ABSTRACT
BACKGROUND The story of protein restriction in renal disease goes back to at least the work of Addis in 1948, and is summarized by Simini.1 Addis hypothesized that protein restriction would not only relieve the symptoms of uraemia, but would also prevent further damage by reducing the load on the remaining nephrons. Brenner et al2 took the story forward by documenting the rise in glomerular capillary pressure and hyperfiltration due to high dietary protein intake, and then Remuzzi and Bertani3 showed that increased protein traffic across the glomerulus could cause progression of renal disease. Attention then focused on the effect of antihypertensive therapies such as ACE inhibitors (for review, see Kasiske et al,4 or Chapter 7), both in hypertensive and non-hypertensive diabetic subjects. These so-called non-hypertensive subjects may not actually be normotensive, and the effect of these agents may be via lowering of blood pressure rather than an intrarenal mechanism.5 There was perhaps a loss of interest in low-protein diets (LPD), especially following the largest ever trial of protein restriction, the Modification of Diet in Renal Disease (MDRD) study,6 which reported that protein restriction did not appear to affect the decline in renal function. However, there were only 25 patients with type 2 diabetes in the MDRD (those with type 1 were excluded from the trial); glomerulonephritis and polycystic disease made up about half, and there was some evidence of variation in response according to the aetiology of the renal impairment. Furthermore, compliance with the LPD was shown to be possible, and when a secondary analysis was performed, taking into account compliance and not intention to treat, the results were more promising.7
