A Case of Hyperreninemic Hypertension with Bilateral Positive Captopril Renography but without Renovascular Stenosis

383 Hypertens Res Vol.31 (2008) No.2 p.383-386 Case Report A Case of Hyperreninemic Hypertension with Bilateral Positive Captopril Renography but without Renovascular Stenosis Takafumi OKURA1), Jun IRITA1), Daijiro ENOMOTO1), Seiko MANABE1), Mie KURATA1), Ken-ichi MIYOSHI1), Tomikazu FUKUOKA1), and Jitsuo HIGAKI1) A 34-year-old woman was admitted to our hospital because of hypertension with hypokalemia. Her past medical history revealed that at age 24 she had been diagnosed with left renal lithiasis and had undergone extracorporeal shock-wave lithotripsy (ESWL). Physical examination showed that her peripheral pulses were intact and no peripheral edema or audible bruits were detected. Her serum potassium concentration was 2.7 mEq/mL, her plasma aldosterone concentration (PAC) was 96.7 ng/dL, and her plasma renin activity (PRA) was 28.1 ng/mL/h. Intrarenal lobar artery flow pattern assessed by Doppler ultrasound showed no abnormality. A renogram demonstrated a normal symmetrical tracing pattern. However, administration of 50 mg captopril induced delayed transit of tracer in both kidneys. Selective angiographic studies showed no stenotic lesions in the proximal to distal renal arteries. Blood sampling from each renal vein showed no laterality of PRA. While the possibility of the Page kidney phenomenon resulting from ESWL could not be excluded completely, the patient was diagnosed as a very rare case of hyperreninemic essential hypertension with positive captopril renography in both kidneys. (Hypertens Res 2008; 31: 383–386) Key Words: hyperreninemia, renovascular stenosis, captopril renography Introduction Case Report The common cause of renovascular hypertension (RVH) in elderly subjects is renal stenosis caused by atherosclerosis and that in young women is medial fibromuscular dysplasia (1). Captopril renography is a very useful technique for diagnosing RVH, since it has a sensitivity and specificity of approximately 90%, for each (2, 3). Captopril renography has been shown to detect bilateral abnormalities in the presence of renal failure (4, 5) and also in a case of atherosclerotic lesions involving both renal arteries (6). We report a rare case of hyperreninemic hypertension with abnormal bilateral captopril renography in the absence of renal artery stenosis and renal failure. A 34-year-old woman was admitted to our hospital because of hypertension with hypokalemia. On admission, her blood pressure was 176/110 mmHg despite the fact that she was taking antihypertensive medication (amlodipine 5 mg, which was discontinued after the admission). Her past medical history showed that at age 24 she had been diagnosed with left renal lithiasis and had undergone extracorporeal shock-wave lithotripsy (ESWL). At 3 months before administration of ESWL, she had a checkup for a headache in a local doctor’s office. She was diagnosed with hypertension with hypokaremia for the first time and treated with amlodipine. No other medication including diuretics was taken until the admission. Physical examination did not reveal signs of the excessive From the 1)Department of Integrated Medicine and Informatics, Ehime University Graduate School of Medicine, Toon, Japan. Address for Reprints: Takafumi Okura, M.D., Ph.D., Department of Integrated Medicine and Informatics, Ehime University Graduate School of Medicine, Shitsukawa, Toon 791–0295, Japan. E-mail: Received April 9, 2007; Accepted in revised form September 2, 2007. 384 Hypertens Res Vol. 31, No. 2 (2008) A B Fig. 1. A basic renogram of a normal symmetrical tracing pattern (A). Administration of 50 mg of captopril induced delayed transit of tracer in both kidneys (B). adrenocortical steroid levels seen in Cushing’s syndrome. Her height was 150 cm and body weight was 44 kg. All peripheral pulses were intact and no peripheral edema or audible bruits were detected. Urine examination showed no hematuria or cast, although the 24-h excretion of protein was 3.7 g. The urinary excretions of potassium and chloride were 35.2 mEq/ day and 81.4 mEq/day, respectively. Serological evaluation for immunoglobulins, complement, anti-nuclear antibodies, antineutrophic cytoplasmic antibody and hepatitis B and C virus were all negative. Biochemical assays showed a serum potassium concentration of 2.7 mEq/mL, serum creatinine concentration of 0.5 mg/dL, plasma aldosterone concentration (PAC) of 96.7 ng/dL and plasma renin activity (PRA) of 28.1 ng/mL/h. Administration of 50 mg captopril caused a marked decrease in blood pressure to pre-shock levels (98/64 mmHg) at 1 h after administration, associated with a further elevation in PRA (44.7 to 64.1 ng/mL/h) and a reduction in PAC (53.5 to 36.2 ng/dL). Ultrasonography revealed normal symmetrical kidneys, with the length of the right measuring 94 mm and that of the left 95 mm. A Doppler ultrasound of the intrarenal lobar arteries showed that the pulsatility index ([max pulse wave velocity − minimum pulse wave velocity]/ mean pulse wave velocity; PI) and resistive index ([max pulse wave velocity − minimum pulse wave velocity]/max pulse wave velocity; RI) were both within the normal range. A renogram using Tc-99m mercaptoacetyltriglycine (MAG3) demonstrated a normal symmetrical tracing pattern (Fig. 1A). However, administration of 50 mg captopril induced delayed transit of tracer in both kidneys (Fig. 1B). These captopril administration tests suggested that the patient’s high blood pressure level was due to bilateral RVH. We next performed computed tomographic renal angiography and selective renal angiography (Fig. 2). These angiographic studies showed no stenotic lesions in the proximal to distal renal arteries. Selective blood sampling from each renal vein showed no laterality of renin secretion. On the basis of these clinical findings, the patient was diagnosed with hyperreninemic essential hypertension. During hospitalization, her blood pressure remained high and the hypokaremia continued, so she was treated with 25 mg spironolactone and 5 mg bisoprolol. After 2 weeks of this treatment, her blood pressure decreased to 122/80 mmHg, her proteinuria fell to 0.4 g/day and her serum potassium level was normalized, without an elevation in creatinine. Discussion In this paper we report the case of a hypertensive patient with hypokalemia due to hyperreninemia and hyperaldosteronism without renal artery stenosis. Secondary hyperaldosteronism and a hyperreninemic state are usually observed in patients with RVH. Angiographically, we did not detect stenosis in the Okura et al: A Case of Hypertension with Hyperreninemia Right renal artery 385 Left renal artery Fig. 2. Selective renal angiography showed no stenotic lesions in the proximal to distal renal arteries in both kidneys. proximal to distal renal arteries in either kidney. Reviewing the patient’s medical history, we noted she had undergone ESWL 10 years previously. ESWL has been reported to initiate the development of hypertension with hyper (...truncated)