[The role of arterial hypertension in developement of chronic renal failure]

The link between the kidney and hypertension has been considered a villain-victim relationship because of the potential two-way causality between high blood pressure (BP) and chronic kidney disease (CKD). Arterial hypertension (AH) per se, but also together with diabetes mellitus, is the most important cause of CKD and end-stage renal disease (ESRD) in the developed world. Pathophysiologicaly, the increment in systemic BP leads to the rise in glomerular pressure. Glomerular hypertension results in glomerular capillary wall stretch, endothelial damage and a rise in protein glomerular filtration. These processes, in turn, cause changes of mesangial and proximal tubular cells, ultimately resulting in the replacement of functional by non-functional connective tissue and the development of fibrosis. One of the most important factors in the progression of CKD is activation of the renin-angiotensin system (RAS). Its effect is not only elevated BP, but also the promotion of cell proliferation, inflammation and matrix accumulation. The terms that clinicians use to identify renal damage associated with hypertension are nephrosclerosis, benign nephrosclerosis, hypertensive kidney disease, or nephroangiosclerosis. Many studies, first in experimental animals and later in humans, have shown that the lowering of BP (and proteinuria) is associated with a slower progression of CKD. It seems that angiotensin-converting enzyme inhibitors (ACEI's) are more renoprotective than other antihypertensives (the protection beyond the antihypertensive effect), although some studies have also confirmed a comparatively beneficial effect of non-dihydropiridine calcium channel blockers (CCBs) and angiotensin II receptor blockers (ARBs). Moreover, it seems that a combination of antihypertensives (e.g. ACEI, CCB, and ARB) has a more effective action than either of the drugs alone. The effects depend first on the degree of BP reduction. The strict BP control has been considered the basis of therapy for slowing renal deterioration.