Growing evidence for treating metabolic acidosis to slow CKD progression

There are two published trials in the last few months that showed the benefit of treating metabolic acidosis in slowing progression of CKD. In a trial of 134 patients with stage IV CKD and serum bicarbonate of 16-20(de Brito-Ashurst et al JASN 2009), patients were randomly assigned to standard care plus oral sodium bicarbonate or standard care only for 2 years. Compared with the control group, decline in GFR was slower with bicarbonate supplementation (5.93 vs. 1.88 ml/min, P < 0.0001). Fewer patients supplemented with bicarbonate developed ESRD (6.5 versus 33%, P < 0.001). Also, nutritional parameters improved significantly with bicarbonate supplementation. In another study that is just published (Phisitkul et al, KI 2010), out of 59 patients with hypertensive CKD and metabolic acidosis on standard care including ACEi, 30 patients were prescribed sodium citrate and the remaining 29, unable or unwilling to take sodium citrate, served as controls. All were followed for 2 years. Urine endothelin-1 excretion, a surrogate of kidney endothelin production, and N-acetyl-beta-D-glucosaminidase, a marker of kidney tubulointerstitial injury, were each significantly lower, while the rate of estimated glomerular filtration rate decline was significantly slower in the treatment group. Although patient groups are similar, the major limitation is that it is not a randomized study. Thus, alkali supplementation seems to be an inexpensive addition to the limited arsenal we have to retard CKD progression. Please see the graphic at the top from editors of KI showing the likely pathway of acidosis exacerbating renal injury.