Is dietary Acid a modifiable risk factor for nephropathy progression?

[11] , endothelin [10] , and aldosterone [10] . Together, these studies suggest that patients with reduced GFR but no metabolic acidosis nevertheless have acid retention that might mediate nephropathy progression. Reducing acid retention with less acid-producing diets that lower net endogenous acid production (NEAP) might slow nephropathy progression in patients with reduced GFR even without metabolic acidosis. Diets of those living in industrialized societies are largely acid-producing due to high intake of acid-producing animal protein and comparatively low intake of baseproducing proteins from fruits and vegetables [12] . These acid-producing diets increase NEAP [13] and typically do so without inducing frank metabolic acidosis in individuals with relatively preserved GFR, but might induce frank metabolic acidosis in those with very low GFR [14] . Diets higher in base-producing protein like fruits and vegetables reduce NEAP [13, 14] and reduce kidney injury in subjects with reduced eGFR without metabolic acidosis [15] . In support of the importance of NEAP in nephropathy progression, high NEAP was associated with faster GFR decline in individuals with reduced GFR [16] , identical to the data of Kanda et al. [17] in this issue of AmerTreating metabolic acidosis in chronic kidney disease (CKD) as per current KDOQI guidelines appears to slow CKD progression [1, 2] and is an added reason to treat CKD-related metabolic acidosis when serum total [HCO 3 ] is <22 mEq/l [3] . This recommendation is based on ‘evidence and opinion’ [3] but cautioned that ‘more research is needed on the long-term effects of correcting acidemia on clinical outcomes...’ [3] . Since these recommendations were issued, epidemiologic studies have shown that CKD patients with ranges of plasma [HCO 3 ] that include those >22 mEq/l are associated with a greater risk for and a faster rate of glomerular filtration rate (GFR) decline [4–6] . In addition, NaHCO 3 slowed the rate of estimated GFR (eGFR) decline in individuals with reduced eGFR but without metabolic acidosis [7] . Animal [8, 9] and human [10] studies support that reduced GFR is associated with acid retention, even with normal plasma [HCO 3 ]. Furthermore, ameliorating this apparent acid retention in animals with reduced GFR but normal plasma [HCO 3 ] by adding dietary alkali or by eating diets that are base-producing rather than acid-producing slows GFR decline [8, 9] . Proposed mediators of acid-induced nephropathy progression include compliment activation Published online: February 7, 2014 Nephrology American Journal of