NDT Advance Access originally published online on October 13, 2005
Nephrology Dialysis Transplantation 2005 20(12):2594-2597; doi:10.1093/ndt/gfi201
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Editorial Comment
Synergy of low nephron number and obesity: a new focus on hyperfiltration nephropathy
Servicio de Nefrología, Hospital 12 de Octubre, Madrid, Spain
Correspondence and offprint requests to: Manuel Praga, Servicio de Nefrología, Hospital 12 de Octubre, Carretera de Andalucía, Km 5,400, 28041 Madrid, Spain. Email: mpragat@senefro.org
Keywords: hyperfiltration nephropathy; obesity-related renal disease; remnant kidney; unilateral renal agenesis; unilateral nephrectomy; nephron number
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Introduction |
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The ‘hyperfiltration theory’, originally postulated by Brenner's group more than 20 years ago, represented a revolutionary advance in defining the mechanisms responsible for the seemingly inexorable progression of renal insufficiency [1]. Brenner's group and others demonstrated that rats submitted to renal ablation (more than five-sixths nephrectomy) developed proteinuria, glomerulosclerosis and progressive renal failure during the months following nephrectomy. They found that the functional and structural changes appearing in the remnant glomeruli correlated with the haemodynamic adaptations observed closely after renal ablation: increments in single nephron glomerular filtration rate (GFR) mediated by preferential vasodilation of afferent glomerular arterioles, together with increments in glomerular transcapillary hydraulic pressure and filtration fraction [1–3]. Attenuation of these haemodynamicadaptations by low protein diets or ACE inhibitors (that induce preferential vasodilation of efferent glomerular arteriole) largely prevents the appearance of glomerulosclerosis and renal failure. Brenner and collaborators postulated that ‘maladaptive’ haemodynamic changes in
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