Acid/Base Metabolism in Chronic Kidney Disease

Abstract Chronic kidney disease (CKD) frequently causes metabolic acidosis. By stage 4 CKD approximately 40% of patients have metabolic acidosis. This is usually a hyperchloremic acidosis with a near-normal anion gap and normal S[K]. When the glomerular filtration rate (GFR) is less than 20 mL/min, a classic high anion gap metabolic acidosis ensues. Although a variety of defects in acid–base regulation have been reported, the predominant defect causing acidosis is an inadequate increase in ammonium excretion in the urine. A variety of complications are caused by this acidosis in conjunction with the other consequences of CKD: loss of muscle mass, loss of bone mineral, insulin resistance, and faster loss of GFR. Increased mortality is associated with the acidosis as well. Treatment of the acidosis may be with sodium bicarbonate, citrate, or diets high in fruits and vegetables. A few single-center trials have suggested that treatment of acidosis improves the progression of chronic kidney disease (CKD) and improves muscle function. Similar treatments have been evaluated in a few studies in patients with normal systemic pH and serum bicarbonate concentration. The rationale for such studies is based on some evidence of retained acid in selected patients with CKD.