Experimental models of distal renal tubular acidosis.
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.
DuBose
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Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
D000136:Acid-Base Equilibrium / Q000502:physiology; D000141:Acidosis, Renal Tubular / Q000139:chemically induced; D000450:Aldosterone / Q000172:deficiency; D000584:Amiloride / Q000633:toxicity; D000666:Amphotericin B / Q000633:toxicity; D000818:Animals; D006801:Humans; D007671:Kidney Concentrating Ability; D007684:Kidney Tubules / Q000503:physiopathology*; D008094:Lithium / Q000633:toxicity; D014050:Toluene / Q000633:toxicity; D014426:Turtles
D014050:Toluene; D000450:Aldosterone; D000584:Amiloride; D000666:Amphotericin B; D008094:Lithium