IntroductionModern acid-producing diets in patients with stage G3-G5 chronic kidney disease (CKD) can cause severe acid accumulation with metabolic acidosis and less severe accumulation causing eubicarbonatemic acidosis in stages G2-G3, each with kidney injury. The impact of these diets on acid accumulation in those with CKD but normal eGFR (G1) is unclear. MethodsWe assessed whether acid accumulation occurs in patients with CKD and normal eGFR, and if added base-producing fruits and vegetables (F&V) or oral NaHCO3 (HCO3-) reduces acid accumulation and/or lowers kidney injury. We randomized 153 macroalbuminuric, non-diabetic, G1 (mean eGFR = 101 ml/min/1.73 m2) participants with hypertension-associated CKD to receive F&Vs in amounts to reduce dietary acid intake 50% (F&V, n=51), oral NaHCO3 to match alkali intake of F&V (HCO3-, n=51), or usual care (UC, n=51) for five years. We assessed acid accumulation by comparing observed to expected increase in plasma total CO2 in response to retained bicarbonate (dose minus urine bicarbonate excretion) two hours after an oral NaHCO3 bolus. ResultsBaseline acid accumulation, eGFR, urine excretion of albumin, N-acetyl-β-D-glucosamine, and angiotensinogen were not different among groups. Five-year acid accumulation [mean(SD)] was lower in F&V [-1.2 (11.0) mmoles] and HCO3- [-1.7 (10.8) mmoles] than UC [5.2 (10.3) mmoles, p<0.003)], consistent with lower acid accumulation in F&V and HCO3-. Five-year urine excretion of albumin, N-acetyl-β-D-glucosamine, and angiotensinogen were lower in F&V and HCO3- than UC, consistent with less kidney injury. ConclusionsDietary acid reduction reduces acid accumulation and kidney injury in patients with CKD and normal eGFR.
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