine was stopped. In conclusion, although the treatment of membranous nephropathy remains difficult, some therapeutical approaches have proved to favour remission and protect renal function
-
Leptospirosis is a re-emerging infectious disease, affecting both animals and humans worldwide. Multiple organ involvement may be encountered in leptospirosis, and early renal involvement is very common, characterized by tubulo-interstitial nephritis and tubular dysfunction. All 12 patients diagnosed in Chang Gung Memorial Hospital (Taiwan) between 1997 and 1999 had acute renal failure, with five patients requiring dialysis. ⋯ To understand the mechanism behind tubular injuries by leptospira infection, outer membrane proteins (OMPs) extracted from pathogenic leptospira were given to tubular cells in culture. Our in vitro experiment showed that OMPs of pathogenic leptospira activate nuclear NFkappaB binding and stimulate downstream inducible nitric oxide (iNOS), monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) expression. These results indicate that leptospiral infection may induce tubulo-interstitial nephritis through a toxic component in the outer membrane followed by expression of inflammatory genes.