Mean serum potassium levels were significantly higher for 9 months in renal allograft recipients receiving cyclosporin than in those receiving prednisolone and azathioprine. Sustained hyperkalaemia (serum potassium 6.0-7.1 mmol/l) inappropriate for their renal function (glomerular filtration rate 21-36 ml/min) developed in seven of forty-three cyclosporin-treated patients. All seven patients had hyperchloraemic acidosis; four were able to acidify their urine to pH less than or equal to 5.4. Six of the seven patients were hypertensive and receiving beta-blockers; one had had bilateral nephrectomy. Despite hyperkalaemia, plasma aldosterone levels were within the normal range in five patients and raised in two. During moderate sodium restriction, plasma renin activity was low or low-normal in five of the seven patients. In these patients a combination of hypoaldosteronism and renal tubular damage leading to a tubular defect of potassium and hydrogen ion secretion is the apparent cause of the hyperkalaemia and hyperchloraemic acidosis. Hyporeninaemia caused by beta-blockade probably blunts the aldosterone response to hyperkalaemia, thereby worsening it.