DuBose T D
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
Semin Nephrol. 1990 Mar;10(2):174-80.
A number of potential defects may impair acidification either directly or indirectly in the CCT, the OMCT, the IMCD, or in all segments. These defects are summarized in Table 1. Findings from studies in animal models of DRTA have enhanced out understanding of the pathophysiological basis of these disorders. Nevertheless, considerable effort needs to be directed in the future toward defining the cellular basis of these defects, especially in the inherited forms of classical hypokalemic DRTA, for which an adequate experimental model does not yet exist.
许多潜在缺陷可能直接或间接损害皮质集合管（CCT）、外髓集合管（OMCT）、内髓集合管（IMCD）或所有节段的酸化功能。这些缺陷总结于表1中。对远端肾小管酸中毒（DRTA）动物模型的研究结果加深了我们对这些疾病病理生理基础的理解。然而，未来仍需投入大量精力来明确这些缺陷的细胞基础，尤其是在经典低钾性DRTA的遗传形式中，目前尚无合适的实验模型。
