Abstract
Metabolic acidosis (MA) in advanced CKD results from a progressive reduction in the capacity of the kidneys to generate sufficient ammonia to excrete the daily production of hydrogen ions (equivalent to approximately 1 mmol/kg body weight) leading to the formation of a new steady state at the cost of a reduction in blood pH. MA is a relatively common complication in patients with advanced CKD, particularly when GFR falls below 30 ml/min (1). MA adversely affects protein and muscle metabolism and bone turnover, compounding the mineral-bone disorder of uremia. In addition, MA is also associated with increased inflammatory mediators, insulin resistance, and corticosteroid and parathyroid hormone production. This may
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