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首页> 外文期刊>American Journal of Physiology >The ugly duckling of urinary acidification: what is the contribution of the thick ascending limb of the loop of Henle to urinary acidification?
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The ugly duckling of urinary acidification: what is the contribution of the thick ascending limb of the loop of Henle to urinary acidification?

机译：尿酸化的丑陋小鸭：厚度升高的升高肢体对尿酸化的贡献是什么？

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the kidney excretes acid in the form of titratable acidity and ammonium as well as in the form of free protons. The latter causes urinary acidification together with the reabsorption of filtered bicarbonate. Inborn or acquired forms of renal tubular acidosis (RTA) reduce the capacity of the kidneys to form ammonium and excrete acids (9). According to the functional defect and predominant site of renal damage, different subtypes of RTA have been classified: type I or distal RTA (dRTA), describing defects localized in the connecting tubule and collecting duct; type II or proximal RTA, caused by defects in the proximal tubule, and type IV or hyperkalemic RTA, summarizing different causes of relative aldosterone insufficiency or resistance in the distal nephron. Some authors use also the term type III RTA or combined RTA, referring to a mixed proximal and distal nephron pathology. Clinically, the distinction of these RTA subtypes depends on the detection of normal anion gap metabolic acidosis for all subtypes combined with bicarbonaturia or other signs of proximal tubule dysfunction (Fanconi syndrome) for type II proximal RTA or inappropriately alkaline urine in the face of metabolic acidosis for type I dRTA and the presence of hyperkalemia for type IV RTA. However, this distinction may not always be as obvious as it seems as compensatory mechanisms may mask overt metabolic acidosis or only partial defects may be present. Thus, specific provocation tests challenging the kidneys' capability to reab-sorb bicarbonate or to produce maximally acidic urine are routinely used to unmask such defects. To date, two types of urinary acidification tests are in clinical use: the ammonium chloride loading test and the furosemide-fludrocortisone (F+F) test. The ammonium chloride loading test introduced by O. Wrong in the 1950s provides a metabolic acid load where hepatic metabolism of ammonium releases protons to be excreted by the kidney (21). A failure of the kidney to acidify urine below pH 5.3 (or, in some centers, 5.5) is diagnostic for type I dRTA. This test, although very reliable and serving as the "gold standard," is very unpleasant for patients as ammonium chloride is poorly palatable and may cause nausea and vomiting. Alternatively, the F+F test may be used, combining a mineralocorticoid such as fludrocortisone with a loop diuretic such as furosemide. This test was first introduced as a single application of furosemide by D. Batlle (1) aiming to provide pathophysiological insights and distinction into different causes of type I dRTA.
机译：肾脏以可滴定的酸度和铵的形式排出酸，也以自由质子的形式排出酸。后者使尿酸化与过滤碳酸氢盐的重吸收。生成或获得的肾小管酸中毒（RTA）降低了肾脏形成铵和排泄酸的能力（9）。根据肾损伤的功能缺陷和主要位点，rta的不同亚型已被分类：I型或远端RTA（DRTA），描述了在连接管和收集管道中局部定位的缺陷; II型或近端RTA，由近端小管中的缺陷和IV型或高痛RTA引起，总结了相对醛固酮不足或抗性在远端肾上的不同原因。一些作者还使用III型RTA或组合RTA，参考混合的近端和远端肾神经学。在临床上，这些RTA亚型的区别取决于所有亚型的正常阴离子间隙代谢酸中毒的检测与双碳酸纤维尿剂（FANCONI综合征）联合的所有亚型，面对代谢酸中毒的近端RTA或不恰当的碱性尿液对于I型DRTA以及IV型RTA的HyperKalemia的存在。然而，这种区别可能并不总是显而易见，因为似乎可以掩盖明显的代谢酸中毒或仅存在部分缺陷。因此，具体的挑衅试验将肾脏碳酸酯碳酸酯或产生最大酸性尿液挑战肾脏的能力，用于揭示这种缺陷。迄今为止，两种类型的尿酸化试验处于临床用途：氯化铵负载试验和呋塞米 - 氟甲基罗（F + F）试验。由O.错误引入的氯化铵负载试验在20世纪50年代中提供了一种代谢酸负载，其中铵的肝脏代谢释放由肾脏排出的质子（21）。肾脏的失败酸化尿液低于pH5.3（或在一些中心，5.5）是I型DRTA的诊断。这项测试虽然非常可靠和用作“黄金标准”，但氯化铵很难令人难以愉快，氯化铵很差，可能导致恶心和呕吐。或者，可以使用F + F试验，与诸如呋喃西胺如呋脲胺的环利尿剂组合，例如Fludrocortisone。首先将该测试作为D. Batlle（1）作为呋塞米的单一应用，旨在提供病理生理学洞察和区别于I型DRTA的不同原因。

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