Key result
Oral sodium bicarbonate supplementation in chronic kidney disease patients decreased electronegative LDL plasma levels from 4.5 to 2.1 U/L (P<0.007).
Why the study?
Does oral sodium bicarbonate supplementation reduce electronegative LDL levels in patients with chronic kidney disease?
Does oral sodium bicarbonate supplementation reduce electronegative LDL levels in patients with chronic kidney disease?
Absolute Event Rate: 2.1% vs 4.5%
p-value: p=< 0.007
Oral sodium bicarbonate supplementation in CKD patients stabilizes renal function and decreases proatherogenic electronegative LDL levels when serum bicarbonate approaches 22 mM.
Hypothesis-generating for bicarbonate in CKD to lower atherogenic LDL; randomized trials needed before clinical consideration.
Background: Chronic kidney disease (CKD) patients develop metabolic acidosis when approaching stages 3 and 4, a period in which accelerated atherogenesis may ensue. Studies in vitro show that low pH may increase low-density lipoprotein (LDL) oxidation, suggesting a role for chronic metabolic acidosis in atherosclerosis. The present study attempted to evaluate the effects of conservative care using oral sodium bicarbonate (NaHCO₃) supplementation on the electronegative LDL [LDL(-)], a minimally oxidized LDL, plasma levels in CKD patients. Methods: Thirty-one CKD patients were followed by a multidisciplinary team during 15 months of care in which 1.0 mmol/kg/day oral NaHCO₃ supplementation was first given in the third month. Blood samples were collected 3 months before the initiation of oral NaHCO₃ supplementation (T1), at the time of the beginning of supplementation (T2), and thereafter, each 4 months (T3, T4 and T5) until month 15 of care. Blood parameters and LDL(-) were measured from these collections. Results: After 12 months of conservative care, creatinine clearance (MDRD) was kept stable, and serum bicarbonate (HCO₃⁻) increased from 20.5 ± 2.9 to 22.6 ± 1.1 m<smlcap>M</smlcap> (p < 0.003). LDL(-) plasma levels declined from 4.5 ± 3.3 to 2.1 ± 0.9 U/L (p < 0.007) after reaching mean serum HCO₃⁻ levels of 22.6 ± 1.1 m<smlcap>M</smlcap>. Conclusions: Conservative care using oral NaHCO₃ supplementation was able to stabilize renal function and decrease serum levels of LDL(-), a modified proatherogenic lipoprotein, only when mean serum HCO₃⁻ levels approached 22 m<smlcap>M</smlcap>. This study constitutes evidence that alkali therapy, in addition to its beneficial effect on renal disease progression, might serve as a preventive strategy to attenuate atherogenesis in CKD patients.
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Rizzetto et al. (2017) studied Chronic kidney disease (CKD) (n=31). Oral sodium bicarbonate (NaHCO3) supplementation vs. Baseline (pre-supplementation) was evaluated on Electronegative LDL [LDL(-)] plasma levels (U/L) (p=< 0.007). Oral sodium bicarbonate supplementation in chronic kidney disease patients decreased electronegative LDL plasma levels from 4.5 to 2.1 U/L (P<0.007).
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