The aetiology of hypertension after renal transplantation in man

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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 (P0.05), 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.