Ambühl P M
Klinik für Nephrologie, Universitätsspital, Zürich.
Ther Umsch. 2006 Sep;63(9):601-7. doi: 10.1024/0040-5930.63.9.601.
Intrinsic defects in tubular transport mechanisms of the kidney may cause impairment of urinary acidification or a loss of base equivalents, thereby inducing systemic metabolic acidosis. Different types of this disorder termed renal tubular acidosis (RTA) can be distinguished based on the localization of the disturbance along the nephron (proximal vs. distal) and their association with potassium transport (hypo-/hyperkalemic). Except for the proximal type RTA results in positive acid balance and negatively impacts on bone metabolism and the formation of kidney stones. The diagnosis is based on analysis of acid/base status, urinary pH and determination of ammonium excretion after an oral acid load. Both functional defects of specific tubular transport mechanisms and global impairment of renal tubular function can be causative of RTA. Their therapy is based on treatment of the primary disease process and correction of acidosis by alkali supplementation.
肾脏肾小管转运机制的内在缺陷可能导致尿酸化受损或碱当量丢失，从而引发全身性代谢性酸中毒。根据沿肾单位（近端与远端）的干扰定位及其与钾转运的关联（低钾血症/高钾血症），可以区分出不同类型的这种疾病，称为肾小管酸中毒（RTA）。除了近端型RTA外，都会导致正酸平衡，并对骨代谢和肾结石的形成产生负面影响。诊断基于酸碱状态分析、尿液pH值以及口服酸负荷后铵排泄的测定。特定肾小管转运机制的功能缺陷和肾小管功能的整体损害都可能是RTA的病因。其治疗基于原发性疾病过程的治疗以及通过补充碱来纠正酸中毒。
