Pathophysiology of Post Transplant Hypertension in Kidney Transplant: Focus on Calcineurin Inhibitors Induced Oxidative Stress and Renal Sodium Retention and Implications with RhoA/Rho Kinase Pathway.

摘要: Post-transplant hypertension is a common occurrence during treatment with calcineurin inhibitors (CNIs) in kidney transplant population. The pathogenesis of vasoconstriction induced by CNIs involves vascular tone alterations and sodium transport regulation. Among the factors involved key role played activation intrarenal renin-angiotensin system enhanced release Angiotensin II (Ang II) increase oxidative stress. A pathway between stress may be identified involvement RhoA/Rho kinase pathway, for induction cardiovascular-renal remodeling, mediated increased nitric oxide (NO) metabolism renal retention via activity thiazide-sensitive chloride cotransporter (NCC) distal tubule. We examined literature data including those coming from our group regarding their remodeling. Based on available data, we have provided support to as an important effector pathophysiology post-transplant retention. Clarification how biochemical molecular mechanisms that regulate processes post work interact, would provide further insights not only into comprehension but could also positive impact clinical ground through identification significant targets. Their specific pharmacologic targeting might multiple beneficial effects whole function. demonstration transplanted patients post-transplanted hypertension, different antihypertensive drugs inducing comparable blood pressure reduction example related proteins and/or Rho retention, helpful choice these which takes advantage beyond reduction.