The aetiology of hypertension after renal transplantation in man.

Abstract

Abstract The renin-angiotensin-aldosterone system was studied in renal allograft patients, 70 per cent of whom were hypertensive. Plasma-renin levels were found to be normal, and a normal increase was observed when patients were changed from the supine to the erect posture (P<0.01). However, aldosterone-secretion rates were found to be approximately four times normal, and a positive correlation between these values and diastolic blood-pressure was observed (r = 0-5, P = 0-05). In patients with intact kidneys a highly significant correlation between plasma-renin activity and aldosterone-secretion rate was observed (r = 0.8, P>0.05), but this normal correlation was not apparent in the patients with transplanted kidneys (r = 0.1, P>0.5). Thus the aldosterone-secretion rates in these patients was not under the control of the renin-angiotensin system. Concurrent studies in adrenalectomized patients showed that they also had elevated aldosteronesecretion rates, and the injection of 14C-labelled cortisone acetate showed that they were capable of converting this steroid into aldosterone or an aldosterone-like metabolite. It is suggested that the hypertension seen after renal transplantation is related to the conversion of prednisone to a mineralocorticoid. Further support for this hypothesis was obtained from studies in patients who had their therapy changed from daily prednisone to alternate-day methylprednisolone. They were found to secrete less aldosterone and all the patients became normotensive following this régime (P >0.1). In addition, patients treated with an aldosterone antagonist, spironolactone, showed a prompt decrease in blood-pressure. It is concluded that the denervated transplanted kidney is able to maintain normal blood-pressure homeostasis in man, and that hypertension Seen after renal allografting is largely due to the therapy with immunosuppressive steroids.