The Role of Bicarbonate in CKD: Evidence Bulks Up

[摘要] The metabolic acidosis that commonly accompanies CKD may be the result of several processes. These include decreased nephron mass with decreased ammonia production, decreased proton secretion, and hyperkalemia which suppresses ammoniagenesis; ultimately, all of these involve the production and trapping of ammonia (1). Metabolic acidosis often occurs early in CKD and leads to non–anion gap metabolic acidosis before the accumulation of organic anions that leads to the high anion gap–type acidosis seen in advanced CKD. The general approach to the treatment of this problem has evolved over the years and continues to evolve. For example, textbooks from the 1990s suggested that serum bicarbonate be kept >20 mmol/L to help alleviate the accompanying bone disease. Bone and mineral guidelines from a decade ago and to the present with Kidney Disease Improving Global Outcomes (KDIGO) have suggested that the HCO3− be kept at ≥22 mmol/L (2). In the past, the concern was primarily about the potential adverse effects on bone, including dissolution of bone to buffer the acid. However, it has also been recognized for many years that muscle and protein catabolism is increased by metabolic acidosis (3). The more recent CKD guidelines also point to evidence showing that acidosis also leads to inflammation, impaired glucose tolerance, cardiac dysfunction, and increased mortality (2). But perhaps most exciting, several studies have suggested that administration of bicarbonate (or other alkali) may slow progression of CKD, presumably by amelioration of acidosis, whether clinically apparent or not.

[学科分类] 泌尿医学

[关键词] Bone marrow necrosis;Sickle cell disease;Hyperhemolysis syndrome