Hypertension is a common cause of chronic kidney disease (CKD) and even more common sequelae of CKD. While strict control of blood pressure is essential to preserve residual renal function, numerous clinical trials have demonstrated that inhibitors of the renin-angiotensin system (RAS), i.e. angiontensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB), reduce the progression of CKD. These studies have examined type I and type II diabetic as well as non-diabetic nephropathies, utilizing end points such as serum creatinine, glomerular filtration rate, time to end-stage renal disease (ESRD), and death. These observations suggest that drugs blocking the RAS offer advantages beyond lowering blood pressure in diabetic and non-diabetic CKD. Therefore, guidelines recommend antihypertensives that block RAS in patients with CKD. Previous studies emphasized amelioration of glomerulosclerosis induced by glomerular hypertension as a renoprotective mechanism of inhibition of RAS. It should also be noted that progression to ESRD is mediated by two final common pathways; tubulointerstitial injury induced by proteinuria, and chronic hypoxia in the tubulointerstitium. Recent research indicates that reduction of proteinuria and improvement of oxygenation of the kidney are crucial mechanisms by which inhibition of RAS mediates renoprotection providing additional rationale for the use of ACEi and ARB to protect the kidney.
Keywords: hypertension, angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, kidney failure, hypoxia, tubulointerstitial injury
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