120 nondiabetic patients with eGFR between 60 and 90 mL/min, and macroalbuminuria (Ualb 200-2000 mg/d) were randomized to receive tablets containing 0.5 mg/kg Na bicarbonate, NaCl, or sucrose (placebo). Over the course of five years, eGFR (measured via creatinine and cystatin methods) and urinary albumin were followed.
The NaHCO3 group showed a statistically significant decrease in the rate of eGFR decline, as well as progression of albuminuria, compared to the two control groups. Interestingly, these results were observed in the absence of a significant difference in serum bicarbonate levels. The authors postulate that perhaps bicarbonate supplementation lessens the degree of tubulointerstitial injury by decreasing urinary endothelin-1 production. Excretion of endothelin-1 and N-acetyl-beta-D-glucosaminidase (NAG), a marker of tubular injury, were decreased in the bicarbonate group, lending support to this hypothesis.
The study does have some limitations, notably the restriction of study eligibility to only patients with presumptive hypertensive nephropathy. None underwent kidney biopsy before or after the study. The mechanism of renal injury in these patients may be markedly different from other forms of renal disease; and the diagnosis category of hypertensive nephropathy itself may include several different mechanisms of disease. The study population was made up of >60% African Americans, and 25% Hispanics, so it may not be applicable to patients of other races. Also, the issue of increased salt intake was not addressed (interestingly, urinary Na excretion did not increase in the NaCl and NaHCO3 groups). Still: the data are compelling, and the treatment is easy and cheap. When taken together with the results from de Brito-Ashurst et al’s finding last year showing slowing of CKD stage IV progression with bicarbonate supplementation, it is becoming easy to argue that maybe all of our patients ought to take a spoonful (or two, or three) of baking soda with their daily meds.