Age and age-related decline in glomerular filtration rate independently increase blood hydrogen ion and decrease plasma bicarbonate concentration, worsening diet-dependent metabolic acidosis.
Cross-Sectional (n=64)
Healthy adults manifest a low-grade diet-dependent metabolic acidosis, the severity of which increases with age due in part to normal age-related decline of renal function.
In 64 apparently healthy adult humans (ages 17-74 yr) ingesting controlled diets, we investigated the separate and combined effects of age, glomerular filtration rate (GFR, index of age-related renal functional decline), renal net acid excretion NAE, index of endogenous acid production (EAP), and blood PCO2 (PbCO2, index of respiratory set point) on steady-state blood hydrogen ion (H+b) and plasma bicarbonate concentration (HCO3-p). Independent predictors of H+b and HCO3-p were PbCO2, NAE, and either age or GFR, but not both, because the two were highly correlated (inversely). H+b increased with increasing PbCO2, NAE, and age and with decreasing GFR. HCO3-p decreased with increasing NAE and age but increased with increasing PbCO2 and GFR. Age (or GFR) at constant NAE had greater effect on both H+b and HCO3-p than did NAE at constant age (or GFR). Neither PbCO2 nor NAE correlated with age or GFR. Thus two metabolic factors, diet-dependent EAP and age (or GFR), operate independently to determine blood acid-base composition in adult humans. Otherwise healthy adults manifest a low-grade diet-dependent metabolic acidosis, the severity of which increases with age at constant EAP, apparently due in part to the normal age-related decline of renal function.
Frassetto et al. (Sun,) conducted a cross-sectional in Healthy (n=64). Age and glomerular filtration rate (GFR) was evaluated on Steady-state blood hydrogen ion ([H+]b) and plasma bicarbonate concentration ([HCO3-]p). Age and age-related decline in glomerular filtration rate independently increase blood hydrogen ion and decrease plasma bicarbonate concentration, worsening diet-dependent metabolic acidosis.