Dietary Acid Load: A Novel Nutritional Target in Chronic Kidney Disease?

Abstract

Nonvolatile acid is produced from the metabolism of organic sulfur in dietary protein, and the production of organic anions during the combustion of neutral foods. Organic anion salts that are found primarily in plant foods are directly absorbed in the gastrointestinal tract and yield bicarbonate. The difference between endogenously produced nonvolatile acid and absorbed alkali precursors yields the dietary acid load, technically known as the net endogenous acid production, and must be excreted by the kidney to maintain acid-base balance. Although typically around 1 mEq/kg/day, dietary acid load is lower with greater intake of fruits and vegetables. In the setting of chronic kidney disease, a high dietary acid load invokes adaptive mechanisms to increase acid excretion despite reduced nephron number, such as increased per nephron ammoniagenesis and augmented distal acid excretion mediated by the renin-angiotensin system and endothelin-1. These adaptations may promote renal injury. Additionally, high dietary acid loads produce low-grade, subclinical acidosis that may result in bone and muscle loss. Early studies suggest that lowering the dietary acid load can improve subclinical acidosis, preserve bone and muscle, and slow decline of glomerular filtration rate in animal models and humans. Studies focusing on hard clinical outcomes are needed.

Red Meat Intake and Risk of ESRD

“…23 Conversely, plant-based proteins (e.g., soy and legumes) and fruits and vegetables have a high basal load. 24 Therapy with alkali has been shown to slow the progression to ESRD in randomized controlled trials. 25 Published data have shown that red meat generally yields greater acid production than other animalsourced protein, although the difference is not that dramatic.…”

A Low-Salt Diet Increases the Estimated Net Endogenous Acid Production in Nondiabetic Chronic Kidney Disease Patients Treated with Angiotensin Receptor Blockade

“…High NEAP levels may rapidly lead to kidney disease progression in CKD patients [1,4,5]. NEAP modulation may be a tool for alteration of the glomerular filtration rate decline.…”

“…We divided the patients into responders and nonresponders in both the intensive- and the conventional-education groups according to the same standard as above. The NEAP was estimated from the protein/potassium ratio in the diet [11,12] as follows: NEAP (mmol/day) = -10.2 + 54.5 [protein intake (g/day)/potassium intake (mmol/day)] [4,5,11,13]. The daily dietary protein intake was estimated based on the 24-hour urine urea nitrogen excretion using the Maroni equation [protein intake = 6.25 × (urine urea nitrogen + 0.031 × ideal body weight)] [14].…”

“…Recently, based on protein intake and the potassium excretion rate, the net endogenous acid production (NEAP) was reported to be a predictor of progressive kidney disease [1,4,5]. Regulation of the NEAP through diet education may be an additional strategy for reducing metabolic acidosis.…”

Dietary Patterns and CKD Progression

“…Potential renal acid load (PRAL) of selected food items (per 100 g serving) is adapted from estimates performed by Remer and Manz [18,19] . Reprinted, with permission [24] . …”