THE PATHOGENESIS OF HYPERTENSION IN AUTOSOMAL-DOMINANT POLYCYSTIC KIDNEY-DISEASE

Citation
D. Wang et S. Strandgaard, THE PATHOGENESIS OF HYPERTENSION IN AUTOSOMAL-DOMINANT POLYCYSTIC KIDNEY-DISEASE, Journal of hypertension, 15(9), 1997, pp. 925-933
Citations number
121
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
02636352
Volume
15
Issue
9
Year of publication
1997
Pages
925 - 933
Database
ISI
SICI code
0263-6352(1997)15:9<925:TPOHIA>2.0.ZU;2-H
Abstract
Background Hypertension is a common and serious complication of autoso mal dominant polycystic kidney disease (ADPKD), often occurring early in the disease before the renal function starts to decrease, The patho genesis of this early hypertension is controversial. Objective To revi ew studies on the pathogenesis of early and late hypertension in ADPKD , Study selection Studies on ADPKD and hypertension were retrieved fro m Medline from the last 20 years, with an emphasis on the last 10 year s. These studies, together with selected published abstracts from rece nt hypertension and nephrology meetings, were reviewed critically, Res ults Cyst growth, renal handling of sodium, activation of the renin-an giotensin-aldosterone system, volume expansion, an elevated plasma vol ume, and increased plasma atrial natriuretic peptide and plasma endoth elin levels have all been found to be associated with hypertension in ADPKD, In some studies an inappropriate activity of the renin-angioten sin-aldosterone system that could be related to cyst growth and intrar enal ischemia was found, An increase in renal vascular resistance has been demonstrated and might be caused by intrarenal release of angiote nsin II, Interestingly, the protective effect of angiotensin convertin g enzyme inhibitors on the renal function could not be demonstrated in ADPKD patients with a moderately decreased renal function. The import ance, if any, of endothelial vasodilatory factors is not known, Sympat hetic nervous activity seems to be increased in ADPKD, but the importa nce of this for the blood pressure level is not known. Conclusion The pathogenesis of hypertension in ADPKD is complex and likely to be depe ndent on the interaction of hemodynamic, endocrine and neurogenic fact ors.