Recovery from renal failure in malignant hypertension associated with primary aldosteronism: effect of an ACE inhibitor

Department of Internal Medicine III

K. Watanabe

Department of Pathology, Fukushima Medical University School of Medicine, Fukushima, Japan Primary aldosteronism is one of the most common causes of secondaryhypertension. However, it is rare for this disease to inducemalignant hypertension associated with vascular organ damage including renalfailure.¹ One of the reasons for this is that,even in the malignant phase, renin activity and subsequent angiotensin II production remain suppressed in primary aldosteronism. Here, we report a case with aldosterone-producing adenoma and increased renin activity complicated by malignant hypertension and renalfailure, which required haemodialysis therapy. This case is noteworthy, because medical therapy with angiotensin-converting enzyme (ACE) inhibitor effectively improved renal function, allowing discontinuation of dialysis.

A 40-year-old woman consulted a physician on 2 January 2000,complaining of dyspnea, general fatigue, anorexia and headache. The patient appeared drowsy and her blood pressure was 260/140mmHg. Serum creatinine was 7.1 mg/dl and severe pleural effusionwas detected on chest X-ray. Optic fundi exhibited papilloedemaand haemorrhage (Keith-Wagener's grade IV). She was admitted to hospital and treated with antihypertensive drugs and intermittent haemodialysis, which was needed three times a week thereafter.Blood pressure was managed by continuous intravenous infusionof nicardipine, which effectively lowered blood pressure to 170/80 mmHg. As renal function had not improved, the patient was transferred to our hospital 2 weeks later. On admission, her height was 156 cm, weight 44 kg and blood pressure 180/80 mmHg while taking the medication described above. On auscultation,there was systolic ejection murmur at the apex and normal respiratory sounds. There was no abdominal or cervical bruit audible. A complete blood count showed normocytic normochromic anaemia. Arterial blood gas analysis indicated metabolic acidosis (pH 7.398, pO₂ 93.2 mmHg, pCO₂ 35.1 mmHg, HCO₃^- 21.2 mmol/l). Serum Na⁺, K⁺, Cl^-, blood urea nitrogen (BUN) and creatinine levels were 135 mEq/l, 5.3 mEq/l, 97 mEq/l, 74 mg/dl and 7.5 mg/dl, respectively. Plasma renin activity (PRA) was over 20 ng/ml/h (normal: 0.3–2.8) and the plasma aldosterone concentration (PAC) was 480 pg/ml (normal: 35–175). She was diagnosed as having malignant hypertension. Blood pressure was controlled at around 160/80 mmHg with multidrug therapy, which consisted of nifedipine, manidipine, doxazosine and then an ACE inhibitor, temocapril . Renal function improved gradually, and haemodialysis was discontinued . Renal biopsy was performed on 8 March 2001. On histological examination, markedreduction of the arterial lumen by mucoid intimal hyperplasiafocally involved by fibrinous matrix was observed, especiallyin the arcuate arteries and interlobular arteries. Electronmicroscopy demonstrated wrinkling and folding of the glomerular basement membrane. PRA was reduced to 0.9 ng/ml/h, although PAC remained elevated (750–940 pg/ml) (Figure 1). Abdominal computed tomography revealed a low-density mass with a diameterof 20 mm in the right adrenal gland. An adrenal scintigram using ¹²⁵I-iodocholesterol showed high uptake in the right adrenalgland compared to the left (right/left=4/1). Plasma cortisoland catecholamines and urinary secretion of 17-OHCS and 17-KSwere within the normal range. These findings indicated she hadprimary aldosteronism. After the diagnosis, spironolactone wasadministered and blood pressure decreased gradually from 170/80 to 120/70 mmHg. Subsequently, retroperitoneal laparoscopic adrenalectomywas performed on 29 June 2000. The resected adrenal tissue contained a golden-yellow mass (20x16 mm), consisting of clear cells histologically. Post-operatively, PAC declined sharply to 90 pg/ml and her bloodpressure was controlled at around 120/70 mmHg without antihypertensive drugs, except temocapril (2 mg/day). Serum BUN and creatinine decreased to 18 mg/dl and 1.9 mg/dl, respectively .After the patient was discharged, serum creatinine remained at 1.9–2.0 mg/dl for an observation period of one year.