How does early chronic kidney disease progress?: A Background Paper prepared for the UK Consensus Conference on Early Chronic Kidney Disease

作者：Wendy Metcalfe · 发表于：Nephrology Dialysis Transplantation · 年份：2007 · DOI：10.1093/ndt/gfm446 · 被引用次数：85 · 研究领域：Birth, Development, and Health、Chronic Kidney Disease and Diabetes、Diet and metabolism studies

Chronic Kidney Disease (CKD) may arise due to a multitude of different insults to renal function. However despite the wide range of pathological processes that may induce renal injury, substantial loss of nephrons provokes a common syndrome characterized clinically by systemic hypertension, proteinuria and a progressive decline in glomerular filtration rate (GFR) and patho-physiologically by progressive interstitial fibrosis, peritubular capillary loss with hypoxia and destruction of functioning nephrons because of tubular atrophy [ 1 ]. Extensive studies suggest that the rate of loss of GFR, that is the rate of progression of CKD, may be largely due to common secondary factors, often unrelated to the initial disease [ 2 ]. Some of these factors such as age and race are not open to intervention. The majority, however, provide at least a potential for intervention in order to slow or halt the progression of early CKD. In rat models, subtotal nephrectomy (remnant kidney model) leads to a compensatory hyperfiltration of the remaining nephrons initially maintaining overall GFR; however, over time glomerular hypertension, proteinuria and progressive CKD develop [ 3 ]. The loss of sufficient renal functional units (nephrons) from whatever insult, puts into place haemodynamic factors that perpetuate renal dysfunction. Indirect studies in humans strongly indicate a very similar response to those that are demonstrated in many animal models of progressive CKD, with increased intraglome...