a Division of Nephrology , Civil and University Hospital Santa Maria della Misericordia , Udine , Italy.
Scand J Clin Lab Invest. 2018 Feb-Apr;78(1-2):31-42. doi: 10.1080/00365513.2017.1408139. Epub 2017 Nov 29.
According to usual literature, the diet-dependent endogenous production of titratable acidity (TA) is contributed by sulphuric and phosphoric acids (NA) and by metabolizable acids (MAs), representing 'net-endogenous acid production' (NEAP). NEAP is mainly neutralised by diet-dependent [Formula: see text] salts of inorganic cations ([Formula: see text]), estimated in foods, faeces and urine from inorganic cation-anion difference (NB). It is claimed that urinary loss of organic acids' anions, '[Formula: see text]', induces metabolizable H ions' retention. Since '[Formula: see text]' is normally lost in urine as '[Formula: see text]' or '[Formula: see text]', no MA retention takes place. Therefore, in our approach, net acid production (NAP) reduces to endogenous sulphuric acidity only. Since in western diets (WDs) alkaline cations exceed inorganic anions (NB excess), acid excess from phosphorus is neutralized. Moreover, the renal reabsorption of ultra-filtered Pi takes place at [Formula: see text] ratios greater than '4/1', which means that the kidney operates as a dietary Pi-dependent NB generator ([Formula: see text] or [Formula: see text]). Since, in standard WDs, HSO generation is less than '[Formula: see text]' production, the sulphuric acidity escaping the intestinal [Formula: see text] absorption is neutralized by [Formula: see text] and excreted as diet-dependent [Formula: see text], without interfering in normal A/B status. Only when extreme acidifying diets are ingested, sulphuric acidity may exceed '[Formula: see text]'. In this case, the excess of sulphuric acidity production is neutralised by the intervention of urinary [Formula: see text] excretion, whose employment is normally restricted to prevent loss of ultra-filtered NB. Finally, the whole body NA balance (NAb(W)) is calculated from the difference 'NA - NA(u)', where abs = intestinal absorption and u = urinary excretion. Being 'NA ≈ NA(u)', NAb(W) approximates zero, confirming WDs as non-acidifying foods.
根据通常的文献，可滴定酸度（TA）的饮食依赖性内源性产生归因于硫酸和磷酸（NA）和可代谢酸（MA），代表“净内源性酸产生”（NEAP）。NEAP 主要由饮食依赖性无机阳离子的[公式：见文本]盐（[公式：见文本]）中和，这些盐在食物、粪便和尿液中通过无机阳离子-阴离子差（NB）估算。据称，有机酸盐阴离子的尿液损失，“[公式：见文本]”，会导致可代谢 H 离子的保留。由于“[公式：见文本]”通常作为“[公式：见文本]”或“[公式：见文本]”在尿液中丢失，因此不会发生 MA 保留。因此，在我们的方法中，净酸产生（NAP）减少到仅内源性硫酸酸度。由于在西方饮食（WDs）中，碱性阳离子超过无机阴离子（NB 过剩），因此磷的酸过剩被中和。此外，超滤液 Pi 的肾重吸收发生在[公式：见文本]比值大于“4/1”的情况下，这意味着肾脏作为饮食 Pi 依赖性 NB 生成器（[公式：见文本]或[公式：见文本]）运作。由于在标准 WDs 中，HSO 的生成小于“[公式：见文本]”的产生，因此逃脱肠道[公式：见文本]吸收的硫酸酸度被[公式：见文本]中和，并作为饮食依赖性[公式：见文本]排泄，而不会干扰正常的 A/B 状态。只有在摄入极端酸化饮食时，硫酸酸度才可能超过“[公式：见文本]”。在这种情况下，过量的硫酸酸度产生通过尿液[公式：见文本]排泄的干预来中和，这种排泄的使用通常受到限制，以防止超滤液 NB 的损失。最后，从“NA - NA(u)”的差异计算全身 NA 平衡（NAb(W)），其中 abs 是肠道吸收，u 是尿排泄。由于“NA ≈ NA(u)”，NAb(W)近似为零，证实 WDs 是非酸化食品。
