Key result
Tubular osteopontin expression is linked to renal interstitial fibrosis in decompensated hypertensive arteriolosclerosis.
Cross-Sectional
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 alpha-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.
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Thomas et al. (1998) conducted a cross-sectional in Essential hypertension. Severe (decompensated) tubulointerstitial injury vs. Minimal (benign) tubulointerstitial injury was evaluated on Osteopontin mRNA and protein expression. In patients with essential hypertension and decompensated arteriolosclerosis, osteopontin mRNA and protein were increased in tubules in association with interstitial fibroblasts and type IV collagen.