Transforming growth factor-beta1 is associated with kidney damage in patients with essential hypertension: renoprotective effect of ACE inhibitor and/or angiotensin II receptor blocker.

Article Details

Citation

Zhu S, Liu Y, Wang L, Meng QH

Transforming growth factor-beta1 is associated with kidney damage in patients with essential hypertension: renoprotective effect of ACE inhibitor and/or angiotensin II receptor blocker.

Nephrol Dial Transplant. 2008 Sep;23(9):2841-6. doi: 10.1093/ndt/gfn159. Epub 2008 Apr 5.

PubMed ID
18390891 [ View in PubMed
]
Abstract

BACKGROUND: Evidence suggests that transforming growth factor-beta1 (TGF-beta(1)) is associated with target organ damage in hypertension. This study aimed to investigate the relationship between TGF-beta(1) 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-beta(1), plasma angiotensin (Ang) II and urinary albumin were quantified by immunoassays. RESULTS: Serum TGF-beta1, plasma Ang II and ACR were highly elevated in patients with EH (P < 0.01). There was a positive correlation between serum TGF-beta1 levels and ACR (r = 0.53, P < 0.01). Significant decreases in TGF beta1 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-beta(1) is highly elevated and strongly associated with urinary albumin excretion in patients with EH. Treatment with benazepril or valsartan attenuates serum TGF-beta(1) levels and microalbuminuria with the combined therapy receiving the greater effect. TGF-beta(1) could be a potential surrogate marker in monitoring the development and progression of kidney damage in EH.

DrugBank Data that Cites this Article

Pharmaco-proteomics
DrugDrug GroupsGeneGene IDChangeInteractionChromosome
BenazeprilApproved InvestigationalAGT183
decreased
benazepril results in decreased expression of AGT protein1q42.2
BenazeprilApproved InvestigationalTGFB17040
decreased
benazepril results in decreased expression of TGFB1 protein19q13.1
ValsartanApproved InvestigationalAGT183
increased
Valsartan results in increased expression of AGT protein1q42.2
ValsartanApproved InvestigationalAGT183
increased
Valsartan results in increased expression of AGT protein1q42.2
ValsartanApproved InvestigationalTGFB17040
decreased
Valsartan results in decreased expression of TGFB1 protein19q13.1
ValsartanApproved InvestigationalTGFB17040
decreased
Valsartan results in decreased expression of TGFB1 protein19q13.1