Abstract
To the Editor
The paper by Milroy and Parai (1) provides further useful evidence for basal vacuolization of renal tubular epithelial cells as a marker for ketoacidosis. Although it has been common practice to use the term “Armanni-Ebstein” to describe this type of histology (1, 2), a review of the literature shows that the original description by Armanni referred instead to a clear cell change (3, 4) that was related to glycogen accumulation (5). However, in recent years the umbrella of “Armanni-Ebstein” has been broadened to include lipid-containing subnuclear vacuoles (6, 7). To clarify this issue we have proposed that the term “Armanni Ebstein phenomenon” be better reserved for cases showing the originally described clear cell change (8). This phenomenon is linked to hyperglycemia and is associated with swelling, loss of shape, clearing of cytoplasm, and an accumulation of cytoplasmic glycogen in the tubular cells of the outer medulla. Conversely, “basal vacuolization” would be a more suitable term for cases showing vacuoles in a subnuclear location, with luminally displaced nuclei and an accumulation of lipids within tubular cells of the cortex, as well as in the outer zone of the me-dulla; a change associated with ketoacidosis (8, 9). The rationale for this distinction is that the two patterns of vacuolization appear both morphologically and pathophysiologically distinct -although they can coexist in conditions such as diabetic ketoacidosis. The advantage of having more precise definitions is that this may assist in further determining the sensitivity and specificity of each of these changes as markers for underlying metabolic disturbances, and may also help in elucidating the particular underlying biochemical and cellular processes that result in these specific changes (8).