Osteopontin expression, tubulointerstitial disease, and essential hypertension.

Abstract A role has recently been proposed for the tubulointerstitium in the pathogenesis of salt-dependent essential hypertension. In this study, biopsies from patients with essential hypertension with either minimal (“benign”) or severe (“decompensated”) tubulointertitial injury were analyzed for the expression of osteopontin, a protein known to modulate tubulointerstitial damage and nitric oxide production. In biopsies from patients with decompensated arteriolosclerosis, osteopontin mRNA and protein were increased in tubules in association with expression of α-smooth muscle actin by interstitial fibroblasts and increased type IV collagen deposition. The relevance of these findings to the pathogenesis of essential hypertension is discussed.