Aliskiren and perindopril reduce the levels of transforming growth factor-β in patients with non-diabetic kidney disease | Zendy

Sławomir Lizakowski | Zendy; Leszek Tylicki | Zendy; Marcin Renke | Zendy; Przemysław Rutkowski | Zendy; Zbigniew Heleniak | Zendy; Maja Sławińska-Morawska | Zendy; Ewa AleksandrowiczWrona | Zendy; Sylwia Małgorzewicz | Zendy; Piotr Rutkowski | Zendy

Open Access

Aliskiren and perindopril reduce the levels of transforming growth factor-β in patients with non-diabetic kidney disease

Author(s) -

Sławomir Lizakowski,

Leszek Tylicki,

Marcin Renke,

Przemysław Rutkowski,

Zbigniew Heleniak,

Maja Sławińska-Morawska,

Ewa AleksandrowiczWrona,

Sylwia Małgorzewicz,

Piotr Rutkowski

Publication year - 2012

Publication title -

american journal of hypertension

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.009

H-Index - 136

eISSN - 1941-7225

pISSN - 0895-7061

DOI - 10.1038/ajh.2012.14

Subject(s) - aliskiren , perindopril , medicine , endocrinology , renin inhibitor , placebo , renin–angiotensin system , excretion , kidney disease , plasma renin activity , kidney , urology , blood pressure , alternative medicine , pathology

It is highly likely that the rise in plasma prorenin and plasma renin during renin inhibitor treatment is induced at least as much by the fall in blood pressure (BP) as it is by the negative feedback of angiotensin II. This could potentially be harmful because high levels of renin and prorenin may stimulate the (pro)renin receptor, thus inducing profibrotic effects. To further understand this relationship, the influence of aliskiren on the urinary excretion of transforming growth factor-β1 (TGF-β1) and procollagen III N-terminal propeptide (PIIINP) was evaluated in patients with nondiabetic kidney diseases.

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