Abstract and Introduction
The neutralization of dietary acid with sodium bicarbonate decreases kidney injury and slows the decline of the glomerular filtration rate (GFR) in animals and patients with chronic kidney disease. The sodium intake, however, could be problematic in patients with reduced GFR. As alkali-induced dietary protein decreased kidney injury in animals, we compared the efficacy of alkali-inducing fruits and vegetables with oral sodium bicarbonate to diminish kidney injury in patients with hypertensive nephropathy at stage 1 or 2 estimated GFR. All patients were evaluated 30 days after no intervention; daily oral sodium bicarbonate; or fruits and vegetables in amounts calculated to reduce dietary acid by half. All patients had 6 months of antihypertensive control by angiotensin-converting enzyme inhibition before and during these studies, and otherwise ate ad lib. Indices of kidney injury were not changed in the stage 1 group. By contrast, each treatment of stage 2 patients decreased urinary albumin, N-acetyl β-D-glucosaminidase, and transforming growth factor β from the controls to a similar extent. Thus, a reduction in dietary acid decreased kidney injury in patients with moderately reduced eGFR due to hypertensive nephropathy and that with fruits and vegetables was comparable to sodium bicarbonate. Fruits and vegetables appear to be an effective kidney protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition in hypertensive and possibly other nephropathies.
Developing safe and effective kidney-protective interventions to slow or stop the progression of established nephropathy is an important strategy in reducing the incidence of complete kidney failure. Such interventions will likely have the greatest benefit in those with no or moderately reduced glomerular filtration rate (GFR) who comprise the largest cadre of subjects with chronic kidney disease (CKD). Hypertension-associated nephropathy is the second leading cause of complete kidney failure in the United States, and most of them with moderately reduced GFR have progressive GFR decline despite blood pressure (BP) reduction with renin–angiotensin system inhibition.[3,4] Because acid-inducing diets increased and strategies to reduce dietary acid with oral alkali- or base-inducing dietary protein decreased kidney injury in animals with normal GFR, and additionally slowed GFR decline in animals with moderately reduced GFR,[6,7] the largely acid-inducing diets of industrialized societies might mediate progressive GFR decline in those with moderately reduced GFR due to hypertensive nephropathy. Supporting this hypothesis, adding oral NaHCO3 to renin–angiotensin system inhibition ameliorated kidney injury and slowed estimated GFR (eGFR) decline in subjects with moderately reduced GFR due to hypertensive nephropathy without metabolic acidosis. Together, these data support the fact that dietary acid reduction is kidney protective in subjects with moderately reduced GFR due to hypertensive nephropathy.
Despite its apparent benefits, dietary acid reduction with NaHCO3 obligates added dietary Na+ that might worsen hypertension and/or volume control in subjects with reduced GFR. Other strategies to reduce dietary acid might be equally or more kidney protective while limiting added Na+. Industrialized society diets are acid-inducing largely because of a high ratio of acid-inducing to base-inducing proteins, the latter being mostly fruits and vegetables (F+V). Consequently, decreasing dietary acid by adding base-inducing F+V might decrease kidney injury as effectively as NaHCO3, but with less added Na+. We compared urine indices of kidney injury in subjects with CKD due to hypertensive nephropathy with normal or moderately reduced eGFR after 30 days of dietary acid reduction with F+V or oral NaHCO3 (HCO3) to compare the kidney-protective efficacy of F+V.
Kidney Int. 2012;81(1):86-93. © 2012 Nature Publishing Group