The role of arterial hypertension in the progression of non-diabetic glomerular diseases.
Arterial hypertension (AH) per se is, together with diabetes mellitus, the most important cause of renal failure and of dialysis in the western world. AH is also a well known consequence of chronic renal disease, and at the same time one of the main factors which causes diabetic and/or non-diabetic chronic renal failure progression. AH is mostly registered in patients with focal segmental glomerulosclerosis and with membranoproliferative glomerulonephritis. The pathophysiology and the mechanism of AH within primary glomerular diseases are complex, including activation of the sympathetic nervous system, the renin-angiotensin system (RAS), sodium retention, volume expansion and decreased synthesis of vasodilatatory substances. As autoregulation of glomerular pressure in chronic glomerular disease is disturbed, the increment in systemic blood pressure 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 chronic renal failure is activation of the RAS. Its effect is not only elevated blood pressure, but also the promotion of cell proliferation, inflammation and matrix accumulation. Many studies, first in experimental animals and later in humans, have shown that the lowering of blood pressure (and proteinuria) is associated with a slower progression of kidney disease. It seems that angiotensin-converting enzyme inhibitors (ACEIs) 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, ACEI + ARB) has a more effective action than either of the drugs alone. However, the effects depend first on the degree of blood pressure reduction. According to comprehensive studies, the achievement of adequate blood pressure (not higher than 130/85 mmHg) is the most important factor. An even lower blood pressure (125/75 mmHg) has been suggested as the limit value in patients with proteinuria of >1 g/24 h and in Blacks.
Ljutić
Dragan
D
Clinical Hospital Split, Split and. Clinical Hospital Centre 'Rebro', Zagreb, Croatia. dragan.ljutic@st.hinet.hr
Kes
Petar
P
D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001795:Blood Pressure Determination; D015897:Comorbidity; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005921:Glomerulonephritis / Q000175:diagnosis* / Q000453:epidemiology* / Q000517:prevention & control; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology*; D007676:Kidney Failure, Chronic / Q000175:diagnosis / Q000453:epidemiology* / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D016032:Randomized Controlled Trials as Topic; D012084:Renin-Angiotensin System / Q000502:physiology*; D018570:Risk Assessment; D012720:Severity of Illness Index; D016896:Treatment Outcome
D000959:Antihypertensive Agents