Klaboch J, Opatrná S, Matoušovic K, Schück O
I.interni klinika fakulty UK a FN Plzen.
Vnitr Lek. 2012 Jul-Aug;58(7-8):519-24.
Renal function disorder is inevitably associated with metabolic acidosis. An adult produces approximately 1 mmol of acids/kg of body weight every day (3 mmol/kg in children), derived from metabolization of proteins from food. Development of metabolic acidosis in patients with kidney disease is based on accumulation of acids and insufficient production of bicarbonates; alkaline loss represents a marginal issue here limited to patients with type II renal tubular acidosis only. The prevalence of this disorder increases with declining glomerular filtration (GFR) from 2% in patients with GFR 1.0-1.5 ml/s/1.73 m2 to 39% in patients with GFR < 0.3 ml/s/1.73 m2 or, alternatively, to 19% in patients with GFR 0.25-0.3 ml/s/1.73 m2. Notwithstanding the primary cause of the renal disease, declining GFR is associated with compensatory increase in ammoniac production in residual nephrons. This is an adaptive mechanism aimed at maintaining sufficient elimination of acids despite reduced volume of functional tissue. However, an increased ammoniac production simultaneously becomes a stimulus for activation of the complement via an alternative route and is thus one of the factors contributing, through this induced inflammation, to progression of tubular interstitial fibrosis that subsequently leads to further GFR reduction. Metabolic acidosis has a number of severe adverse effects on the organism, e.g. deterioration of kidney bone disease through stimulation of bone resorption and inhibition of bone formation, inhibition of vitamin D formation, increased muscle catabolism, reduced albumin production, glucose metabolism disorder, increased insulin resistance, reduced production of thyroid hormones, increased accumulation of β2-microglobulin etc. Non-interventional studies suggest that alkali supplementation may slow down progression of chronic nephropathies. However, this approach, safe and inexpensive, has not been widely implemented in clinical practice yet. With respect to dialyzed patients, abnormal levels of bicarbonates are associated with increased mortality. Both metabolic acidosis and alkalosis, rather regularly seen in a considerable number of patients, have a negative effect on patient survival. Alkali substitution from a dialysis solution is the main pillar of metabolic acidosis management in patients on hemo- as well as peritoneal dialysis. Available technologies allow individualization of the treatment and this should be observed.
肾功能障碍不可避免地与代谢性酸中毒相关。成年人每天每千克体重产生约1毫摩尔酸（儿童为3毫摩尔/千克），这些酸来源于食物中蛋白质的代谢。肾病患者代谢性酸中毒的发生基于酸的蓄积和碳酸氢盐生成不足；碱丢失在此仅为II型肾小管酸中毒患者的一个次要问题。这种疾病的患病率随着肾小球滤过率（GFR）的下降而增加，从GFR为1.0 - 1.5 ml/s/1.73 m²的患者中的2%增加到GFR < 0.3 ml/s/1.73 m²的患者中的39%，或者在GFR为0.25 - 0.3 ml/s/1.73 m²的患者中为19%。尽管肾病的主要病因不同，但GFR下降与残余肾单位中氨生成的代偿性增加相关。这是一种适应性机制，旨在尽管功能组织体积减少但仍能保持足够的酸排泄。然而，氨生成增加同时会通过替代途径激活补体，因此是通过这种诱导的炎症促进肾小管间质纤维化进展进而导致GFR进一步降低的因素之一。代谢性酸中毒对机体有许多严重的不良影响，例如通过刺激骨吸收和抑制骨形成使肾性骨病恶化、抑制维生素D形成、增加肌肉分解代谢、减少白蛋白生成、葡萄糖代谢紊乱、胰岛素抵抗增加、甲状腺激素生成减少、β2 - 微球蛋白蓄积增加等。非干预性研究表明补充碱可能会减缓慢性肾病的进展。然而，这种安全且廉价的方法在临床实践中尚未得到广泛应用。对于透析患者，碳酸氢盐水平异常与死亡率增加相关。代谢性酸中毒和碱中毒在相当数量的患者中相当常见，二者均对患者生存有负面影响。透析液中的碱替代是血液透析和腹膜透析患者代谢性酸中毒管理的主要支柱。现有技术允许治疗个体化，应予以遵循。
