LAUSR

Sir, We would like to thank Professor Madea and his colleagues for their very pertinent comments about the etiology of both Armanni–Ebstein, or the so-called clear-cell, change and basal lipid vacuolization in renal tubular epithelial cells, as detailed in our recent paper (1,2). We agree completely that the pathogenesis of both clear-cell change and basal vacuolization is complex and undoubtedly interrelated to a variety of underlying metabolic disturbances (3–5). As in many situations, the morphological response of tissues is likely to be relatively limited, with similar phenotypes possibly arising from a wide variety of insults and pathological processes. We were pleased, however, to have clarified that the original studies by both Armanni and Ebstein referred to clear-cell change rather than to subnuclear basal vacuolization (6). Madea et al.’s study correlating the level of ketones in various bodily fluids with the amount of fat staining in renal tubular cells serves to demonstrate that there may be a “dose relationship” between the amount of ketones that renal tubular cells are exposed to and their subsequent accumulation of lipid. It also supports our recent findings that the incidence of basal lipid vacuolizations increases with the degree of ketoacidosis (7). Unfortunately, we were limited in our own studies by the lack of tissues available for oil red-0 staining and so cannot comment meaningfully on whether we could replicate that particular finding. However, the suggestion that lipid staining should form a routine part of the assessment of renal tubular vacuolization is well made.