Developments in molecular biology have led to major improvements in our understanding of the physiology and pathophysiology of renal tubular function. It is now possible to subdivide the various types of renal tubular acidosis, for example, by the precise biochemical defect rather than simply the tubular location. Thus, distal (or type 1) RTA may be a consequence of impaired distal tubular H+ excretion, either due to increased permeability to H+ or to impaired secretion, the latter, in turn, being a consequence of a variety of defects that include carbonic anhydrase type 2 deficiency, mutations in anion transport protein AE1, or deficiency of collecting duct proton transport ATPase. Whilst specific knowledge of the molecular defect is not necessary to either diagnose or manage these disorders, it is likely that future classification of acid-base disorders will change to recognize the underlying defect.
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