Transforming growth factor-β1 is associated with kidney damage in patients with essential hypertension: renoprotective effect of ACE inhibitor and/or angiotensin II …

S Zhu, Y Liu, L Wang, QH Meng - Nephrology Dialysis …, 2008 - academic.oup.com
S Zhu, Y Liu, L Wang, QH Meng
Nephrology Dialysis Transplantation, 2008academic.oup.com
Background. Evidence suggests that transforming growth factor-β1 (TGF-β1) is associated
with target organ damage in hypertension. This study aimed to investigate the relationship
between TGF-β1 levels and kidney damage and renoprotective effects of angiotensin-
converting enzyme inhibitor and/or angiotensin II type 1 receptor blocker in patients with
essential hypertension (EH). Methods. A total of 156 patients with EH were enrolled and
grouped according to albumin-to-creatinine ratio (ACR). Of these, 90 patients with EH …
Abstract
Background. Evidence suggests that transforming growth factor-β1 (TGF-β1) is associated with target organ damage in hypertension. This study aimed to investigate the relationship between TGF-β1 levels and kidney damage and renoprotective effects of angiotensin-converting enzyme inhibitor and/or angiotensin II type 1 receptor blocker in patients with essential hypertension (EH).
Methods. A total of 156 patients with EH were enrolled and grouped according to albumin-to-creatinine ratio (ACR). Of these, 90 patients with EH underwent a 12-week antihypertensive trial with administration of benazepril, valsartan or both. Serum TGF-β1, plasma angiotensin (Ang) II and urinary albumin were quantified by immunoassays.
Results. Serum TGF-β1, plasma Ang II and ACR were highly elevated in patients with EH (P < 0.01). There was a positive correlation between serum TGF-β1 levels and ACR (r = 0.53, P < 0.01). Significant decreases in TGF β1 and ACR were obtained in all groups at the end of 12-week antihypertensive therapy compared to the baseline values, with the combined group to a greater extent (P < 0.01). Plasma Ang II levels were significantly decreased in the benazepril group but increased in the valsartan group (P < 0.05) while no significant change was observed in the combined group.
Conclusions. TGF-β1 is highly elevated and strongly associated with urinary albumin excretion in patients with EH. Treatment with benazepril or valsartan attenuates serum TGF-β1 levels and microalbuminuria with the combined therapy receiving the greater effect. TGF-β1 could be a potential surrogate marker in monitoring the development and progression of kidney damage in EH.
Oxford University Press