Expression of cell adhesion molecules in tubulointerstitial nephritis associated with Sjögren's syndrome.

The tissue distribution of cellular adhesion molecules (ICAM- I, ELAM- I, VCAM-1) was studied in specimens from six normal human kidneys and in six biopsies from kidneys with tubulointerstitial nephritis associated with Sjagren's syndrome. In addition, the expression of cellular adhesion molecules was examined both in four renal biopsies from cases of tubulointerstitial nephritis of diverse pathogenesis and in six lip biopsies from cases of Sjogren's syndrome. ICAM- I was expressed on vascular endothelial cells in normal kidneys, in all specimens of tubulointerstitial nephritis and in salivary glands. On tubular epithelial cells, ICAM-I appeared slightly in normal kidney;; otherwise tubular epithelial ICAM- I was observed in and around the foci of cellular infiltration in all cases of tubulointerstitial nephritis. ELAM- I and VCAM-I were observed on the newly generated vessels in massive cellular infiltrates in some cases of tubulointerstitial nephritis associated with Sjogren's syndrome; by contrast, they were not seen in normal kidneys and in cases of tubulointerstitial nephritis of diverse pathogenesis. In the lip biopsies from salivary glands, ICAM- I was observed on ductal epithelial cells in and around the foci of cellular infiltration, and ELAM-I and VCAM-I occasionally appeared on the newly generated vessels in massive cellular infiltrates. Chronic and progressive inflammation may be facilitated by such ELAM-I and VCAM-I expression on newly generated vessels. The adhesion molecules were thought to play a role in the pathogenesis of tubulointerstitial nephritis and sialoadenitis associated with Sjogren's syndrome. It was thus concluded that the same inflammatory process that took place in the salivary glands to induce the characteristic tissue change of Sjogren's syndrome likely was operative in the renal tubulointerstitial tissue as well.