Robert Deicher1, Walter H Hörl. 1. Department of Medicine III, Division of Nephrology and Dialysis, University Hospital of Vienna, Austria.
Abstract
PURPOSE OF REVIEW: About a dozen controlled clinical trials examined the effect of anaemia correction on the progression of chronic kidney disease. None of these studies fulfilled the stringent criteria of a randomized controlled trial as suggested by the CONSORT statement, yet evidence emerged that anaemia sustains mitogenic and fibrogenic stimuli by lowering local partial oxygen tension. This review addresses the question of why and how anaemia could possibly enhance the progression of chronic kidney disease, and summarizes relevant clinical trials. RECENT FINDINGS: The discovery of hypoxia-inducible factor, a transcription factor stabilized under hypoxic conditions, with DNA-binding properties towards about 50 target genes including erythropoietin, has largely encouraged the hypothesis that tissue hypoxia may serve as another common mechanism for the progression of chronic kidney disease besides hypertension or proteinuria. In addition, anaemia-mediated alterations of renal sympathetic nerve activity and anaemia-related increments of oxidative stress may contribute to a progressive nephron loss. Conclusive evidence from clinical trials is scarce. SUMMARY: Pathophysiological concepts suggest some impact of anaemia on the progression of chronic kidney disease. The urge for more sound clinical intervention trials is met by the ongoing ECAP study (Effect of early Correction of Anaemia on the Progression of chronic kidney disease).
PURPOSE OF REVIEW: About a dozen controlled clinical trials examined the effect of anaemia correction on the progression of chronic kidney disease. None of these studies fulfilled the stringent criteria of a randomized controlled trial as suggested by the CONSORT statement, yet evidence emerged that anaemia sustains mitogenic and fibrogenic stimuli by lowering local partial oxygen tension. This review addresses the question of why and how anaemia could possibly enhance the progression of chronic kidney disease, and summarizes relevant clinical trials. RECENT FINDINGS: The discovery of hypoxia-inducible factor, a transcription factor stabilized under hypoxic conditions, with DNA-binding properties towards about 50 target genes including erythropoietin, has largely encouraged the hypothesis that tissue hypoxia may serve as another common mechanism for the progression of chronic kidney disease besides hypertension or proteinuria. In addition, anaemia-mediated alterations of renal sympathetic nerve activity and anaemia-related increments of oxidative stress may contribute to a progressive nephron loss. Conclusive evidence from clinical trials is scarce. SUMMARY: Pathophysiological concepts suggest some impact of anaemia on the progression of chronic kidney disease. The urge for more sound clinical intervention trials is met by the ongoing ECAP study (Effect of early Correction of Anaemia on the Progression of chronic kidney disease).
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