Hypertension following renal transplantation: the role of the host's kidney.
Renin, aldosterone and exchangeable sodium were measured in 38 hypertensive and 56 normotensive renal transplant recipients with good renal function and without renal artery stenosis. Response to competitive blockade of angiotensin II using saralasin was studied in 20 of the hypertensive group. Hypertension was uncommon when bilateral nephrectomy had been performed. When diseased kidneys remained in situ, blood pressure after transplantation correlated well with blood pressure on dialysis. Plasma renin activity was higher in hypertensive patients despite higher exchangeable sodium levels. Urinary aldosterone was also higher and correlated well with blood pressure and plasma renin activity. Angiotensin II blockade produced a fall in blood pressure proportional to plasma renin activity. These observations suggest that hypersecretion of renin is an aetiological factor in the hypertension of renal transplant recipients. It appears to act both through the stimulation of aldosterone secretion, with resultant salt retention, and through the direct vasoconstrictor action of angiotensin II. Since renin levels were lower in patients subjected to bilateral nephrectomy the source of the excess renin is probably the host's kidneys.
D000328:Adult; D000450:Aldosterone / Q000652:urine; D001794:Blood Pressure / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D016030:Kidney Transplantation; D008875:Middle Aged; D011183:Postoperative Complications / Q000503:physiopathology; D012083:Renin / Q000097:blood; D012504:Saralasin; D012964:Sodium / Q000378:metabolism; D014184:Transplantation, Homologous
D000450:Aldosterone; D012964:Sodium; D012083:Renin; D012504:Saralasin