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Effect of metabolic acidosis on progression of chronic kidney disease.

METABOLIC ACIDOSIS, TRADITIONALLY defined as a reduction in serum HCO3 concentration ([HCO3 ]) often associated with a detectable reduction in blood pH, is a common accompaniment of progressive chronic kidney disease (CKD) (7). The metabolic acidosis even when mild is not without consequences: increased degradation of muscle protein with muscle wasting (1), reduced albumin synthesis with resultant hypoalbuminemia (2), production or exacerbation of bone disease along with stunting of growth in children (8, 9), and impairment in glucose tolerance (11), are among its major consequences. The mechanisms underlying these effects appear to be complex, involving several different pathways, although treatment of the metabolic acidosis with base usually lessens the severity of or completely reverses these abnormalities (8). Studies performed in animals and humans have confirmed that metabolic acidosis is also a risk factor for progression of CKD (3, 8, 12‐14). Administration of either citrate (5) or sodium bicarbonate (12) to rats with CKD decreased the severity of tubulointerstitial disease and/or the decline in glomerular filtration rate compared with controls receiving sodium chloride. Also, the chronic administration of base to Han.SPRD rats, an animal model of polycystic kidney disease, decreased the cystic enlargement and prevented development of interstitial inflammation, chronic fibrosis, and severe renal failure (18).